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41 publications mentioning mmu-mir-455

Open access articles that are associated with the species Mus musculus and mention the gene name mir-455. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 371
These data demonstrate that miR-455-3p can inhibit the expression of DNMT3A to regulate DNA methylation of cartilage-specific genes, thus regulating pathways such as the PI3K-Akt signaling pathway and ultimately inhibiting the cartilage degeneration during chondrogenic differentiation. [score:9]
The increased expression of miR-455-3p and decreased expression of DNMT3A upregulate cartilage-specific genes and pathways, thereby attenuating cartilage degeneration during chondrogenic differentiation. [score:8]
Our previous study showed that miR-455-3p functions as an activator for early chondrogenic differentiation of ATDC5 cells, and directly targets and inhibits the expression of Runt-related transcription factor 2 (RUNX2) [15]. [score:8]
Overexpression of miR-455-3p upregulated p-Akt expression (Fig.   5b−f). [score:8]
Moreover, our results also demonstrated that miR-455-3p targets the 3′-UTR of DNMT3A mRNA and downregulates its expression. [score:8]
Our study reveals that overexpression of miR-455-3p inhibits matrix degeneration and increases the expression of the cartilage-specific genes COL2A1, COL11A1, and SOX6 during the degenerate stage of chondrogenic differentiation (days 21−35). [score:7]
miR-455-3p overexpression downregulates the DNA methylation of cartilage development-related genes such as SOX6 and Smad3. [score:7]
miR-455-3p inhibits the expression of DNMT3A, and DNMT3A also modulated expression of miR-455-3p. [score:7]
Meanwhile, inhibition of miR-455-3p resulted in a significant increase in the expression of DNMT3A and a decrease in SOX9 expression (Fig.   2d−f). [score:7]
Overexpression of miR-455-3p inhibits the degenerate process during chondrogenic differentiation by regulating DNA methylation of cartilage development-related genes and pathways. [score:7]
negative controls, respectively To further investigate whether miR-455-3p regulates DNMT3A expression in vitro and in vivo, we inhibited and overexpressed miR-455-3p. [score:6]
Notably, safranin O staining showed that overexpression of miR-455-3p did not affect cartilage development between days 0 and 14, but later inhibited matrix degeneration from days 21 to 35 (Fig.   4a). [score:6]
High expression levels of miR-455-3p can inhibit degeneration of the cartilage matrix and increase the expression of cartilage-specific genes, and miR-455-3p deletion mice showed accelerated cartilage degeneration compared with wild mice. [score:6]
We have demonstrated that miR-455-3p inhibits the degeneration process during the chondrogenic differentiation of hBMSCs, and directly targets DNMT3A by interaction with the 3′-UTR. [score:6]
MiR-455 is located in an intronic region of COL27A1 [24], Swingler et al. reported that miR-455-3p is highly expressed during the chondrogenesis of ATDC5 cells, and that it regulates TGFβ signaling and suppresses the Smad2/3 pathway [25]. [score:6]
Using miRNA target prediction algorithms, we found that miR-455-3p has a potential target in DNMT3A, which does regulate DNA methylation. [score:6]
Our results demonstrated that miR-455-3p regulated the expression of DNMT3A, and DNMT3A also modulated miR-455-3p expression in vitro. [score:6]
To further investigate whether miR-455-3p regulates DNMT3A expression in vitro and in vivo, we inhibited and overexpressed miR-455-3p. [score:6]
We also demonstrated that miR-455-3p promotes chondrogenic differentiation by suppressing the expression of HDAC2 and HDAC8, thereby maintaining an appropriate level of histone H3 acetylation at the COL2A1 promoter to promote the production of type II collagen [14]. [score:5]
negative controls, respectively Our previous study [14] revealed that while moderate and high levels of miR-455-3p expression were detected in proliferating and prehypertrophic chondrocytes, little to no miR-455-3p expression was observed in hypertrophic chondrocytes in vivo by in situ hybridization in E16.5 mouse limbs. [score:5]
Overexpression of miR-455-3p and the use of a DNA methylation inhibitor could optimize the process of chondrogenic differentiation. [score:5]
Together these data indicate that miR-455-3p does modulate DNMT3A expression by binding to the 3′-UTR, and that DNMT3A is a target of miR-455-3p. [score:5]
Normal chondrocytes were transfected with miR-455-3p mimic, a non-specific control (NC) mimic, miR-455-3p inhibitor, NC inhibitor. [score:5]
Fig. 2Normal chondrocytes were transfected with miR-455-3p mimic, a non-specific control (NC) mimic, miR-455-3p inhibitor, NC inhibitor. [score:5]
TargetScan analysis identified DNMT3A as a potential target of hsa-miR-455-3p (Fig.   3a). [score:5]
Treatment with DNMT3A siRNA resulted in significantly decreased expression of DNMT3Aand H3K4me3 (Fig.   2n, o), and increased expression of miR-455-3p, aggrecan, and SOX9 (Fig.   2n−p). [score:5]
negative controls, respectivelyOur previous study [14] revealed that while moderate and high levels of miR-455-3p expression were detected in proliferating and prehypertrophic chondrocytes, little to no miR-455-3p expression was observed in hypertrophic chondrocytes in vivo by in situ hybridization in E16.5 mouse limbs. [score:5]
The expression levels of miR-455-3p were assessed by qRT-PCR, and the expression of DNMT3A was assessed by qRT-PCR and western blotting. [score:5]
Our study demonstrated that miR-455-3p plays a role similar to 5-azacytidine in repressing DNMT3A expression and inhibiting DNA methylation. [score:5]
The effect of overexpressed (a, b) or inhibited (c, d) miR-455-3p on DNMT3A, RUNX2, and SOX9 were detected by RT-PCR. [score:5]
Therefore, we concluded that miR-455-3p may regulate the chondrogenic differentiation of hBMSCs by directly targeting DNMT3A to affect genomic methylation levels. [score:5]
Treatment with miR-455-3p resulted in significantly decreased mRNA expression of DNMT3A and an increase in SOX9 expression (Fig.   2b, e, f). [score:5]
miR-455-3p directly targets DNMT3A. [score:4]
The inhibitory rate of miR-455-3p on the wild-type 3′-UTR DNMT3A was 44.3%, while it decreased to 16.0% with the mutation of the DNMT3A 3′-UTR (Fig.   3b). [score:4]
These contrary expression patterns between miR-455-3p and DNMT3A indicated the co-regulation of chondrogenesis. [score:4]
Ning T miR-455 inhibits cell proliferation and migration via negative regulation of EGFR in human gastric cancerOncol. [score:4]
Overexpression of miR-455-3p reduced the methylation of cartilage development-related genes. [score:4]
Zhao Y Microrna-455-3p functions as a tumor suppressor by targeting eif4e in prostate cancerOncol. [score:4]
These results suggest that miR-455-3p may affect the expression of DNMT3A and regulate cartilage metabolism. [score:4]
Zhang Z miR-455-3p regulates early chondrogenic differentiation via inhibiting RUNX2FEBS Lett. [score:4]
These results show that the upregulation effect of the miR-455-3p agomir in hBMSCs can continue for more than 28 days during chondrogenic differentiation. [score:4]
Our previous studies demonstrated that miR-455-3p regulated hMSC chondrogenic differentiation by targeting RUNX2 [15], HDAC2, and HDAC8 [14]. [score:4]
The expression of miR-455-3p (a), DNMT3A (b) were detected by qRT-PCR. [score:3]
The normal chondrocytes were transfected with miR-455-3p mimic or inhibitor (RiboBio, Guangzhou, China) at a concentration of 50 nM; they were also transfected with DNMT3A-siRNA or NC (RiboBio, Guangzhou, China). [score:3]
These data suggest that miR-455-3p inhibits the degeneration process of chondrogenic differentiation by activating canonical pathways such as the PI3K-Akt signaling pathway through the reduction of its methylation levels. [score:3]
Previously, we found high expression levels of miR-455-3p in human adipose-derived stem cells (hADSCs) during chondrogenic differentiation [13]. [score:3]
Recent studies have shown that miR-455-3p functions as suppressors of hypoxia signaling [24] and gastric cancer [26]. [score:3]
Analysis of miR-455-3p and DNMT3A expression during chondrogenesis. [score:3]
Notably, we observed high DNMT3A expression levels in palms of miR-455-3p deletion mice (Fig.   2l, m), while low levels were detected in wild-type mice (Fig.   2j, k). [score:3]
We then extracted the RNA on day 28 of chondrogenic differentiation to detect the expression of miR-455-3p and cartilage-related mRNAs. [score:3]
Expression pattern of miR-455-3p and DNMT3A during chondrogenic differentiation of hBMSCs. [score:3]
Therefore, we overexpressed miR-455-3p in hBMSCs and induced them to differentiate into chondrocytes in micromass culture. [score:3]
DNMT3A modulated expression of endogenous miR-455-3p in normal chondrocytes. [score:3]
The in vivo study showed high DNMT3A expression levels in miR-455-3p deletion mice and low levels in wild-type mice. [score:3]
However, whether miR-455-3p regulates cartilage development and degeneration by adjusting DNA methylation level is not clear. [score:3]
MiR-455-3p directly targets DNMT3A by interaction with the 3′-UTR. [score:3]
We extracted the RNA on days 28 of the chondrogenic differentiation to detect the expression of miR-455-3p (b), COL2A1, COL11A1, and SOX6 (c) by RT-PCR. [score:3]
The experiment was performed in triplicate and a representative image is shown To assess whether DNMT3A modulated expression of miR-455-3p in normal chondrocytes, we transfected with DNMT3A siRNA. [score:3]
Treatment with the miR-455-3p agomir significantly increased the expression of miR-455-3p (Fig.   4b), COL2A1, COL11A1, and SOX6 (Fig.   4c). [score:3]
The expression of miR-455-3p increased rapidly in hBMSC chondrogenic differentiation beginning on day 7, peaked at 21 days, and was followed by a marked decrease from days 28 to 35 (Fig.   1a). [score:3]
The expression of DNMT3A in palm of wild mice (j, k) and miR-455-3p deletion mice (l, m), scale bar, 100 μm. [score:3]
MiR-455-3p regulates the expression of DNMT3A in vitro and in vivo. [score:3]
miR-455-3p inhibits cartilage degenerate process in vitro and in vivo. [score:3]
Significant differential CpG methylation between overexpressed miR-455-3p and control groups in hBMSCs induced to differentiate to chondrocytes. [score:3]
Additionally, a luciferase reporter assay demonstrated that miR-455-3p regulates DNMT3A expression by binding to the DNMT3A 3′-UTR. [score:3]
qPCR of miR-455-3p and target mRNAs were performed using SYBR [®] Premix Ex Taq™ II (Takara) and KOD SYBR [®] qPCR Mix(Toyobo), according to the manufacturer’s instructions, respectively. [score:3]
Immunohistochemistry analysis of DNMT3A (Fig.   1c) also showed a similar trend to RT-PCR, suggesting that miR-455-3p may affect the expression of DNMT3A. [score:3]
For example, collagen type V alpha 1 (COL5A1), a gene that promotes the anabolism of cartilage [20], was hypomethylated with the overexpression of miR-455-3p, and is also related to the PI3K-Akt signaling pathway and the ECM−receptor interaction pathway. [score:3]
To assess whether DNMT3A modulated expression of miR-455-3p in normal chondrocytes, we transfected with DNMT3A siRNA. [score:3]
miR-455-3p inhibits the degenerate process during chondrogenic differentiation of hBMSCs. [score:3]
DNMT3A siRNA was transfected into normal chondrocytes, then RT-PCR and western blot were used to detect the expression of DNMT3A, Aggrecan, Sox9, H3K4me3 (n, o) and miR-455-3p (p). [score:3]
Previous studies also demonstrated that miR-455-3p modulates cartilage development and degeneration 14, 15. [score:2]
We also identified eight miRNAs with over twofold increases in regulation during chondrogenic differentiation of hADSCs, such as miR-320c, miR-92a-3p, and miR-455-3p [13]. [score:2]
In summary, this study demonstrates that miR-455-3p and DNMT3A co-regulate chondrogenic differentiation of hMSCs by modulating DNA methylation. [score:2]
The mmu-miR-455-3p global knockout mice were generated by a transcription activator-like effector nuclease (TALEN) system. [score:2]
Thus, we hypothesized that miR-455-3p plays an important role in hMSC chondrogenic differentiation by regulating the ability of DNMT3A to modulate DNA methylation. [score:2]
Co-transfection of DNMT3A 3′-UTR luciferase reporter plasmids with miR-455-3p resulted in significantly decreased luciferase activity (44.3%), and the mutation of the miR-455-3p binding sequence significantly diminished this effect (Fig.   3b). [score:2]
Recent studies have shown that miR-455-3p regulates certain pathological processes, such as cancer [17]. [score:2]
In this study, we first identified the co -regulating activity of DNMT3A and miR-455-3p in DNA methylation during the degenerate stage of chondrogenic differentiation. [score:2]
Situ hybridization of knee cartilage (g, h) showed the miR-455-3p expression in miR-455-3p deletion mice (h) was repressed compared with wild mice (g), scale bar, 100 μm. [score:2]
To the best of our knowledge, this study is the first to demonstrate the co-regulation between DNMT3A and miR-455-3p in vivo and the chondrogenic differentiation of hBMSCs in vitro. [score:2]
These results not only reveal the important role of DNA methylation in chondrogenic differentiation, but also demonstrate that miR-455-3p can regulate this process by affecting DNA methylation. [score:2]
Luciferase reporter assays were performed on the DNMT3A 3′-UTR and the mutated 3′-UTR in the presence or absence of miR-455-3p overexpression. [score:2]
We compared miR-455-3p expression between 6-month wild-type mice and homozygous mice by in situ hybridization. [score:2]
Lalevee S Lapaire O Bühler M miR455 is linked to hypoxia signaling and is deregulated in preeclampsiaCell Death Dis. [score:2]
We subsequently demonstrated that miR-455-3p plays a role in regulating OA and the chondrogenic differentiation of hMSCs 14– 16. [score:2]
As described previously, hBMSCs transfected with miR-455-3p agomir or normal controls were induced to differentiate into chondrocytes in micromass culture. [score:1]
The experiment was performed in triplicate and a representative image is shownWe constructed miR-455-3p deletion mice and proved the successful deletion. [score:1]
To characterize the expression patterns of miR-455-3p and DNMT3A during chondrogenic differentiation, hBMSCs were induced to differentiate into chondrocytes in micromass culture in vitro. [score:1]
The ECM−receptor interaction was also hypomethylated (P = 0.002, FDR = 0.015), as shown in Table  3. To confirm the DNA methylation analysis results, we overexpressed miR-455-3p in hBMSCs and induced them to differentiate to chondrocytes in micromass culture for 28 days, and immunohistochemistry of Akt and p-Akt were used to evaluate the PI3K/Akt signaling pathway. [score:1]
Sections were subjected to in situ hybridization analysis using the miR- 455-3p-specific probe (Servicebio, Wuhan, China), or treated with PBS instead of the miR-455-3p probe as negative control. [score:1]
We also observed thinner cartilage thickness in miR-455-3p deletion mice at 6 months of age than we did in wild-type mice. [score:1]
The knee joint of miR-455-3p deletion mice and wild-type mice were harvested at 6 months and fixed by incubation in DEPC -treated 10% formalin at 4 °C overnight. [score:1]
Wild-type (WT) mice (d) and miR-455-3p deletion (KO) mice (e) were stained with Safranin O at 6 months of age, scale bar, 100 μm. [score:1]
The wild-type (miR-455-3p+/+), heterozygous (miR-455-3p+/−), and homozygous (miR-455-3p−/−) mice were obtained through the mating of heterozygous male and female mice. [score:1]
A luciferase reporter carrying the 3′-UTR of DNMT3A or mutant DNMT3A in which the binding site of miR-455-3p was mutated (Luc-DNMT3A-UTR-mut) was introduced into 293T cells along with negative miR-control (miR-Control), miR-455-3p, respectively. [score:1]
Fig. 4hBMSCs were transfected with miR-455-3p agomir induced to differentiate to chondrocytes in micromass culture. [score:1]
miR-455-3p deletion mice showed more hypertrophic chondrocytes (black arrow) and thinner cartilage than WT mice (f). [score:1]
Heatmap of the 1733 significant differentially DNA methylation sites in miR-455-3p group comparing with control group (a). [score:1]
The experiment was performed in triplicate and a representative image is shown We constructed miR-455-3p deletion mice and proved the successful deletion. [score:1]
Chen W Microrna-455-3p modulates cartilage development and degeneration through modification of histone H3 acetylationBiochim. [score:1]
The results showed miR-455-3p were significantly decreased on cartilage (Fig.   2g−i), bone (Supplementary Figure  2a, b, e), and meniscus (Supplementary Figure  2c, d, e). [score:1]
The chondrocytes isolated from normal cartilage were transfected with either miR-455-3p or anti-miR-455-3p (Fig.   2a, c). [score:1]
We also observed the cartilage thickness of hip joint in wild-type mice (Fig.   4d) and miR-455-3p deletion mice at 6 months (Fig.   4e); the miR-455-3p deletion mice exhibited more hypertrophic chondrocytes and thinner cartilage than wild mice (Fig.   4f). [score:1]
We detected 803,869 methylated CpG sites and observed 1733 differentially methylated sites (P < 0.01) representing 1023 distinct genes and nearby genomic regions when comparing miR-455-3p groups with control groups (Fig.   5a, Supplementary Figure  3a). [score:1]
Fig. 3Alignment of the nucleotide sequence of miR-455-3p, 3′-UTR DNMT3A, and 3′-UTR mutant DNMT3A mRNA (a). [score:1]
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2
[+] score: 264
Other miRNAs from this paper: hsa-mir-455, hsa-mir-640
We identified for the first time that upregulation of miR-455-3p expression could promote the migration of HUVECs while downregulation of miR-455-3p could inhibit the migration. [score:11]
Our results also showed that there is no change in iNOS expression either in miR-455-3p overexpressed cells or in downregulated ones (Supplementary Figure S1a and 1b). [score:8]
DNAJB12, DNAJB14, HERPUD1 mRNA expression did not change either in miR-455-3p overexpressed or in miR-455-3p downregulated HUVECs (Fig. 4a,b). [score:8]
Secondly, inhibiting expression of miR-455-3p to 50% (Fig. 2d) leaded to decreased expression of eNOS protein and NO content (Fig. 2e,f). [score:7]
H [2]S induced increasing expression of miR-455-3p were blocked when the expression of miR-455-3p were inhibited. [score:7]
Inhibiting expression of miR-455-3p not only leaded to increased expression of CUL3 but also blocked the effects of NaHS on CUL3 production (Fig. 4e,f). [score:7]
CUL3 could associate with other proteins to form ubiquitin ligase complex 18. and Western blot results showed thatHydrogen sulfide increases miR-455-3p, thus downregulates CUL3 and inhibits the proteasome degradation of eNOS protein. [score:6]
HUVECs were transfected with 0.05 nM, 0.5 nM, 5 nM has-miR-455-3p agomir to overexpress miR-455-3p and 150 nM has-miR-455-3p antagomir to downregulate it. [score:6]
However, neither overexpression nor downregulation of miR-455-3p has any effect on phosphorylation or dimerization of eNOS. [score:6]
Moreover, downregulation of miR-455-3p attenuated eNOS expression and NO content in HUVECs. [score:6]
We also found that the promoting effect of H [2]S on eNOS expression was abolished by the inhibition of miR-455-3p. [score:5]
Interestingly, we found that HUVECs with overexpressed miR-455-3p have decreased CUL3 expression both in mRNA and protein levels (Fig. 4c,d). [score:5]
Conversely, when endogenous miR-455-3p expression was inhibited by miR-455-3p antagomir, cell migration was blunted (Fig. 5c,f). [score:5]
The effects of exogenous H [2]S on the expression of eNOS, miR-455-3p and NO production in mice, and comparison of miR-455-3p expression and H [2]S production between atherosclerosis patients and chronic venous insufficiency patients. [score:5]
Ubiquitin-proteasome pathway inhibitor MG-132 blocked the effects of H [2]S and miR-455-3p on eNOS expression. [score:5]
We also found that increased expression of miR-455-3p was involved in NaHS induced eNOS expression, NO production, and HUVEC migration. [score:5]
To explore the mechanism of miR-455-3p on eNOS expression, we first identified potential targets for miR-455-3p by employing database miRecords (http://c1. [score:5]
H [2]S promotes miR-455-3p and eNOS expression in HUVECsCultured HUVECs were harvested after treated with vehicle or NaHS for 24 h. Then total RNA was extracted and real-time PCR experiments were performed to determine the expression of miR-455-3p. [score:5]
Figure 2i,j showed that inhibiting expression of miR-455-3p has no effects on phosphorylation or coupling levels of eNOS. [score:5]
Interestingly, the effects of H [2]S on eNOS expression and NO production were blocked by miR-455-3p inhibition (Fig. 2e,f). [score:5]
miR-455-3p mediates H [2]S induced eNOS expressionAs shown in Fig. 2a, HUVECs transfected with 5 nM miR-455-3p agomir showed an increased expression of miR-455-3p for nearly 200-folds. [score:5]
HUVECs with all three dosages of miR-455-3p overexpression have elevated eNOS expression (Fig. 2b). [score:5]
H [2]S and miR-455-3p downregulate the proteasome degradation pathway of eNOS protein. [score:4]
How to cite this article: Li, X. -H. et al. H [2]S regulates endothelial nitric oxide synthase protein stability by promoting microRNA-455-3p expression. [score:4]
Inhibition of miR-455-3p also blocked the pro-migration effect of H [2]S. These results indicate that miR-455-3p played an important role in H [2]S and eNOS mediated migration of HUVECs, and involves in the regulation of NO production. [score:4]
H [2]S and miR-455-3p downregulate the proteasome degradation pathway of eNOS proteinThe mRNA levels of eNOS were detected by and the results showed that there was no significant change either by NaHS treatment or miR-455-3p agomir transfection (Fig. 3a). [score:4]
No significant change was observed in kidney miR-455-3p expression. [score:3]
As shown in Fig. 2g,h, overexpression of miR-455-3p (5 nM) has no effects on phosphorylation or coupling levels of eNOS. [score:3]
Western blots and results showed that NaHS administration increased the expression of miR-455-3p and eNOS protein levels in skeletal muscle, heart and aorta. [score:3]
5 nM miR-455-3p agomir was chosen to perform the following experiments since it caused highest eNOS expression. [score:3]
Proteasome inhibitor MG-132 was used to detect whether miR-455-3p is involved in the ubiquitination and degradation of eNOS or not. [score:3]
As shown in Fig. 2a, HUVECs transfected with 5 nM miR-455-3p agomir showed an increased expression of miR-455-3p for nearly 200-folds. [score:3]
H [2]S promotes migration of HUVECs through increased expression of eNOS and miR-455-3p. [score:3]
eNOS and miR-455-3p expression increased in mice tissues after H [2]S administrationTo investigate if H [2]S could influence miR-455-3p and eNOS expression in vivo, 8-week-old mice were injected intraperitoneally with normal saline or 50 μmol/kg/day NaHS for one week. [score:3]
The effects of miR-455-3p on eNOS expression, NO production and eNOS coupling. [score:3]
CUL3 is the target gene of miR-455-3p in HUVECs. [score:3]
As shown by our results, overexpression of miR-455-3p dramatically elevated the protein levels of eNOS and NO content in HUVECs. [score:3]
When we decreased the dosage of miR-455-3p agomir to 0.5 nM or 0.05 nM, the expression level of miR-455-3p increased 8 or 2 folds respectively. [score:3]
Changes in miR-455-3p expression is more profound than NO content. [score:3]
miR-455-3p mediates H [2]S induced eNOS expression. [score:3]
To further investigate in vivo effects of H [2]S on miR-455-3p and their potential effects on the pathogenesis of diseases, we detected the expression of miR-455-3p in mouse healthy tissues. [score:3]
miRecords predicted several target genes of miR-455-3p such as DNAJB12, DNAJB14, HERPUD1 as well as CUL3 which are all related to proteasome degradation (Supplementary Table S1). [score:3]
While the increase range of NO content is only 10 to 30 percent, miR-455-3p expression increased in heart tissues for 2-fold, muscle tissues for 1.5-fold and aorta tissues for nearly 6-folds (Fig. 6a,b). [score:3]
Nevertheless, exogenous H [2]S remarkably increased both NO content (Fig. 6a) and miR-455-3p expression (Fig. 6b) in heart, muscle and aorta tissues. [score:3]
The has-miR-455-3p agomir oligonucleotide (5′-GCAGUCCAUGGGCAUAUACAC-3′), the has-miR-455-3p antagomir oligonucleotide (target sequence 5′-GUGUAUAUGCCCAUGGACUGC-3′), the agomir negative control and the antagomir negative control were synthesized by Biotend (Shanghai, China). [score:3]
Both H [2]S and miR-455-3p induced eNOS expression (Fig. 3b,c) and NO production (Fig. 3d,e) were blocked with the presence of MG-132 (1 μM). [score:3]
CUL3 is the target gene of miR-455-3p. [score:3]
After adding MG-132 to HUVECs, we found that the promoting effect of H [2]S and miR-455-3p on eNOS expression was abolished. [score:3]
Firstly, we examined NO production after miR-455-3p overexpression. [score:3]
The effects of exogenous H [2]S on miR-455-3p, eNOS and iNOS expression in HUVECs. [score:3]
eNOS and miR-455-3p expression increased in mice tissues after H [2]S administration. [score:3]
Our results indicate that H [2]S and miR-455-3p may participate in the compensation mechanism of eNOS expression in atherosclerotic plaque. [score:3]
Cultured HUVECs were harvested after treated with vehicle or NaHS for 24 h. Then total RNA was extracted and real-time PCR experiments were performed to determine the expression of miR-455-3p. [score:3]
Several predicted target genes of miR-455-3p such as DNAJB12, DNAJB14, HERPUD1 as well as CUL3 are related to proteasome degradation (Supplementary Table S1). [score:3]
H [2]S promotes miR-455-3p and eNOS expression in HUVECs. [score:3]
So that, we speculated that the stability of eNOS might be regulated by miR-455-3p. [score:2]
We found that proteasome degradation pathway of eNOS is regulated by H [2]S and miR-455-3p. [score:2]
As demonstrated in Fig. 5b,e, HUVECs overexpressing miR-455-3p showed a remarkable increase of migration when compared to the control groups. [score:2]
We also detected the expression of miR-455-3p in those patients and found that miR-455-3p levels increased in atherosclerotic plaques when compared with normal arterioles (Fig. 6f). [score:2]
Our results indicate the post-transcriptional regulation of NO production by H [2]S and miR-455-3p. [score:2]
As shown in Fig. 1a compared with vehicle group, the expression of miR-455-3p was increased with NaHS administration. [score:2]
In heart, muscle and aorta, miR-455-3p seems to play a vital role in eNOS regulation, while in kidney and liver, it does not play a decisive role. [score:2]
To investigate the mechanism of NO production regulation, we transfected agomir or antagomir of miR-455-3p in HUVECs to study its effect on eNOS expression, phosphorylation as well as the coupling of eNOS. [score:2]
However, the number of human samples is small in our experiments, more clinical samples and animal studies are needed to further investigate whether the compensation effect on NO production during atherosclerotic plaque formation is caused by increased H [2]S concentration and miR-455-3p expression. [score:1]
Taken together, the current work discovered for the first time that miR-455-3p was involved in the pro-migration effect of H [2]S on endothelial cells and mediates the effect of H [2]S on eNOS protein stability through ubiquitination pathway. [score:1]
However, eNOS protein level (Fig. 3b,c) and NO content (Fig. 3d,e) increased after H [2]S administration and miR-455-3p transfection. [score:1]
To investigate the role of miR-455-3p in HUVEC migration, miR-455-3p overexpression was achieved by agomir transfection. [score:1]
Synthesis and transfection of has-miR-455-3p agomir and antagomir. [score:1]
In liver, miR-455-3p levels increased while eNOS protein levels and NO production decreased. [score:1]
To investigate if H [2]S could influence miR-455-3p and eNOS expression in vivo, 8-week-old mice were injected intraperitoneally with normal saline or 50 μmol/kg/day NaHS for one week. [score:1]
Our results also showed that NO production and eNOS protein levels decreased in liver tissues (Fig. 6a,c) while miR-455-3p increased in liver tissues (Fig. 6b) after NaHS administration. [score:1]
Our results showed that eNOS protein levels, miR-455-3p levels as well as NO content did not change in kidney tissues (Fig. 6a–c). [score:1]
Elevated miR-455-3p caused increased NO production (Fig. 2c). [score:1]
miR-455-3p and eNOS protein levels in kidney did not change after NaHS administration. [score:1]
The mRNA levels of eNOS were detected by and the results showed that there was no significant change either by NaHS treatment or miR-455-3p agomir transfection (Fig. 3a). [score:1]
The role of eNOS and miR-455-3p during H [2]S -mediated migration of HUVECs. [score:1]
[1 to 20 of 76 sentences]
3
[+] score: 197
Other miRNAs from this paper: mmu-mir-122, hsa-mir-122, hsa-mir-455
Based on current findings, we cautiously propose that the upregulation of miR-455-3p—may be a compensatory to the amyloid beta toxicity in disease process. [score:6]
Expression of miR-455-3p was found to be significantly upregulated in AD serum samples,, AD mouse mo del, and AD cell lines (Kumar et al., 2017). [score:6]
miR-455-3p expression is upregulated in different AD mo dels and sources. [score:6]
Up-regulation of miR-455-5p by the TGF-β-SMAD signalling axis promotes the proliferation of oral squamous cancer cells by targeting UBE2B. [score:6]
To understand the roles of miR-455-3p in AD, expression of these genes needs to be studied by using miR-455-3p modulation approaches (mimics/inhibitors). [score:5]
MicroRNA-455-3p functions as a tumor suppressor by targeting eIF4E in prostate cancer. [score:4]
However, we don't know the exact reason for the upregulation of miR-455-3p in AD brains and further, we still do not know molecular mechanism(s) of its increased levels. [score:4]
However, we need further research to understand the nature of miR-455-3p upregulation, not only serum but also in affected tissues from AD patients and AD cell and mouse mo dels. [score:4]
MicroRNA-455 suppresses non-small cell lung cancer through targeting ZEB1. [score:4]
Upregulation of miR-455-3p in different cell and mouse mo dels of AD proven its biomarker potential for AD. [score:4]
We found miR-455-3p levels were upregulated in the fibroblasts and B-lymphocytes from AD patients relative to healthy control subjects. [score:4]
In this direction, next phase of our study is to determine the effect of miR-455-3p on its AD related target genes. [score:4]
Hence, upregulation of miR-455-3p in AD may be a “good” or “bad” signal for the cells. [score:4]
Up regulation of miR-455-3p expression in AD. [score:4]
To determine the diagnostic performance of miR-455-3p expression in AD patients, ROC curve was plotted using (ΔCT) values of miR-455-3p in AD patients and healthy controls. [score:3]
Interaction of miR-455-3p at these sites will influence the expression level of APP genes. [score:3]
Total RNA was extracted from the postmortem brains of healthy controls (n = 15) and AD patients (n = 27) and expression of hsa-miR-455-3p was quantified by real-time RT-PCR analysis. [score:3]
Alteration of miR-455-3p expression in AD cell lines indicates the strong molecular association of miR-455-3p with AD progression. [score:3]
showed a negative correlation r = −0.146 (with 95% confidence interval: −0.498 to 0.247; P = 0.466) between brains postmortem interval and miR-455-3p expression level (Figure 3A). [score:3]
As shown in Figures 3C,D, donors' age for fibroblasts (r = −0.396, 95% confidence interval: −0.821 to 0.310; P = 0.256), and B-lymphocytes (r = 0.235, 95% confidence interval: −0.391 to 0.713; P = 0.461), we did not find statistical significance, between donors age with miR-455-3p levels for fibroblasts and B-lymphocytes, indicating that donors age do not affect miR-455-3p expression levels. [score:3]
Our previous study reported the higher expression of miR-455-3p in patients with AD and other AD sources. [score:3]
We analyzed miR-455-3p expression levels in relation to (1) postmortem interval, (2) AD patients' age, and also (3) donors' age of fibroblasts, and (4) B-lymphocytes using Pearson correlation coefficients (r). [score:3]
Correlation of miR-455-3p expression with patients' demographic data. [score:3]
Figure 3Scattered plot diagrams showing the Pearson correlation coefficient (r) values of miR-455-3p expression with (A) autolysis time (B) Age of (C) Age of AD fibroblast cells and (D) Age of. [score:3]
MicroRNA-455 regulates migration and invasion of human hepatocellular carcinoma by targeting Runx2. [score:3]
Our study was the first to reveal the higher expression level of miR-455-3p in persons with AD. [score:3]
MiR-455-3p target genes were analyzed using various on-line miRNA algorithms (diana-microt, microrna. [score:3]
Each algorithm was run for miR-455-3p and validated/predictive target genes were analyzed. [score:3]
However, exact molecular link between miR-455-3p, AD, and target genes needs to be determined. [score:3]
Similarly, expression of miR-455-3p was quantified in the skin fibroblast cells generated form familial AD patients (n = 4), sporadic AD patients (n = 6), and healthy control subjects (n = 8). [score:3]
Current focus of our laboratory is to understand the role of miR-455-3p in APP processing and amyloid beta modulation, using miR-455-3p mimics and inhibitor treatments. [score:3]
Similarly, in B-lymphocytes, miR-455-3p level was significantly upregulated in sporadic AD cases compared to controls (P = 0.044). [score:3]
S. No Representative miRNA Ortholog of target gene Representative transcript Gene name 3P-seq tags + 5 Conserved sites total Cumulative weighted context++ score Total context++ score Aggregate PCT 1 hsa-miR-455-3p. [score:3]
Expression of miR-455-3p was quantified and its diagnostic potential was examined in different sources. [score:3]
ROC curve was analyzed for miR-455-3p expression in fibroblast cells form familial and sporadic AD patients vs. [score:3]
Figure 1Expression of hsa-miR-455-3p in AD patients. [score:3]
In-silico analysis for miR-455-3pMiR-455-3p target genes were analyzed using various on-line miRNA algorithms (diana-microt, microrna. [score:3]
Interestingly, fold-change analysis indicated the significantly higher expression of miR-455-3p in AD patients. [score:3]
Simultaneously, miR-455-3p target several key genes those are involved in the AD. [score:3]
MiR-455-5p acts as a novel tumor suppressor in gastric cancer by down -regulating RAB18. [score:3]
InROC curve was analyzed for miR-455-3p expression in fibroblast cells form familial and sporadic AD patients vs. [score:3]
MicroRNA-455-3p as a potential peripheral biomarker for Alzheimer's disease. [score:2]
MiR-455 has been implicated in various human diseases specially cancer and chondrogenesis (Chen et al., 2016). [score:2]
MicroRNA-455 (MiR-455) is identified as a member of broadly conserved family non-coding RNA and expressed in most of the phylum such as Eukaryota, Metazoa, Chordata, Craniata, Vertebrata, Euteleostomi; Mammalia, and Primates etc. [score:2]
MicroRNA-455-3p inhibits tumor cell proliferation and induces apoptosis in HCT116 human colon cancer cells. [score:2]
Figure 4 Schematic representation of miR-455-3p roles in AD pathogenesis. [score:1]
miR-455-3p having at least one or two binding site at 3′UTR of the genes and total context [++] score ranges from −0.1 to −0.46. [score:1]
However, in neurodegenerative diseases, role of miR-455-3p is barely investigated. [score:1]
Our current study on AD postmortem findings revealed that miR-455-3p levels are significantly increased in a large number (n = 27) of AD brains and a significant AUC value also strengthen its biomarker potential. [score:1]
These observations strongly suggest that miR-455-3p is a potential biomarker for sporadic AD. [score:1]
We also predict that two potential binding sites of miR-455-3p at the 3′UTR of APP gene may be involved in the modulation of full-length APP. [score:1]
Current findings is the continuation of our past study to elaborate the biomarker potential of miR-455-3p in more details. [score:1]
For e. g., miR-455-3p binds at the two sequence sites of 3′ UTR of APP gene at sequence position 522–528 and 3,139–3,145. [score:1]
A total of 323 predicted transcripts/human genes were identified with conserved miR-455-3p. [score:1]
Further, we also predict that miR-455-3p affects the APP processing and amyloid beta production. [score:1]
Many other reports identified the role of miR-455-3p in several cancers and chondrogenic differentiation (Chen et al., 2016; Cheng et al., 2016; Li et al., 2016; Liu et al., 2016; Qin et al., 2016; Zheng et al., 2016; Zhao et al., 2017). [score:1]
However, data from postmortem AD brains and cells showed significant ROC curve data further confirmed that the miR-455-3p as a valuable molecule capable of discriminating the patients with AD from healthy individuals. [score:1]
One of the most suitable identified candidate in our study was microRNA-455-3p. [score:1]
The curve was plotted based on the ΔCT value of miR-455-3p in AD patients and control samples. [score:1]
As mentioned above, our recent lab study on AD serum samples and other AD sources/AD mouse mo del unveiled the miR-455-3p as potential biomarker candidate for AD (Kumar et al., 2017; Figure 4). [score:1]
1 and hsa-miR-455-3p. [score:1]
Hence, results obtained from, AD fibroblast, and AD B-lymphocyte were conclusively confirmed the decisive role of miR-455-3p in AD assessment. [score:1]
Whereas a positive correlation r = 0.355 (with 95% confidence interval: −0.029 to 0.647; P = 0.069) was observed between the age of and miR-455-3p level (Figure 3B). [score:1]
MicroRNA-455-3p modulates cartilage development and degeneration through modification of histone H3 acetylation. [score:1]
In-silico analysis for miR-455-3p function in AD In-silico analysis was performed to understand the functions of miR-455-3p and its possible role in AD pathogenesis. [score:1]
In order to expose the roles and functions of miR-455-3p in AD, in-silico analysis provides the valuable information. [score:1]
In-silico analysis for miR-455-3p. [score:1]
Hence, these analyses indicated the possible way the miR-455-3p involved in AD pathogenesis. [score:1]
InSimilarly ROC curve for miR-455-3p was analyzed in B-lymphocytes of AD patients. [score:1]
Both cell types showed the significantly higher levels of miR-455-3p, especially in sporadic AD cases but not in familial AD. [score:1]
Thus, results showed a trend of reduced levels of miR-455-3p with increased postmortem interval and increased trend of miR-455-3p with patients' age. [score:1]
In-silico analysis for miR-455-3p function in AD. [score:1]
Similarly ROC curve for miR-455-3p was analyzed in B-lymphocytes of AD patients. [score:1]
Analysis showed the variations in miR-455-3p level among these groups, however significant difference (P = 0.044) in (–ΔCT) value was reported between sporadic AD cases (−13.98 ± 0.73) and controls (−15.50 ± 0.80; Figure 1C). [score:1]
Further, we checked the level of miR-455-3p in B-lymphocytes obtained from familial AD patients (n = 6), sporadic AD patients (n = 6), and healthy controls (n = 10). [score:1]
Analysis showed the significant area under ROC curve (AUROC) value of miR-455-3p (AUROC = 0.792) with the 95% confidence interval was 0.637–0.948 (P = 0.0018). [score:1]
As per miRbase database, a total of 3,102 reads of miR-455-3p has been detected by deep sequencing in 62 experiments (www. [score:1]
The reaction was set in the 7900HT Fast Real Time PCR System (Applied Biosystems, USA) using following reaction conditions: initial denaturation at 95°C for 5 min, denaturation at 95°C for 10 s, annealing at 60°C for 15 s, and extension at 72°C for 25 s. The relative levels of miR-455-3p in the AD patients vs. [score:1]
Further, in-silico analysis was performed to understand the roles and downstream application of miR-455-3p in AD. [score:1]
Thus, analysis showed that ROC analysis of miR-455-3p in B-lymphocytes was not significant. [score:1]
Figure 2ROC curve analysis of hsa-miR-455-3p in (A), (B) AD fibroblast cell lines, and in (C) B-lymphocytes cells from AD patients. [score:1]
In-silico analysis was performed to understand the functions of miR-455-3p and its possible role in AD pathogenesis. [score:1]
Role of miR-455 has been identified in Human Colon Cancer (Zheng et al., 2016), prostate cancer (Zhao et al., 2017), hepatocellular carcinoma (Qin et al., 2016), gastric cancer (Liu et al., 2016), oral squamous cancer cells (Cheng et al., 2016), and non-small cell lung cancer (Li et al., 2016). [score:1]
Beside brain tissues, we also investigated the and B-lymphocytes for miR-455-3p expression. [score:1]
Details about predictive and validated transcripts were obtained by searching hsa-miR-455-3p. [score:1]
Further, high level of miR-455-3p in and lymphoblasts indicate that increased levels of miR-455-3p is a typical feature of AD—both in the brain and peripheral cells. [score:1]
Findings from this study, will provide the valuable information about miR-455-3p role in AD and in search of pre-clinical biomarker for early AD detection. [score:1]
Therefore, current findings together with our recently published study in Human Molecular Genetics (Kumar et al., 2017), strongly suggest that miR-455-3p as a potential biomarker and a possible therapeutic candidate for AD. [score:1]
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4
[+] score: 114
However, Calr was down-regulated and GRP78 was upregulated with the upregulation of miR-455 in the left ventricular tissue of the miR455 -treated mice (Fig. 7). [score:10]
To the best of our knowledge, this study is the first to demonstrate that miR-455 is downregulated in pressure overload -induced cardiac hypertrophy in vivo and that this downregulation increases the mRNA and protein levels of Calr, the predicted target of miR-455. [score:9]
The normalization of miR-455 gene expression levels, which were downregulated during hypertrophy, aggravated cardiac hypertrophy in the short term, but attenuated pathological remo deling in the long term. [score:6]
In this study, using a target prediction algorithm (23), we identified calreticulin (Calr) as the putative target gene of miR-455. [score:5]
miR-455 inhibits myocardial fibrosis and decreases the expression of molecular markers of cardiac fibrosis at 4 weeks after TAC. [score:5]
Calr is a direct target of miR-455 that is involved in miR-455 -mediated effects in mouse hearts after TAC. [score:4]
The restoration or downregulation of miR-455 at different time periods may lead to a pioneering therapeutic strategy to reverse cardiac hypertrophy and alleviate function deterioration. [score:4]
Compared to treatment with GFP, treatment with miR-455 significantly increased Bcl-2 expression and decreased Bax expression. [score:4]
The results of RT-qPCR revealed that miR-455 significantly decreased the mRNA expression level of Calr, but did not alter the mRNA expression level of GRP78 as compared with GFP (Fig. 7). [score:4]
These 3 genes were upregulated in the mice following aortic coarctation, particularly in the miR-455 -treated mice. [score:4]
The expression of the mature miR-455 in the hypertrophied hearts induced by pressure overload was restored by Ad -mediated miR-455 gene transfer in vivo (Fig. 2). [score:3]
The gene expression of miR-455 was significantly decreased in the GFP -treated hearts, but was significantly increased in the miR-455 -treated hearts after TAC. [score:3]
The different effects of miR-455 on myocardial hypertrophy in the short and long term may be related to its target gene, Calr. [score:3]
miR-455 gene expression in vivo. [score:3]
However, the expression of Myh7 was higher in the GFP -treated mice than in the miR-455 -treated mice at 4 weeks. [score:3]
miR-455 modulates the expression of molecular markers of cardiac hypertrophy. [score:3]
In conclusion, the Ad-13 -mediated normalization of miR-455 expression aggravates the hypertrophic phenotype, but attenuates the progressive deterioration of left ventricular function. [score:3]
These results indicate that Calr and not GRP78 is the target of miR-455. [score:3]
Mature miR-455 expression was quantified by RT-qPCR using the All-in-One miRNA qRT-PCR Detection system following the manufacturer’s instructions (GeneCopoeia, Guangdong, China). [score:3]
miR-455 inhibits heart myocardial apoptosis. [score:3]
This study found no evidence to prove that miR-455 directly influences the different genes. [score:2]
The change observed may be due to an indirect effect of miR-455 on the different genes. [score:2]
Furthermore, the expression levels of these 3 genes significantly increased in the miR-455 -treated mouse hearts compared with the GFP -treated mouse hearts. [score:2]
Therefore, we evaluated whether the expression levels of Calr and GRP78 are regulated by miR-455 in vivo in hypertrophy induced by pressure overload. [score:2]
Thus, miR-455 may be important in myocardial hypertrophy. [score:1]
This study assessed the short-term and long-term effects of miR-455 gene transfer in pressure overload -induced cardiac hypertrophy in vivo using a cardiotropic Ad-13 vector that efficiently transduced cardiac tissues. [score:1]
The mRNA sequence of Calr was predicted to contain a conserved ‘seed’ sequence complementary to miR-455 in the 3′-UTR (Fig. 1). [score:1]
Ad-13 containing miR-455 precursor. [score:1]
This study is also the first to reveal the short-term and long-term effects of miR-455 on pressure overload -induced cardiac hypertrophy. [score:1]
Our findings on the different effects of miR-455 are in agreement with other data demonstrating the effects of Calr on cardiomyocytes (28, 30). [score:1]
Treatment with miR-455 reduced LVAWd, but did not enlarge left ventricular cavity dimension (LVIDd) and did not lower LV contractility. [score:1]
By contrast, treatment with miR-455 significantly decreased fibrosis (Fig. 5). [score:1]
The precursor of the miRNA, mmu-miR-455 (miRBase accession no. [score:1]
However, these increased levels of myocardial fibrosis-related genes following pressure overload were significantly decreased in the mice treated with miR-455. [score:1]
Thus, the myocardial state during the application of miR-455 for the treatment of myocardial hypertrophy is highly important. [score:1]
miR-455 aggravates cardiac hypertrophy in mice 2 weeks after TAC. [score:1]
However, the association between miRNA-455 and Calr during cardiac hypertrophy remains unclear. [score:1]
The mice were randomly selected to receive a tail vein injection of either miR-455 (5.0×10 [9] ifu/ml, n=12) or GFP (1.0×10 [9] ifu/ml, n=24) at 0.1 ml (viral genomes) per animal at 1, 8, 15 and 21 days following surgery. [score:1]
These results suggest that miR-455 gene transfer is effective in the prevention of cardiac remo deling and dysfunction during a 4-week period of pressure overload. [score:1]
Furthermore, this change may differ when hypertrophy results from other causes than TAC with or without miR-455 transfection. [score:1]
miR-455 gene transfer preserves cardiac adaptation and function at 4 weeks after TAC. [score:1]
Thus, the miR-455 -treated hearts maintained a state of myocardial hypertrophy. [score:1]
Cardiac fibrosis and apoptosis were alleviated in the miR-455 -treated mice. [score:1]
In the present study, we established a mouse mo del of hypertrophy by transverse aortic constriction (TAC) in order to investigate the effects of the aberrant expression of miR-455 on cardiac hypertrophy induced by pressure overload and to elucidate the potential cellular and molecular mechanisms of action of this miRNA. [score:1]
However, the association between miRNA-455 (miR-455) and cardiac hypertrophy remains unclear. [score:1]
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5
[+] score: 73
Both miR-146b, which has previously been shown to be up-regulated in macrophages and miR-455 were also up-regulated in this experiment, however their p values were 0.16 and 0.10 respectively. [score:7]
Both pri- and mature miR-455 were also up-regulated by LPS, however in contrast to the other miRNAs tested the up-regulation of the mature miR-455 was faster and more transient than for the other pri-miRNAs tested (Fig. 1A & B). [score:7]
In response to heat killed C. albicans miR-155 and miR-455 were the most highly up-regulated of the miRNAs tested. [score:4]
Only 2 miRNAs, miR-155 and miR-455, were more than 2-fold up-regulated with a p-value of less than 0.05 (Table 1). [score:4]
We show here that miR-155, miR-146a, miR-146b, miR-125a and miR-455 can be up-regulated by the TLR4 agonist LPS as well as by heat killed C. albicans which most likely signals via a combination of TLRs and the C-type lectin dectin-1 [24], [25]. [score:4]
org) for miR-125a and miR-455 however suggest they may target some proteins involved in inflammatory signaling, including IRF4, MLK2, IL-1 receptor protein 1, OTBU2 and c-maf, suggesting that these miRNAs may also play a role in limiting inflammation. [score:3]
Effect of MAPK inhibitors on the transcription of miR-155, miR-455, miR-146 and miR-125a. [score:3]
Both the LPS and heat killed C. albicans stimulated transcription of pri-miR-155, pri-miR-455, pri-miR-146a and pri-miR-125a as well as the LPS induced transcription of pri-miR-146b were reduced by pretreatment with the IKKβ inhibitors, suggesting that IKKβ plays a critical role in the induction of these miRNAs (Fig. 7A and B). [score:3]
The transcription of miR-455 and miR-125a has not previously been studied in immune cells, while miR-146 has been reported to be an NFκB target gene. [score:3]
Effect of IKKβ inhibitors on the transcription of miR-155, miR-455, miR-146 and miR-125a. [score:3]
The targets for miR-125a and miR-455 are not well established. [score:3]
However, while the fold up-regulation of miR-455 was similar between LPS and heat killed C. albicans, LPS gave a much higher fold stimulation of miR-155 than heat killed C. albicans (150 compared to 7 fold). [score:3]
Consistent with pri-miR-125 and pri-miR-455 being co-transcribed with Ncrna00085 and Col27a1 respectively, the induction of both these mRNAs was also blocked by IKKβ inhibitors (data not shown). [score:3]
For pri-miR-155, pri-miR-455 and pri-miR-146a this would suggest that NFκB plays a direct role in the transcription of these miRNAs. [score:2]
To extend the results from the array experiment, the transcriptional regulation of miR-125-5p and 3p, miR-155, miR-146a, miR-146b and miR-455 by either heat killed C. albicans or LPS was examined using Taqman qPCR based methods, in samples from BMDMs generated independently from those used for the array studies. [score:2]
The regulation of miR-125a and miR-455 in response to either of these stimuli has not previously been examined. [score:2]
Similar to miR-455, Col27a1 mRNA transcription was induced by both LPS and heat killed C. albicans (Fig. 3B). [score:1]
0013669.g002 Figure 2Heat killed Candida albicans stimulates the transcription of miR-155, miR-455, miR-146 and miR-125a. [score:1]
miR-155 is located in the exon of the non-protein coding BIC gene, while miR-146b and miR-455 are encoded in the introns of Tmem180 and Col27a1 respectively. [score:1]
In contrast, while IL-10 alone was a relatively weak stimulus for pri-miR-455 transcription, a combination of both IL-10 and LPS resulted in a much greater stimulation of pri-miR-455 than either LPS or IL-10 alone at 1 h, although this synergistic effect of LPS and IL-10 was not seen at 6 h (Fig. 8A). [score:1]
miR-455 is encoded in intron 10 of the Col27a1 gene. [score:1]
miR-455 is encoded within an intron of the Col27a1 gene, which encodes type XXVII collagen. [score:1]
Similar to pri-miR-455, Col27a1 transcription was induced by LPS or heat killed C. albicans. [score:1]
Heat killed Candida albicans stimulates the transcription of miR-155, miR-455, miR-146 and miR-125a. [score:1]
The levels of pri-miR-155, pri-miR-455, pri-miR-146a, pri-miR-146b and pri-miR-125a were determined by Q-PCR. [score:1]
Unexpectedly SB203580 did result in a small increase in pri-miR-155, and to a lesser extent, pri-miR-455 levels. [score:1]
0013669.g008 Figure 8 A) BMDMs were stimulated with either 100 ng/ml IL-10, 100 ng/ml LPS or a combination of both IL-10 and LPS for 1 or 6 h. Total RNA was isolated, and the levels of pri-miR-155, pri-miR-455, pri-miR-146a, pri-miR-146b, pri-miR-125a were determined by Q-PCR. [score:1]
miR-146b, mir-155, miR-455 and miR-125a are located in annotated genes. [score:1]
LPS stimulates the transcription of miR-155, miR-455, miR-146 and miR-125a. [score:1]
A) BMDMs were stimulated with either 100 ng/ml IL-10, 100 ng/ml LPS or a combination of both IL-10 and LPS for 1 or 6 h. Total RNA was isolated, and the levels of pri-miR-155, pri-miR-455, pri-miR-146a, pri-miR-146b, pri-miR-125a were determined by Q-PCR. [score:1]
The induction of pri-miR-155, pri-miR-455 and pri-miR-146a was not reduced by pre-treatment with PD184352, SB203580 or a combination of both PD 184352 and SB203580 indicating that the initial induction of these miRNAs in response to LPS was independent of MAPK signaling (Fig. 6A). [score:1]
This would be consistent with the processing of miR-455 from the intron of the Col27a1 transcript. [score:1]
IL-10 did however have a synergistic effect with LPS on pri-miR-455 induction, however this appeared to be restricted to early time points. [score:1]
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6
[+] score: 54
Less is known about the cellular targets and function of miR-450b-3p, miR-455*, miR-543 and miR-872 (all downregulated in our studies). [score:6]
Of the ten miRNAs downregulated in Ercc1 [−/−] MEFs, eight (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b) were also down-regulated in both the progeroid and old WT mouse livers compared to the WT young (20 week) control mouse livers (Figure 1). [score:6]
One miRNA, miR-24-2*, was upregulated and three miRNAs, miR-204, miR-218, miR-455* were downregulated in P7 Ercc1 [−/−] MEFs grown in 20% O [2] compared to P3 Ercc1 [−/−] MEFs (Table 4). [score:6]
Of the 8 downregulated miRNAs in Ercc1 [−/Δ] and WT old mouse liver compared to WT young mouse liver (Figure 1), three miRNAs (miR-449a, miR-455*, miR-128) were also downregulated in the kidneys of progeroid mice compared to WT young mice (Figure 2). [score:5]
MiR-455*, miR-497 and miR-543 were significantly downregulated in P7 Ercc1 [−/−] MEFs compared to P7 WT MEFs (Table 1) and P7 versus P3 Ercc1 [−/−] MEFs (Table 3)grown at 3% O [2], suggesting that these miRNAs may be dysregulated as a result of deficient DNA repair and/or sequential passaging. [score:4]
Three miRNAs (miR-128, miR-449a and miR-455*) are downregulated in late passage MEFs as well as liver and kidney tissues of both progeroid Ercc1 [−/Δ] and WT old mice. [score:4]
Eight miRNAs (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b) are significantly downregulated in the livers of progeroid Ercc1 [−/Δ] and naturally aged mice compared to young adult mice (Figure 1). [score:3]
Three of these miRNAs (miR-128, miR-449a and miR-455*) were also downregulated in the kidneys of progeroid and WT old mouse compared to the young WT mouse kidneys (Figure 2). [score:3]
We show that three of the above miRNAs (miR-449a, miR-455* and miR-128) were downregulated in kidney tissues from Ercc1 [−/Δ]progeroid and WT old mice compared to the young mice. [score:3]
Additionally, we identified six downregulated miRNAs (miR-301a, miR-326, miR-455*, miR-497, miR-543 and miR-872) in late-passage P7 Ercc1 [−/−] MEFs compared to the WT MEFs grown in 3% O [2] (Table 1). [score:3]
Previously confirmed gene targets of the miRNAs identified in this study that are linked to cellular senescence and aging (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b) are listed in Supplemental Table S1. [score:3]
Additionally, we demonstrate that several miRNAs differentially expressed in the Ercc1 [−/−] MEFs (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b) were also dysregulated in liver tissues of both progeroid Ercc1 [−/Δ] and old WT mice compared to young WT mice. [score:3]
In summary, we identified several miRNAs that are similarly dysregulated in senescent primary MEFs and senescent tissues of progeroid and naturally aged mice (miR-449a, miR-455*, miR-128, miR-497, miR-543, miR-450b-3p, miR-872 and miR-10b). [score:2]
MiR-455* was downregulated in late passage cells compared to early passage in both analyses. [score:2]
We analyzed the levels of 13 miRNAs confirmed to be dysregulated in P7 Ercc1 [−/−] MEFs compared to P3 Ercc1 [−/−] MEFs (miR-680, miR-320, miR-22, miR-449a, miR-455*, miR-675-3p, miR-128, miR-497, miR-543, miR-450b-3p, miR-872, miR-369-5p and miR-10b) in RNA samples prepared from the livers of WT young (20 weeks), the progeroid Ercc1 [−/Δ] mice, and WT old mice (30 months). [score:1]
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7
[+] score: 50
We observed that mir455 mimics downregulated the expression of MMP9 while mir455 inhibitors upregulated the expression (Fig. 7A). [score:13]
We found that downregulation of MMP9 was associated with upregulation in the levels of mir29b and mir455 in the exosomes. [score:7]
We observed that mir455 tightly regulated the expression of MMP9 since the use of mir455 mimics diminished the expression of MMP9 (A). [score:6]
Although qRT-PCR confirmed the presence of all the microRNAs in the exosomes, the expression of mir29b and mir455 was significantly upregulated in the exercise group as compared to the non-exercise group. [score:5]
The use of mimics and inhibitors in the HL-1 cell line 27 confirmed that mir455 directly regulated MMP9. [score:5]
Of the four microRNAs there was significant upregulation of mir29b and mir455 (* P < 0.05) in the exercise group. [score:4]
The evidence provided by this study that exosomes released in exercise contain microRNAs (mir29b, mir455) to silence MMP9 can be extrapolated to replace MMP9 inhibitors which have not been successful so far for managing cardiac remo delling 23. [score:3]
Figure 6Expression of mir29b, mir455, mir323-5p and mir466. [score:3]
We used mimics and inhibitors for mir455 and mir29b in the HL-1 cell line (as described in our previous study 27) to evaluate the expression of MMP9. [score:3]
Interestingly, we observed mir29b and mir455 in the exosomal population after exercise in type 2 diabetic mice which suggests that the exosomal content varies and depends upon the cells of origin at time of secretion. [score:1]
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8
[+] score: 48
The results showed that 5 miRNAs (miR-130b-5p (formerly designated as miR-130b*), miR-196a, miR-455-3p, miR-455-5p, and miR-801) or 2 miRNAs (miR-133b and miR-145) were significantly up-regulated or down-regulated, respectively in laryngeal cancers (Figure 1A). [score:7]
Interestingly, recent study have reported that decreased expression of miR-455-5p was correlated with vascular invasion, poor overall survival, and poor disease-free survival in endometrial serous adenocarcinoma suggesting the potential involvement of miR-455-5p in cancer progression [44]. [score:5]
One known target of miR-455-3p is TTK (also known as MPS1) protein kinase [59] which regulates mitotic spindle formation and cell proliferation [60] [61]. [score:4]
While miR-130b-5p, miR-455-3p, miR-455-5p, and miR-801 were up-regulated in laryngeal cancer in our study, much less study has been performed on these miRNAs before. [score:4]
Significant up-regulation of miR-455-5p and miR-196a in multiple laryngeal cancer samples. [score:4]
Significant up-regulation of miR-455-5p was observed in cancers compared with NCs and benign samples. [score:3]
Furthermore, expression levels of miR-196a and miR-455-5p were significantly higher in cancer tissues when compared with neighboring controls (miR-196a, p = 0.0460; miR-455-5p, p = 0.0286) (Figure 2A), while expression level of miR-133b was significantly lower in cancer samples compared with controls (p = 0.0274) (Figure 2B). [score:3]
Significant expressional differences between matched pairs were reproduced in miR-133b, miR-455-5p, and miR-196a, among which miR-196a being the most promising cancer biomarker as validated by qRT-PCR analyses on additional 84 tissue samples. [score:3]
Up-regulated miR-455-5p may have different roles in the biology of laryngeal cancer compared with endometrial carcinoma. [score:3]
Statistically significant differences of the expression levels of miR-196a, miR-455-5p, and miR-133b were observed between matched pairs. [score:3]
miR-455-3p has been reported to be differentially expressed in smokers compared to nonsmokers [59]. [score:2]
Thus, of these 4 miRNAs, 3 miRNAs (i. e., miR-196a, miR-455-5p and miR-133b) showed significantly different expression levels in cancer tissues when compared with their matched control tissues and further quantification of miRNAs was performed using 48 laryngeal samples. [score:2]
When 48 samples were studied, the expression level of miR-455-5p was significantly higher in cancers compared with adjacent noncancerous counterparts and benign laryngeal tissues (p = 0.0113). [score:2]
miR-455-5p instead of miR-455-3p was used in further studies, because miRNAs 3p and 5p are generated from either side of the same precursor stem to have similar sequences and recent report suggested the potential involvement of miR-455-5p in cancer progression [44]. [score:1]
0071480.g003 Figure 3(A) Expression levels of miR-455-5p and miR-196a were measured by TaqMan® qRT-PCR using 48 tissue samples. [score:1]
Thus, qRT-PCR analysis was performed on residual 4 miRNAs (i. e., miR-130b-5p, miR-196a, miR-455-5p, and miR-133b). [score:1]
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9
[+] score: 47
The expression of miRNA-455 is detected in adrenal, ovarian granulosa, and mo del Leydig cell lines, and its expression is downregulated by trophic hormones or their second messenger, cyclic AMP [50]. [score:8]
As shown, the expression levels of miR-342 and miR-455 in SV were significantly downregulated, while miR-29a and miR-203 were upregulated when compared to those of the P21 mice. [score:8]
Among the list, members of the miR-29 family, miR-203, miR-762, and miR-1224, showed upregulation, whereas members of the miR-107 family, miR-127 and miR-130a/b, miR-342-3p, miR-351, miR-379, miR-455, and miR-467a, were downregulated in both strains. [score:7]
Two upregulated (miR-29a and miR-203) and two downregulated (miR-342 and miR-455) miRNAs shown in the microarray analyses were selected for q-PCR analysis. [score:7]
The four downregulated miRNAs are miR-107, miR-145, miR-342, and miR-455. [score:4]
Reduced expression of miR-455 was evident in our microarray analysis and q-PCR validation, and it might reflect a reduction of intermediate cells in the SV during aging. [score:3]
One of the putative targets of miR-455 is PAX6, which has been shown to play a critical role in the self-renewal and differentiation of neural stem cells. [score:3]
It is speculated that the loss of miR-455 and its subsequent effect on PAX6 expression may disrupt the normal progression of melanogenesis. [score:3]
These miRNAs include miR-107, miR-127, miR-130a/b, miR-145, miR-342, miR-351, miR-379, miR-455, and miR-467. [score:1]
miR-455 is also detected in primary melanoma cell lines and metastatic melanomas [51], [67]– [69]. [score:1]
These miRNAs include miR-29a/b, miR-100, miR-107, miR-130b, miR-193b, miR-343-3p, miR-351, and miR-455. [score:1]
miRNA-455 is also important for chondrogenesis [51]. [score:1]
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10
[+] score: 35
Out of the up-regulated miRs, miR-146a and miR-455 have known targets (Table 3). [score:6]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 A) C2C12 myotubes were treated with 10ng/ml of TWEAK for 18h following isolation of total RNA enriched with small RNAs. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 In order to understand the interaction between different genes, we generated common networks using Ingenuity Pathway Analysis (IPA) software. [score:4]
Recent studies have suggested that miR-455 is linked to the up-regulation of brown adipocyte formation. [score:4]
We studied the expression of miR-1-1, miR-1-2, miR-133a, miR-133b, miR-206, miR-146a, and miR-455. [score:3]
The up-regulation of this miR-455 in our miRNA-array and QRT-PCR assays further signifies its potential role in TWEAK -induced skeletal muscle-wasting (Figure 4A). [score:3]
The expression of a few miRs including miR-146a and miR-455 was found to be significantly increased in response to TWEAK treatment. [score:3]
TWEAK increased the expression of miR-715, miR-146a, miR-455, miR-322, mir-98, and miR-470 in C2C12 myotubes. [score:3]
Moreover, TWEAK also significantly increased the expression of miR-715, miR- 146a, miR-455, miR-322, mir-98, and miR-470 in TWEAK -treated C2C12 myotubes (Figure 3B). [score:3]
TaqMan qRT-PCR analysis of miR-1-1, miR-1-2, miR-133a, miR-133b, miR-206, miR-146a, miR-206, miR146a, and miR-455 in TWEAK -treated C2C12 cells. [score:1]
In addition, Eisenberg et al [34] have reported that the levels of miR-455 were increased about two fold in dystrophic muscle of facioscapulohumeral muscular dystrophy, limb girdle muscular dystrophy 2A, and nemaline myopathy. [score:1]
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11
[+] score: 33
As miR-199a, miR-455 and miR-1192 were up-regulated in PPARγ DN animals this may indicate that PPARγ normally inhibits their expression directly (e. g. by recruiting transcriptional inhibitors to those promoters) or indirectly (by the PPARγ specific transctivation of a transcriptional inhibitor). [score:14]
Interestingly, only four of the 21 regulated miRNAs (miR-199a, miR-455, miR-592, and miR-1192) were solely dependent on the genotype; independent of diet, the expression of miR-199a, miR-455 and miR-1192 was up-regulated in PPARγ DN animals whereas miR-592 was down-regulated in these mice compared to wt. [score:9]
The expression of four miRNAs was only dependent on the PPARγ expression status of the animals; miR-199, miR-455 and miR-1192 were upregulated in mice with dominant -negative PPARγ irrespective of the diet given to the animals, the fourth, miR-592, was reduced in mutant animals (“a” in Fig. 5C). [score:8]
In MSCs, some miRNAs were differentially regulated in both cell passages early after IBMX, DMX treatment with fold-changes >2 at day 2 after induction (e. g. miR-455; Fig. 3). [score:2]
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12
[+] score: 31
Morphine also induced a dose -dependent down-regulation of miR-448-5p, mir-204-5p, and miR-455-5p expression with corresponding changes in their mRNA targets involved in neurodevelopment, neurotransmission, and inflammation. [score:9]
In our neonatal mice, three miRs, miR-448-5p, mir-204-5p, and miR-455-5p, which targeted 9 of the 63 experimentally determined differentially expressed mRNAs, exhibited decreased expression in MS5 -treated hippocampus. [score:7]
Fig 4 illustrates the dose -dependent effects of morphine on array expression (panel A) and RT-PCR expression (panel B) of miR-204-5p, miR-448-5p, miR-455-3p, and miR-574-3p. [score:5]
However, despite the suppression of both mir-204-5p and miR-455-5p, Ap1s2 was still decreased. [score:3]
The miR-455-5p was decreased and both Prg4 and Pdzd2 were correspondingly increased as expected based on classical miR-mRNA regulation. [score:2]
The following TaqMan RT-PCR assays from Life Technologies were used to assess expression of mmu-miR-455, mmu-miR-574-3p, mmu-miR-448-5p, mmu-miR-45c-5p, mmu-miR-34c-3p, mmu-miR-204, mmu-miR-1839-3p, mmu-miR-153, mmu-miR-1983, mmu-miR-214 in mouse: 002455 (mmu-miR-455), 002349 (mmu-miR-574-3p), 464921_mat (mmu-miR-448-5p), 000428 (mmu-miR-45c-5p), 001197 (mmu-miR-204), 002584 (mmu-miR-34c*), 121203_mat (mmu-miR-1839-3p), 001191 (mmu-miR-153), 121204_mat (mmu-miR-1983), 002306 (mmu-miR-214) and 001973 (U6 snRNA). [score:2]
miR array profiling identified ten specific miRs that were altered (>1.5 fold, p < 0.05) by morphine (miR-204, miR-448, miR-455, miR-574, miR-34c, miR-34c*, miR-1839, miR-153, miR-1983 and miR-214) and RT-PCR analysis was performed for those ten miRs. [score:1]
RT-PCR analysis was performed for miR-448, miR-34c, miR-34c*, miR-204, miR-1839-3p, miR-153, miR-1983, miR-214, miR-455, miR-574-3p. [score:1]
The miR mir-455-5p was associated with 3 altered mRNAs (Prg4, Pdzd2, and Ap1s2). [score:1]
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13
[+] score: 19
Other miRNAs from this paper: mmu-mir-29b-1, mmu-mir-29b-2
We checked the expression of micro RNAs 122a which we reported earlier to be involved in TIMP4 regulation and mir29b and mir455‐5p, which were reported to be involved in MMP9 regulation. [score:5]
Since mir29b and mir455‐5p regulate the expression of MMP9, the high MMP9 levels in AVF mice can be partially attributed to these two microRNAs. [score:4]
We also evaluated the expression of mir29b, and mir455‐5p which we have reported to regulate the expression of MMP9 6. Although, there are no studies in heart that explain epigenetic silencing of TIMP4 due to methylation, but there is a report in lung cancer which shows that CpG islands in the TIMP4 promoter region get methylated 15. [score:4]
E. M., AVF versus WT, Student's t‐test, n = 6) and down‐regulated expression of mir29b and mir455‐5p in AVF mice as compared to WT (* P < 0.05, ±S. [score:3]
We also evaluated mir29b and mir455‐5p which have been shown to regulate MMP9 6. We observed down‐regulated expression of these two microRNAs in AVF mice as compared to WT mice. [score:2]
To validate this hypothesis, we created heart failure mo del by creating AV fistula in C57 BL/6 mice and looked into the promoter methylation (methylation specific PCR, high resolution melting, methylation sensitive restriction enzyme and Na bisulphite treatment followed by sequencing), histone modification (Ch IP assay) and micro RNAs that regulate TIMP4 (mir122a) and MMP9 (mir29b and mir455‐5p). [score:1]
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14
[+] score: 19
We conclude that miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543 represent an FGF2 -dependent system of multiple miRNAs that target specific genes operating in pathways and processes related to the lens differentiation (via c-Maf, Med1/PBP, N-myc, and Nfat5), miRNA-regulated RNA processing (via Cpsf6 and Tnrc6b) and nuclear/chromatin -based processes (via Med1/PBP, As1l, and Kdm5b/Jarid1b/Plu1). [score:4]
The current data suggest that multiple miRNAs, including miR-9, miR-137, miR-155, miR-301a, miR455, and miR-543 (Figure 7A and Figure 8A), regulate c-Maf expression through its 3′-UTR. [score:4]
To determine whether the aforementioned miRNAs identified in rat lens explant system are also expressed during mammalian lens development in vivo, we conducted ISH analysis of miR-9, miR-143, miR-155, miR-301a, miR-381, and miR-455 in E14.5 and newborn (P0) lenses. [score:4]
We found that seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, target at least two “early” genes examined (i. e., c-Maf, N-Myc, and Nfib). [score:3]
At this stage both miR-381 (H) and miR-455 (J) expression domains are restricted to the equatorial zone of the lens in proliferating, migrating, and differentiating lens cells. [score:3]
Seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, and connections to specific functional groups of genes are shown. [score:1]
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15
[+] score: 18
miR-504-3p and miR-455-3p were downregulated at magnetic field intensities of 1 mT and 3 mT, but upregulated in response to a 2 mT electromagnetic field. [score:7]
miR-504-3p and miR-455-3p were downregulated at magnetic field intensities of 1 mT and 3 mT and upregulated in response to a 2 mT electromagnetic field (E and G). [score:7]
Following the network analysis and confirmation of the miRNA array data via real-time PCR, we examined the effect of the magnetic field intensity on the expression levels of miR-30e-5p, miR-210-5p, miR-224-5p, miR-196b-5p, miR-504-3p, miR-669c-5p and miR-455-3p (Fig 6). [score:3]
However, miR-30e-5p, miR-210-5p, miR-224-5p, miR-196b-5p, miR-504-3p, miR-669c-5p and miR-455-3p may be closely related to the epigenetic mechanism associated with ELF-EMF exposure at a magnetic field intensity of 3 mT (Fig 5B). [score:1]
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16
[+] score: 16
The most significantly downregulated (mmu-miR-31, mmu-miR-455, mmu-miR-744, mmu-miR-695, mmu-miR-181a, mmu-miR-181d, mmu-miR-182, mmu-miR-190, mmu-miR-194) and upregulated miRNAs (mmu-miR-34c, mmu-miR-124, mmu-miR-142–3p, mmu-miR-706, mmu-miR-29c) were analyzed. [score:7]
The results of the miRNA– messenger RNA regulatory networks indicated that the common target gene between mmu-miR-181d and mmu-miR-455 was motile sperm domain containing 1 (MOSPD1); that between mmu-miR-31 and mmu-miR-182 was RNA polymerase II, TATA box -binding protein–associated factor (TAF4A); that between mmu-miR-455 and mmu-miR-182 was reticulon 4 (RTN4); that between mmu-miR-182 and mmu-miR-190 was brain-derived neurotrophic factor (BDNF); that between mmu-miR-142–3p and mmu-miR-34c was protein phosphatase 1, regulatory subunit 10 (PPP1R10); and that between mmu-miR-142–3p and mmu-miR-124 was leucine rich repeat containing 1 (LRRC1). [score:5]
The common target gene between mmu-miR-181d and mmu-miR-455 was motile sperm domain containing 1 (MOSPD1), that between mmu-miR-31 and mmu-miR-182 was RNA polymerase II, TATA box binding protein (TBP) -associated factor (TAF4A), that between mmu-miR-455 and mmu-miR-182 was reticulon 4 (RTN4), that between mmu-miR-182 and mmu-miR-190 was brain-derived neurotrophic factor (BDNF), that between mmu-miR-142–3p and mmu-miR-34c was protein phosphatase 1, regulatory subunit 10 (PPP1R10), and that between mmu-miR-142–3p and mmu-miR-124 was leucine rich repeat containing 1 (LRRC1). [score:4]
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17
[+] score: 16
Of these, eight (miR-193b, miR-199a-3p/hsa-miR-199b-3p, miR-455-3p, miR-210, miR-381 (also known as miR-381-3p), miR-92a, miR-320c, and miR-136) were upregulated, while the other four (miR-490-5p, miR-4287, miR-BART8*, and miR-US25-1*) were downregulated during this process [22]. [score:7]
We demonstrated that miR-193b regulates early chondrogenesis by targeting transforming growth factor β 2 (TGFB2) and TGFBR3 [23], and that miR-455-3p might promote early chondrogenesis by targeting RUNX2 [24]. [score:6]
Zhang Z. Hou C. Meng F. Zhao X. Zhang Z. Huang G. Chen W. Fu M. Liao W. MiR-455-3p regulates early chondrogenic differentiation via inhibiting Runx2 FEBS Lett. [score:3]
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18
[+] score: 15
Bone morphogenetic protein receptor 2 (BMPR2) is known to be targeted by miR-19a, −20a and miR-25 [28] and predicted to be targeted by miR-455. [score:5]
Of these miRNAs, 145 were expressed in both human and mouse BAT (Additional file 4), including 23 miRNAs that had the same name but their sequences differed by few nucleotides between the species (i. e. miR-155, miR-193b, miR-455). [score:3]
The miR-193b-365 cluster and miR-455 are known to regulate mouse brown fat development and were identified in our selection of 25 BAT-enriched miRNAs common to mice and humans. [score:3]
miR-455 expression levels are also increased in mature murine brown adipocytes and positively correlate with uncoupling protein 1 (UCP1) levels suggesting a potential metabolic role in brown adipocytes [10]. [score:3]
miR-193b null mice have elevated levels of miR-455 suggesting a compensatory effect in the absence of the miR-193b-365 cluster. [score:1]
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19
[+] score: 9
miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107 were differentially expressed in mouse fibrotic lung tissues. [score:3]
We found that miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107 were differentially expressed in a BLM -induced mouse mo del of pulmonary fibrosis (Fig. 1C). [score:3]
Five miRNAs, miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were validated to be dysregulated in the lung tissues from mice with silica -induced fibrosis (n = 6 per group) (Fig. 1B). [score:2]
The expression of mature miRNAs was assayed using TaqMan MicroRNA Assays (Applied Biosystems, Foster City, CA) specific for hsa-miR-486 (ID 001278), hsa/mmu-miR-21a (ID 000397), hsa-miR-455 (ID 001280), hsa-miR-151-3p (ID 002254), mmu-miR-1a (ID 002222), mmu-miR-133b (ID 002247), mmu-miR-5128 (ID 462199_mat), mmu-miR-223 (ID 002295), mmu-miR-146b (ID 001097), mmu-miR-133a (ID 001637), mmu-miR-449a (ID 001030), mmu-miR-122 (ID 002245), mmu-miR-351-3p (ID 464446_mat), mmu-miR-193a-5p (ID 002577), mmu-miR-151-3p (ID 001190), mmu-miR-574-3p (ID 002349), mmu-miR-3107/486 (ID 001278). [score:1]
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20
[+] score: 8
Potentially, editing of these miRNAs could therefore be a side effect of other regulatory functions performed by ADARs, which might in turn explain why the deeply conserved editing sites of miR-140*, miR-301a and miR-455 all lie outside of the seed sequence and other parts of the miRNA that may influence targeting properties [22]. [score:4]
One of these events, editing of miR-455 at position 17, had been verified by ADARB1 overexpression experiments in human cell lines [13]. [score:3]
Remarkably, we found that miR-301a and miR-455 were edited in bony fishes, implying that both miRNAs have experienced site-specific RNA editing during the past 450 million years [20]. [score:1]
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21
[+] score: 8
Interestingly, we were able to identify 8 differentially expressed miRNAs related to UPR including miR-30c-2-3p, miR-455, miR-125a-5p, miR-17-5p, miR-143-3p, miR-16-5p, miR-181d-5p and miR-34a-5p in VAT/BAT based on literature and IPA [®] (Figure 3). [score:3]
Same direction of fold change was observed for seven miRNAs including miR-455-3p, miR-30c-2-3p, miR-222-3p, miR-99b-5p, miR-199a-3p, miR-143-3p, and let-7a-5p. [score:2]
Another miRNA, miR-455: calreticulin association was identified previously in murine cardiomyocytes [32] However, we did not observe any significant changes in miR-455-3p in adipose tissue. [score:1]
The miRNAs we tested were let-7a-5p, miR-30a-5p, miR-30c-2-3p, miR- 99b-5p, miR-143-3p, miR-199a-3p, miR-221-3p, miR-222-3p, miR-455-3p, and miR-708-5p. [score:1]
We also performed qPCR for selected miRNAs that were related to ER stress (miR-125b-5p, miR-143-3p and miR-222-3p, miR-30c-2-3p, and miR-455-3p), in BAT and VAT of LFD and HFD fed mice (Figure 6). [score:1]
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22
[+] score: 8
The selection of the miRNAs is based on their potential role in the pathology of the lung (mmu-miR-1, 146b, -203, -21, -223, -29b, -29c) or on their high and significant differential expression in the mo del (mmu-miR-455, -574-5p, -672, -690) or for their high (mmu-let-7b a, mmu-miR-145) or low (mmu-miR-450a-5p) signal intensity in microarray analysis. [score:3]
Among these miRNAs, miR-455 has been reported to be implicated in brown adipocyte differentiation [53], while the functions or targets of the others are not determined yet. [score:3]
Among these data, 40 out of 42 (95%) gave results and trends similar to those obtained by microarray profiling, except for mmu-miR-29c at ST and LT (Figure 2), although the magnitude of the observed regulation was not always identical (mmu-miR-455 at LT and mmu-miR-450a at IT). [score:2]
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23
[+] score: 7
The upregulated miRNAs included mmu-miR-34a-5p, mmu-miR-129b-5p, mmu-miR-451a, mmu-miR-144-5p and mmu-miR-129b-3p, whereas highly downregulated miRNAs included mmu-miR-100-5p, mmu-miR-99a-5p, mmu-miR-33-5p, mmu-miR-125a-5p, mmu-miR-128-1-5p, mmu-miR-181b-1-3p, mmu-miR-188-5p, mmu-miR-196b-5p, mmu-miR-211-5p, mmu-miR-224-5p, mmu-miR-455-3p, mmu-miR-504-5p, mmu-miR-592-5p, mmu-miR-5107-3p, mmu-miR-5120, and mmu-let-7i-3p. [score:7]
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24
[+] score: 7
The quantitative RT-PCR analysis confirmed that all four of the selected up-regulated hsa (Homo sapiens)-miRNAs (miR-205, miR-182, miR-135b, and miR-455-3p) were significantly up-regulated in NPC tissues (Fig. 1C). [score:7]
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25
[+] score: 5
Interestingly, the certain miRNAs, such as miR-96, miR-140, miR-151, miR-185, miR-378, miR-455, miR-532, and miR-874, presumably targeting a 3’UTR of INSR, were upregulated by more than 1.5-fold in the liver of HFD mice compared to NFD-fed control, whereas the levels of other selected miRNAs remained unaffected (S2 Fig). [score:5]
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26
[+] score: 5
Bioinformatics analysis identified the key biochemical signaling and cellular plasticity pathways that are targeted by miR-19b, miR-133a and miR-455. [score:3]
We confirmed that miR-455 was significantly decreased (t [(8)]=3.16, P=0.0134) in sperm of runners. [score:1]
miR-190b and miR-19b-2 were increased and miR-133a-1, miR-133a-2 (same gene sequences mapped to different chromosomes) and miR-455 were decreased. [score:1]
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27
[+] score: 5
Several miRNAs are regulated by Sox9 (e. g. miR-140 and miR-455) [13– 15] or regulate Sox9 expression (e. g. miR-675 and miR-145) [16, 17]. [score:5]
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28
[+] score: 5
Furthermore, we identified miR-9, miR-455, and miR-1224 as microRNAs downregulated upon myelination and reduced following Dicer ablation from Schwann cells. [score:4]
Only three microRNAs met these criteria: miR-9, miR-455, and miR-1224. [score:1]
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29
[+] score: 5
Other miRNAs from this paper: mmu-mir-30c-2, mmu-mir-211, mmu-mir-708
The expression of calreticulin, an ER chaperone involved in glycoprotein folding, is regulated by miR-455 and ncRNA-RB1, a lncRNA that shares a bidirectional promoter with the RB1 gene. [score:5]
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30
[+] score: 4
Quantitative analysis of miR-32-5p, miR-142-5p, miR-455-3p and miR-1249-3p expression was performed with reverse transcription polymerase chain reaction (RT-PCR) using the TaqMan MicroRNA Reverse Transcription kit (Applied Biosystems, Waltham, MA, USA) and 10 ng of total RNA. [score:3]
Thus, we shortlisted four miRNAs—miR-32-5p, miR-142-5p, miR-455-3p and miR-1249-3p. [score:1]
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31
[+] score: 3
The mG [+] cells also expressed higher levels of miR-143, miR-145 and miR-455 (Fig. 2D), known as adipogenic miRNAs [7]. [score:3]
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32
[+] score: 3
We found that our transcript sequence could be a target of three miRNAs: hsa-miR-455-5p, has-miR-640 and has-miR-1909-3p. [score:3]
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33
[+] score: 3
Of the nine miRNAs were specifically expressed in cashmere goat dorsal skin [18], only four of them were examined in the present study: miR-1, miR-374, miR-455-3p and miR-92b. [score:3]
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34
[+] score: 3
The rest of the differentially expressed miRNAs between strains have been found to be altered in different neurodegenerative mo dels (28a-5p, miR-337-3p, miR-431-5p, miR-455-5p). [score:3]
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35
[+] score: 2
Other miRNAs from this paper: mmu-mir-29b-1, mmu-mir-30a, mmu-mir-146a, mmu-mir-320, mmu-mir-29b-2
Chaturvedi P Kalani A Medina I Familtseva A Tyagi SC Cardiosome mediated regulation of MMP9 in diabetic heart: role of mir29b and mir455 in exerciseJ. [score:2]
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36
[+] score: 2
Moreover, there is also the first demonstrated elevated levels of miR-874-3p, miR-7a-5p, miR-455-5p, miR-129-1-3p, miR-151-5p, miR-3473b, and down regulated levels of miR-345-3p, novel_mir_8 and let-7 k in the kidneys of db-/db- mice. [score:2]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
Recently, we reported that SR-BI, which delivers the bulk of the cholesterol substrate for steroidogenesis, is regulated by two specific miRNAs, miRNA-125a and miRNA-455, in rat granulosa cells, a mo del mouse Leydig cell line and the rat adrenal gland [19]. [score:2]
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38
[+] score: 2
miR-24, miR-186, and miR-455 are regulators of NCT [12]. [score:2]
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39
[+] score: 1
2 mmu-miR-204* mmu-let-7b mmu-miR-30c mmu-miR-500* mmu-miR-219-3p mmu-miR-362-3p mmu-miR-455* mmu-miR-3098-5p mmu-miR-193 DEmiRNAs in bold were confirmed using. [score:1]
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40
[+] score: 1
We focused our analysis on 12 miRNAs (miR-22, miR-29a-3p, miR-34a, miR-126, miR-140-3p, miR-141, miR-181c-5p, miR-202, miR-455-5p, miR-508-3p, miR-517a-3p and miR-576-3p). [score:1]
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41
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-211, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Among these, 16 precursors were found amongst the 43 conserved between human, mouse, cow and goat in our analysis (let-7 g, mir-101-2, mir-103, mir-107, mir-128-1, mir-1306, mir-140, mir-15b, mir-16b, mir-211, mir-218-1, mir-26a-1, mir-32, mir-33a, mir-455, let-7-2), so the location of these precursors appears to be highly conserved in all vertebrates. [score:1]
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