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49 publications mentioning rno-mir-223

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-223. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 255
TS1,target site 1 (a pooly conserved binding site); TS2, target site 2 (a conserved binding site); Bottom panel: with targets and their mutant along with miR-223/miR-Con overexpressing vectors. [score:9]
above demonstrate that miR-223 contributes to hypoxia -induced phosphorylation of MYPT1 by targeting RhoB and more importantly, has a direct inhibitory effect on MLC2 expression. [score:8]
Overexpression of miR-223 caused a remarkable decrease in MLC2 protein levels, while miR-223 inhibition increased the expression of MLC2. [score:7]
Chemically synthesized miRNA mimics or inhibitors to overexpress or inhibit miR-223 and each unrelated negative control (miR-Con or anti-Con), were purchased from Ribobio (Guangzhou, China). [score:7]
The correlation between the expression of RhoB and miR-223 was ascertained in primary culture of PASMC and in an in vivo PAH rat mo del by both miR-223 overexpression and/or knockdown approaches. [score:6]
To determine whether miR-223 expression in PASMC parallels expression in lungs of hypoxic mice, we isolated PASMC from Sprague-Dawley rats and exposed them to hypoxia. [score:5]
Our study demonstrates that miR-223 regulation directly targets RhoB and MLC2 to affect vascular remo deling and hypoxia -induced pulmonary hypertension. [score:5]
Here, we discovered that treatment with miR-223 agomir markedly attenuates chronic hypoxia -induced pulmonary vascular remo deling in vivo, due to its post-transcriptionally inhibitory effects on RhoB and MLC2 expression. [score:5]
Cells at 70% confluence after overnight culture on petri dishes were transfected with miR-223 mimic, mimic control (miR-Con) (50 nmol/L), or miR-223 inhibitors (anti-223), inhibitor control (anti-Con) (100 nmol/L) by Lipofectamine 2000 (Invitrogen). [score:5]
TargetScan predicted RhoB having two miR-223 target sites and defined site 1 as poorly conserved and site 2 as a conserved site. [score:5]
Therefore, a small molecular drug, like miR-223, may improve efficacy by targeting the RhoB/Rho Kinase/MLC2 signaling in pulmonary vascular diseases. [score:5]
miR-223 overexpression and inhibition. [score:5]
We elucidate a RhoB/ROCK -associated regulatory pathway that is suppressed by miR-223 and the decrease of miR-223 in hypoxia leads to pathologic changes in PASMC (as summarized in Fig. 7). [score:4]
The results above clearly show that RhoB is a direct target of miR-223 in PASMC. [score:4]
To determine how miR-223 regulates PASMC proliferation, migration and consequently pulmonary vascular remo deling, we identified the miR-223 target proteins involved in these processes. [score:4]
miR-223 is downregulated by hypoxia in PASMC. [score:4]
Identification of RhoB and MLC2 as direct targets of miR-223. [score:4]
Validation of miR-223 downregulation by hypoxia in mouse lungs (B), rat lungs, n = 8 (C) and rat pulmonary arteries (PA), n = 8 (D) was performed by qRT-PCR. [score:4]
In our study, we uncovered that there are gender differences in downregulation of serum levels of circulatory miR-223 in patients with CHD-PAH. [score:4]
Reporter gene analysis revealed that mutation of site 2 resulted in complete loss of the inhibitory activity of miR-223, while site 1 mutation showed no activity change compared to wild type construct, although it indicates that there may be more bases pairing with miR-223. [score:4]
This study reveals that miR-223 is rapidly downregulated in response to hypoxia in PASMC and is critical to chronic hypoxia -associated pulmonary vascular pathology, such as smooth muscle cell proliferation, migration and actomyosin reorganization, which ultimately results in vascular remo deling and distal arteriole muscularization. [score:4]
During the preparation of this manuscript, Meloche et al. most recently showed that miR-223 was downregulated in PAH-PASMCs and lungs of monocrotaline -treated PAH rats. [score:4]
Here we further corroborated RhoB as a direct target of rno-miR-223 in rat PASMC. [score:4]
Overexpression of miR-223 using agomir antagonized the hypoxic effects on pulmonary artery pressure and distal arteriolar muscularization in vivo. [score:3]
Comparable results were obtained when expression of miR-223 was studied in human PASMC (hPASMC) under hypoxic conditions (Fig. 1E, right panel). [score:3]
The results fit well with a recent report that hsa-miR-223 interacts with RhoB, in which the authors proposed that some AU-rich motif located upstream of distal miR-223 -binding site enhances the miRNA function, independent of the miRNA target sequence being tested 41. [score:3]
Moreover, the altered migration in miR-223 -expressing cells was associated with a decrease in stress fiber levels, a feature reflected by the higher F-actin content in cells that have active actomyosin contraction (Fig. 2D). [score:3]
miR-223 inhibits PASMC proliferation, migration and stress fiber formation. [score:3]
It was previously reported that the 3′-UTR of RhoB could be targeted by hsa-miR-223 in human cell lines 41. [score:3]
After RVSP recording, whole blood were collected via right ventricular puncture, filled in 1.5 ml tubes, centrifuged for 3,000 × g for 10 min at 4 °C, and serum collected for detection of miR-223 expression levels. [score:3]
Rats were injected with either agomir control (miR-Con) or agomir specifically expressing miR-223 (miR-223). [score:3]
Mutation of the downstream binding site (Mut 2) completely antagonized the inhibitory effect of miR-223 in the luciferase assay. [score:3]
HEK293 cells were seeded in 24-well plates and after the cells reached 80~90% confluence, each well of cells was transfected with 100 ng of 3′-UTR reporter vectors or mutated 3′-UTR reporter vectors, 900 ng of miR-223 expressing plasmid (pLVX-CMV-miR-223) with 2 μl of Lipofectamine 2000 (Invitrogen, Carlsbad, CA). [score:3]
Notably, a negative correlation of total MLC2 expression and miR-223 levels was found in rPASMC and hPASMC (Fig. 5D). [score:3]
A negative correlation between the expression of miR-223 and RhoB protein was detected in mouse lungs, as well as in rat and human PASMC exposed to hypoxia (Fig. 4A). [score:3]
We have not explored the miR-223 expression and RhoB/ROCK/MLC pathway in pulmonary artery endothelial cells (PAECs), the abnormality of which also contributes to the pathology of pulmonary arterial hypertention. [score:3]
In order to validate RhoB as a direct target of miR-223, we performed a reporter gene assay to ascertain the interactions between miR-223 and RhoB 3′-UTR. [score:3]
Our data show that increasing the expression of miR-223 abrogated the hypoxia -induced increase in proliferation, migration, as well as stress fiber assembly in both rPASMC and hPASMC. [score:3]
miR-223 inhibition also enhanced the phosphorylation of MYPT1 and MLC2, partially mimicking the effects of hypoxia. [score:3]
Hypoxia decreases miR-223 expression in lungs, pulmonary artery and pulmonary arterial smooth muscle cells. [score:3]
The mRNA level of RhoB in both hypoxia -treated rPASMC and hPASMC was also negatively correlated with miR-223 expression (Fig. 4B). [score:3]
Rangrez et al. found that overexpressing miR-223 in aortic vascular smooth muscle cells (VSMCs) increased proliferation and markedly enhanced cell migration 38, demonstrating miR-223 may function in a tissue-specific manner. [score:3]
Conversely, miR-223 inhibition augmented the proliferation of PASMC under normoxic conditions (Supplementary Figure S2A, B). [score:3]
miRNA target prediction with FINDTAR3 indicated a potential miR-223 binding site in the 3′-UTR of MLC2. [score:3]
This study identifies miR-223 as a potential target in experimental PAH and the possible benefits of miR-223 agomir therapy in its treatment. [score:3]
In this study, we discovered a decrease in expression of miR-223 in hypoxia -induced PAH mouse lungs, pulmonary artery and isolated PASMC. [score:3]
Conversely, overexpression of miR-223 reduced the levels of phosphorylated MYPT1 and MLC2 (Fig. 5D). [score:3]
Rho GTPase activation assay showed that miR-223 not only repressed the expression of RhoB but also markedly reduced its activity (Fig. 5C). [score:2]
The results revealed that standing out from 1040 miRNAs measured, there were five significantly changed miRNAs between normoxia and hypoxia (p < 0.01) and miR-223 (also called miR-223-3p) was the most significantly downregulated miRNA (Fig. 1A). [score:2]
It still remains unknown if there is a relationship between miR-223 reduction in female serum and gene regulatory abnormality on X chromosome in CHD-PAH patients. [score:2]
For miRNA assay, the mature miR-223 expression level was determined according to S-Poly(T) method, as we previously reported 53 54. [score:2]
To confirm the consequences of miR-223 on cell proliferation, EdU incorporation assay and PCNA immunoblotting were also performed in cells transfected with miR-223 inhibitor. [score:2]
Furthermore, enhanced expression of miR-223 also inhibited hypoxia -induced increase in cell migration in both rPASMC and hPASMC, as measured using a chamber invasion assay of cells passing through a transwell filter (Fig. 2C). [score:2]
Data are shown as means ± SE, ** p < 0.01. miR-223 attenuates hypoxia -induced smooth muscle cell proliferation, migration and actomyosin reorganization, and the consequent vascular remo deling and pulmonary hypertension by regulating the RhoB/MLC pathway. [score:2]
MiR-223 targets RhoB and MLC2 in pulmonary arterial smooth muscle cells. [score:2]
Further, we demonstrated the 3′-UTR of MLC2 mRNA was post-transcriptionally regulated by miR-223. [score:2]
An independent quantitative real-time PCR (qRT-PCR) assay confirmed the decreased expression of miR-223 in mouse lungs in response to hypoxia (Fig. 1B). [score:2]
Notably, the two target sites when tested in the assay exhibited substantial differences in their susceptibility to miR-223 mediated repression. [score:2]
How to cite this article: Zeng, Y. et al. MicroRNA-223 Attenuates Hypoxia -induced Vascular Remo deling by Targeting RhoB/MLC2 in Pulmonary Arterial Smooth Muscle Cells. [score:2]
Upper panel: putative miR-223 binding sites in the 3′-UTR of RhoB or MLC2 along with the mutation sites. [score:2]
They reported that miR-223 played anti-proliferative and pro-apoptosis roles in PAH-PASMC by directly repressing PARP-1 40. [score:2]
Co-transfection of HEK-293 cells with pre-miR-223 and a luciferase construct containing the two putative miR-223 binding sequences within the 3′-UTR of RhoB resulted in a significant decrease (about 50%, p < 0.01) in luciferase activity, indicating direct interaction between them. [score:2]
EdU incorporation assay and PCNA immunoblotting showed that miR-223 overexpression significantly prevented the increase in cell proliferation induced by hypoxia (Fig. 2A,B). [score:2]
As miR-223 locus is located on the X chromosome, a new study was carried out on 13 male CHD-PAH patients/ healthy donors or 17 female CHD-PAH patients/ healthy donors to determine whether gender differences exist (Supplementary Table S1). [score:1]
All the results above indicate that miR-223 is involved in the proliferative and migratory responses in PASMC to hypoxia. [score:1]
miR-223 agomirs (30 nmol), agomir control (30 nmol), or the normal saline (NS) were injected intravenously (tail vein, 0.3 ml) at day 7 and 14. [score:1]
A recent study on circulating miRNAs as potential markers for pulmonary hypertension by using a microarray approach identified that plasma miR-223 levels were decreased in these patients 34. [score:1]
To confirm our findings in vivo, we determined the effect of administering an agomir of miR-223 or an unrelated agomir control on right ventricular systolic pressure (RVSP) and pulmonary vascular muscularization in rats exposed to chronic hypoxia. [score:1]
We observed a 50% decrease in miR-223 levels, with a maximal decrease after 6 to 12 hours of hypoxia (Fig. 1E, left panel). [score:1]
It also suggests a potential use of miR-223 levels as a circulating biomarker for clinical diagnosis in women with CDH-PAH. [score:1]
Serum miR-223 is a potential circulating biomarker for PAH. [score:1]
These results point to miR-223 as a miRNA that is decreased by hypoxia in PASMC. [score:1]
Recently, Shi et al. reported that miR-223 antagonizes angiogenesis by abrogating VEGF and bFGF -induced cell proliferation, migration and tube formation in vascular endothelial cells 27. [score:1]
Another study on 7 male and 17 female CHD-PAH patients/ healthy donors (Supplementary Table S2) showed significant decrease in circulating miR-223 levels in CHD-PAH patients and confirmed the gender-related alteration (Fig. 6C,D). [score:1]
The decrease in miR-223 was also observed in rat lungs and in pulmonary arteries (PA) following 3-weeks of hypoxia (Fig. 1C,D, respectively). [score:1]
Serum miR-223 as a potential circulating biomarker for CHD-PAH. [score:1]
org), we found two potential miR-223 binding sites within RhoB 3′-UTR (Fig. 5A). [score:1]
Rats for in vivo studies were randomized into four groups (n = 8 each): 1) a normoxic control group, 2) a hypoxic control group, 3) a hypoxic group injected with agomir control, and 4) a hypoxic group injected with miR-223 agomir (Ribobio). [score:1]
We observed similar results with the cell proliferative marker PCNA, indicating that miR-223 has an anti-proliferative effect in experimental PAH. [score:1]
The miR-223 expression level in human serum samples was normalized to hsa-miR-16-5p and calculated using the 2 [(−ΔCt)] method. [score:1]
Our results show that pulmonary artery pressure and distal arteriolar muscularization following chronic hypoxia were significantly decreased when level of miR-223 was preserved. [score:1]
Coincident with the effects on pulmonary vascular pressure, the ratio of right to left ventricle plus septum weight [RV/(LV + S)] in rats treated with miR-223 agomir also showed an attenuated increase in hypoxia (Fig. 3B). [score:1]
Our results show that the levels of circulating miR-223 in CHD-PAH manifest a gender related difference. [score:1]
In an early study, Caruso et al. reported that miR-223 was decreased in chronic hypoxia -treated PAH rat lungs 37. [score:1]
Levels of miR-223 in 30 normal versus 30 CHD-PAH patients (A), 13 male normal versus 13 male CHD-PAH patients, and 17 female normal versus 17 female CHD-PAH patients (B), a second group of 24 normal versus 24 patients (C), 7 male normal versus 7 male patients, and 17 female donors versus 17 female patients (D), respectively were normalized to hsa-miR-16-5p and represented in scatter plots. [score:1]
Schematic mo del showing the role of miR-223 in pulmonary arterial hypertension in response to hypoxia. [score:1]
We found that serum miR-223 levels in patients were lower than that in healthy donors but with no significant difference (p = 0.058) (Fig. 6A). [score:1]
miR-223 attenuates chronic hypoxia -induced pulmonary vascular remo deling. [score:1]
These results are of great clinical significance as it highlights miR-223 as a potential diagnostic circulating biomarker in female CHD-PAH patients. [score:1]
In addition, we measured the protein levels of these two targets in rats with hypoxia -induced PAH with miR-Con and miR-223 agomir treatment. [score:1]
It will be of great interest to study whether miR-223 agomir shows better effect by intratracheal nebulization. [score:1]
To assess the role of miR-223 in modulating cell proliferation, cells were transfected with miR-223 mimic, which increased miR-223 levels in cultured rPASMC and hPASMC (Supplementary Figure S1). [score:1]
The miR-223 expression level was normalized to SNORD44 (in human tissue sample), rno-miR-16-5p (in rat serum sample) or snoRNA202 (in mice or rat tissue sample) and calculated using the 2 [(−ΔΔCt)] method. [score:1]
Serum levels of miR-223 in female CHD-PAH patients were significant lower than that in healthy female donors, but there was no difference between male CHD-PAH subjects and control subjects (Fig. 6B). [score:1]
Rat and human PASMC were transfected with mimic control (miR-Con) or miR-223 mimic (miR-223) and exposed to hypoxia (3% O [2]) or normoxia for 24 h in triplicate. [score:1]
Our results point to a gender-specific response in circulating miR-223 in pulmonary hypertension associated with CHD. [score:1]
These hypoxia -induced changes in RhoB were opposite to the effects on miR-223, pointing to a negative relationship between them. [score:1]
Expression of serum miR-223 was measured by qRT-PCR in healthy human donors (normal) and CHD-PAH patients. [score:1]
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[+] score: 136
Thus, upregulation of oncogenic miR-223, -31, and -21 is accompanied by down-regulation of their respective tumor suppressor target Fbxw7, Stk40 and Pdcd4. [score:11]
miR-223, -31, -21 upregulation correlates with down-regulation of their tumor-suppressor targets. [score:11]
We then determined whether upregulation of oncogenic miR-223, -31, and -21 in ZD3T, ZD6T, and ZD12T esophagus is accompanied by down-regulation of their respective tumor suppressor targets, FXBW7 [25, 61], STK40 [60, 62, 63], and PDCD4 [64], by using qPCR (n = 7-10 rats/group). [score:11]
That the tumor suppressor genes Fxbw7, Pdcd4, and Stk40 were downregulated at the mRNA and protein level in marked-ZD tumor group (Figure 6) and that they were predicted to interact to alter network of target proteins [65, 66, 77] (Figure 7) provide support that miR-223, miR-21, and miR-31 have an important role in ESCC and may be useful prognostic biomarkers and therapeutic targets for ESCC. [score:10]
Analysis of esophageal expression of Fbxw7, Stk40, and Pdcd4 (respective tumor suppressor targets of miR-223, miR-31, and -21) in Zn-modulated rats at tumor endpoint. [score:7]
That the three tumor suppressor targets are predicted to interact to alter network of cancer-related proteins [65, 66, 77] provide support that miR-223, miR-21, and miR-31 have an important role in ESCC and may be useful therapeutic targets in ESCC. [score:7]
We selected 8 miRNAs in ZD3T esophageal tissue (miR-223, -21, -31, -146a, -146b, -221, -194, and -106b) and two miRNAs (miR-31, -223) in ZD6T and ZD12T esophageal tissues, Figure 4B shows that the Taqman data confirmed the upregulation of all 8 selected miRNAs in ZD3T vs ZST samples, and the upregulation of miR-223 and miR-31 in ZD6T and ZD12T samples. [score:7]
In ESCC, patients with high miR-223 expression have a significantly poorer prognosis, presumably because of repression of the function of its tumor suppressor target FBXW7 [25]. [score:7]
miR-223, miR-21, and miR-31 can target many important tumor suppressor genes, including FXBW7 [25, 61], STK40 [60, 62, 63], and PDCD4 [64]. [score:5]
Figure 7 A. The displayed esophagus-specific nine-gene network shows predicted functional relationships among the genes that are most functionally related to Stk40, Pdcd4 and Fbxw7 (tumor-suppressor targets of miR-31, mir-21 and miR-223, respectively). [score:5]
To explore the esophagus-specific functional relationships for Fbxw7, Stk40, and Pdcd4 (tumor-suppressor targets of miR-223, -31, -21), we employed FNTM for the rat. [score:5]
A. The displayed esophagus-specific nine-gene network shows predicted functional relationships among the genes that are most functionally related to Stk40, Pdcd4 and Fbxw7 (tumor-suppressor targets of miR-31, mir-21 and miR-223, respectively). [score:5]
miR-223, miR-21, and miR-31 are the top -upregulated species in the high ESCC-burden, marked-ZD esophagus. [score:4]
This 15-miRNA signature (Figure 3B, marked by asterisks) was defined by strong to modest upregulation of oncogenic miR-223, -21, -31, -146a, -146b, -27a, -221, -27b, -194, -24, -203, -183, -130b, -106b, and -22 (up 3.6 to 1.4 fold). [score:4]
Importantly, the high ESCC-burden, marked-ZD esophagus showed a 15-miRNA signature (with miR-223, -21, and -31 as the top-up-regulated species), thus differentiating it from the low ESCC-burden, mild-ZD esophagus with a 2-miRNA signature (miR-223, -31). [score:4]
By contrast, low ESCC-burden, ZD6T and ZD12T esophagus displayed, respectively, a 3-miRNA signature (miR-223, -31, -27b) and a 2-miRNA signature (miR-223, -31; up 2.9 and 1.5 fold) with modest upregulation (Figure 3B). [score:4]
The mechanism(s) by which miR-223 and miR-21 are upregulated by ZD remains to be elucidated. [score:4]
Thus, moderate and mild-ZD induces alterations in miRNA expression, including miR-31 and miR-223. [score:3]
Cellular localization of miR-223, miR-31 and miR-21 expression in human ESCC tissue. [score:3]
Our study suggests that miR-223, miR-31 and miR-21 alone or in combination could be used as therapeutic targets for treatment of ESCC. [score:3]
In addition, miR-223 and miR-31 dysregulation is common to marked-ZD and moderate/mild-ZD tumor groups (Figure 4A). [score:2]
Whether miR-223 and miR-21 co-localize in the same ESCC tissue is not known. [score:1]
miRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, rno-miR-21, rno-miR-31, rno-miR-223, hsa-miR-31, hsa-miR-223, negative controls (rno-miR-31) with mismatches at two position, were purchased from Exiqon (Vedbaek, Denmark). [score:1]
Figure 4 A. Venn diagram showing miR-223 and miR-31 are common to ZD3T, ZD6T, and ZD12T esophagi (cutoff point of P < 0.05 and fold difference >1.3), and scatterplot showing their fold change vs ZST. [score:1]
A limitation of this study is the fact that the underlying biological mechanisms of the key dysregulated miRNAs in ESCC development, namely, miR-223, miR-21, and miR-31, were not investigated. [score:1]
In situ hybridizationmiRCURY locked nucleic acid (LNA)™ microRNA detection probes, namely, rno-miR-21, rno-miR-31, rno-miR-223, hsa-miR-31, hsa-miR-223, negative controls (rno-miR-31) with mismatches at two position, were purchased from Exiqon (Vedbaek, Denmark). [score:1]
A. Venn diagram showing miR-223 and miR-31 are common to ZD3T, ZD6T, and ZD12T esophagi (cutoff point of P < 0.05 and fold difference >1.3), and scatterplot showing their fold change vs ZST. [score:1]
miR-223 acts as an oncomiR in several solid tumors, including ESCC, gastric, ovarian, and bladder cancers [25, 80– 82]. [score:1]
Localization of miR-223, miR-31, and miR-21 in human esophageal squamous cell carcinoma (ESCC) tissue by in situ hybridization (ISH). [score:1]
B. Validation of eight representative miRNAs in ZD3T esophagus; and miR-223 and miR-31 in ZD6T and ZD12T esophagi. [score:1]
Following deparaffinization, rehydration in graded alcohol and proteinase K treatment, tissue sections were hybridized with miR-31 probe (20 nM), miR-223 or miR-21 probe (50 nM) in hybridization buffer (Exiqon) at 50°C - 57°C for 14 h in a hybridizer (Dako, Glostrup, Denmark). [score:1]
These results represent the first simultaneous in situ detection of miR-223, -21, and -31 in human ESCC. [score:1]
Among which, miR-31 [15, 16, 30, 60] and miR-223 [25, 26, 34] are oncomiRs for human ESCC. [score:1]
miR-223, -31, and -21 ISH signal (blue, 4-nitro-blue tetrazolium and 5-brom-4-chloro-3′-indolylphosphate; counterstain, nuclear fast red) was moderate to intense and abundant in near serial formalin-fixed, paraffin-embedded sections of ESCC tumor tissue. [score:1]
All 12 cases showed intense to moderate miR-31, miR-223, and miR-21 ISH signal in near serial sections of moderately to poorly differentiated ESCC tumor samples (Figure 5). [score:1]
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[+] score: 130
In contrast, the miRNA panel from lung specimens of MCT rats overexpressing hPGIS exhibited restoration of dysregulated miRNA levels to levels of naïve control rats, with downregulation of miRNAs that had been increased by MCT (miR-17, miR-21, and miR-223), and upregulation of miRNAs that had been decreased by MCT (miRs 424 and 503), Fig 5C]. [score:10]
The upregulation of miR-21 and miR-223 for all tissues examined indicates the possibility they are ubiquitously upregulated in all tissues affected by PAH, while other miRNAs may have a more tissue-specific dysregulation, for example miR-124 which is predominantly dysregulated in adventitial fibroblasts. [score:9]
Consistent with upregulation of miR-223, levels of IGF1R mRNA were downregulated in PA of MCT PAH rats, whereas the decreased miR-328 expression would have been expected to increase IGF1R mRNA levels. [score:9]
We also report downregulation of miR-223 in MCT PAH with specific inhibition of miR-223 that failed to attenuate MCT PAH, whereas overexpression of hPGIS reversed dysregulation of multiple miRNAs in lung specimens and attenuated MCT PAH [33]. [score:9]
Overexpression of miR-223 has been shown to downregulate expression of IGFR1 in HeLa, leukemia, hepatoma, and human embryonic stem cells [46– 48]. [score:8]
Since miRs 17, 21, and 223 were significantly upregulated in the PA of MCT PAH rats, we performed qPCR for BMPR2 and IGF1R mRNA, as these miRNAs have been associated with downregulation of BMPR2 (miR 17, 21 and 145) and IGF1R (miR-223 and 328). [score:7]
In the current study, miR-328 expression was modestly reduced in lung, but not PA, of MCT PAH rats, whereas miR-223 was consistently upregulated in all tissues and plasma. [score:6]
Inhibition of miR-223 did not attenuate MCT PAH, whereas human prostacyclin synthase overexpression restored miRNA levels in MCT PAH to levels detected in naïve rats. [score:5]
We do not know the much about miR-223 dysregulation in humans with PAH, but data showing upregulation of miR-223 by 1.5-fold in miRNA microarray heat maps of buffy coat blood specimens of human subjects with PAH are encouraging [36]. [score:5]
To evaluate a potential pathogenic relationship between miR-223 upregulation and PAH, we performed specific inhibition of this miRNA by injecting MCT PAH rats with A223 or a nonspecific control oligonucleotide, A-control. [score:4]
To explore whether findings from miR-223 dysregulation in cardiovascular disease could be extended to PAH [31, 32], we measured expression of miR-223 in MCT PAH rats. [score:4]
As shown in Fig 1, miR-223 was upregulated in lung, PA, RV, and plasma of MCT PAH rats. [score:4]
As shown in Fig 1, miR-223 was upregulated in lung, PA, and RV of MCT PAH rats. [score:4]
A223 inhibition of miR-223 did not attenuate MCT PAH, whereas hPGIS through modulation of multiple miRNAs did. [score:3]
These observations led us to evaluate the expression and function of miR-223 in MCT PAH by administering a specific inhibitor of miR-223 (A223) to MCT PAH rats. [score:3]
Based on TargetScan predictions, miR-223 binds to the seed region of IGF1R at position 234–241. [score:3]
0147827.g003 Fig 3Expression levels of miR-223 relative to saline-saline (naïve) control animals. [score:3]
In this study, we examined the expression of a panel of miRNAs in the monocrotaline (MCT) PAH rat mo del, evaluated the functional role of a specific miR-223 inhibitor on attenuation of PAH, and determined the results of human prostacyclin synthase (hPGIS) -mediated attenuation of MCT PAH on this miRNA panel. [score:3]
Finally, we evaluated the effects of these interventions on BMPR2 mRNA levels and also on IGF1R mRNA levels, which TargetScan predictions identify as a target for miR-223. [score:3]
Specific inhibition of miR-223 in MCT PAH rats. [score:3]
Subsequently, MCT PAH rats were injected with a specific inhibitor (antagomiR) for miR-223 (A223) or a nonspecific control oligonucleotide (A-control) 4 days after MCT administration, then weekly. [score:3]
Preliminary results with a limited number of human PAH lung specimens in our laboratory have shown a more modest increase (~1.25 fold) in miR-223 expression (data not shown). [score:3]
However, since hemodynamically and clinically, right ventricular systolic pressure is equivalent to pulmonary artery systolic pressure, it is highly unlikely that the reduction in miR-223 expression in lung and PA specimens induced by A-223 to naïve rat levels reduced PASP since no changes in RV mass or RVSP were detected (Fig 4). [score:3]
Expression levels of miR-223 relative to saline-saline (naïve) control animals. [score:3]
MiRNA-223 inhibitor (antagomiR-223, designated below as A223) was synthesized and purchased from Exiqon, Inc. [score:3]
Subsequently, dysregulation of miR-223 has been demonstrated in animal mo dels and humans with acute myocardial infarction and heart failure [31, 32]. [score:2]
The A223 -mediated reduction in levels of miR-223 in MCT PAH rats was specific, as levels of the remaining miRNAs in our panel were unchanged (Fig 3E). [score:1]
A223 significantly decreased miR-223 expression in the lung and PA, but not RV, of MCT PAH rats to levels measured in vehicle controls (Fig 3A–3D), whereas A-control did not. [score:1]
Because A223 administration to MCT PAH rats reduced miR-223 levels to levels in naïve rats, but did not attenuate MCT PAH, we hypothesized that restoration of BMPR2 signaling was a requirement for attenuation of MCT PAH. [score:1]
Expression levels of miR-17-5p, miR-21-5p, miR-126-3p, miR-145-5p, miR-150-5p, miR-204-5p, miR-223-3p, miR-328-3p, miR-424-5p (mmu-miR-322, the mouse/rat ortholog for hsa-miR-424), and miR-503-5p were evaluated. [score:1]
Our data showed a reduction in miR-223 expression by A223 administration in PA and lung in MCT PAH to levels measured in naïve rats, whereas, A-control administration did not. [score:1]
MiR-223 has previously been considered a myeloid specific miRNA, but has been shown to be dysregulated in cardiovascular medicine with a potential role as a biomarker of acute myocardial infarction and heart failure [9, 10]. [score:1]
Its sequence (5’-ATTTGACAAACTGAC-3’) is complimentary to miR-223-3p. [score:1]
The functional effects of specific inhibition of miR-223 by A223 on MCT PAH were also evaluated. [score:1]
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4
[+] score: 125
QSYQ Promote Ischemic CMECs Angiogenesis by Regulating mir-223-3p Expression, Possibly Related to Upregulation of RPS6KB1/HIF-1 α Signaling PathwayPrevious research showed that HIF-1 α was an important transcription regulating factor for VEGF [15] and angiogenesis could be induced by upregulation of VEGF mRNA expression [16]. [score:13]
To further explore the function target and mechanisms of QSYQ in the regulation of ischemic CMECs angiogenesis based on miRNA, we used the optimum dosage and window period of QSYQ as the intervention group, used gene chip to analyze the miRNA active expression changes from intervention group, M group, and N group, and found that expression of mir-223-3p in intervention group was downregulated 0.117 times as much as M group, denoting a very significant difference. [score:11]
Compared with N group, there was significant upregulation of mir-223-3p expression in M group (P < 0.01) and downregulation in Q-L group (P < 0.05); compared with M group, there was significant downregulation of mir-223-3p in Q-L group (P < 0.01, Figure 5(b)). [score:10]
The previous experiment results showed that mir-223-3p was a direct target of rats ischemic CMECs angiogenesis, decreased expression of VEGF, MAPK, PI3K, and so forth, inhibited proliferation and migration of ischemic CMECs, via affecting RPS6KB1/HIF-1 α signal pathway, and thereby suppressed angiogenesis of ischemic myocardium. [score:10]
Among these, mir-223-3p showed the most significant expression changes, suggesting that QSYQ promote ischemic cardiac angiogenesis through regulating mir-223-3p expressions, which also involves upregulation of RPS6KB1/HIF-1 α signaling pathway, and these have provided experimental evidence for research on miRNA array analysis of ischemic CMECs and drug intervention. [score:9]
Results showed that, compared with M group, mRNA and protein expression of the above-mentioned molecules in the Q-L group were significantly elevated (P < 0.01 or P < 0.05, Figures 7 and 8), suggesting that QSYQ induced expression of related molecules on the RPS6KB1/HIF-1 α signaling pathway via downregulating mir-223-3p expression during CMECs angiogenesis and thereby promoted ischemic cardiac angiogenesis. [score:9]
In conclusion, the study suggests that QSYQ can promote angiogenesis by downregulating mir-223-3p expressions and elevating expressions of factors on the RPS6KB1/HIF-1 α signaling pathway, including VEGF, MAPK, and PI3K. [score:8]
Compared with M group, the expression of mir-223-3p was downregulated 0.117 times in Q-L group, which showed a significant expression difference (P < 0.01). [score:7]
QSYQ Promote Ischemic CMECs Angiogenesis by Regulating mir-223-3p Expression, Possibly Related to Upregulation of RPS6KB1/HIF-1 α Signaling Pathway. [score:7]
In the previous study [3], we found that microRNA-223-3p (mir-223-3p) was the core miRNA of angiogenesis of rats ischemic cardiac microvascular endothelial cells (CMECs), which targeted Rps6kb1 and inhibited angiogenesis of ischemic myocardium via regulating RPS6KB1/HIF-1 α signal pathway. [score:6]
The results of mRNA and protein expression of Rps6kb1 as the target of mir-223-3p demonstrated the segregation phenomenon between them, which was consistent with the mechanism of miRNA negative regulation. [score:6]
To further understand the mechanism of regulation of mir-223-3p expression by QSYQ in ischemic CMECs angiogenesis, we analyzed the signaling pathway of predicted RPS6KB1/HIF-1 α and used real-time PCR and western-blot to test mRNA and protein expression, respectively, of related molecules in the signaling pathway: HIF-1 α, VEGF, MAPK, PI3K, and AKT. [score:6]
It is concluded that QSYQ can downregulate mir-223-3p expression, activate RPS6KB1/HIF-1 α signaling pathway, and promote ischemic cardiac angiogenesis. [score:6]
It had been confirmed in previous study that Rps6kb1 was the target gene of mir-223-3p in regulating angiogenesis of ischemic CMECs. [score:4]
Considering the link between differences in miRNA expression and angiogenesis, mir-223-3p was identified as the key miRNA during the proliferation period in the Q-L group. [score:3]
Real-time PCR was used to verify the results from miRNA chip experiments on mir-223-3p expression and the results were found to be consistent. [score:3]
To further discuss the mechanism of the regulation on mir-223-3p after the intervention from QSYQ, we tested related molecules HIF-1 α, VEGF, MAPK, PI3K, and AKT with real-time PCR and western-blot. [score:2]
Thus, we concluded that mir-223-3p was the core miRNA for regulating ischemic CMECs angiogenesis by QSYQ. [score:2]
After comprehensive analysis, we confirmed mir-223-3p as the core miRNA from QSYQ in regulating ischemic CMECs angiogenesis. [score:2]
Real-time PCR analysis on mir-223-3p agreed with chip results. [score:1]
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5
[+] score: 89
In particular, the NP expression of miR-223, which inhibited the nociceptive spinal signalling, was increased. [score:5]
Interestingly, miR-223-3p, miR-760-5p and miR-145-5p, were also significantly up-regulated after correction for multiple testing (Fig.   2). [score:4]
The down-regulation of miR-223, in contrast, has been reported to increase the release of IL-6 and IL-1β [35]. [score:4]
Moreover, the present results demonstrated that miR-223, miR-760 and miR-145 may be up-regulated in NP and released in exosome-like vesicles (ELV) when the NP tissue is exposed to the dorsal nerve roots. [score:4]
** p < 0.0001 Fig.  2Fold expression of a miR-223, b miR-760 and c miR-145 in nucleus pulposus (NP) tissue frozen directly (native) or 180 min after NP application onto the dorsal nerve roots (exposed) after harvesting. [score:4]
Therefore, the up-regulation and release of miR-223 from the NP cells close to the nerve roots could influence on the activity in nearby neuronal tissues, i. e., the DRG or spinal cord. [score:4]
Moreover, previous data show that miR-223 through the NR2B subunits in neuronal tissue may inhibit NMDA induced Ca [2+] influx [37]. [score:3]
Fig.  3Fold expression of a miR-223, b miR-760 and c miR-145 in cell-free medium frozen after nucleus pulposus (NP) incubation for 5 min or 3 h. Overall linear mixed mo del, beta = 0.65, **p < 0.001, 95% CI (0.28, 1.01), nanoparticle tracking analysis, western blot analysis and qPCR were used to demonstrate exosome-like vesicles (ELV) in the media conditioned for 3 h by NP. [score:3]
The increased miR-223 expression was, however, only observed in those who recovered (sex, age and smoking were included as covariates). [score:3]
In serum samples from our patients with lumbar radicular pain, the extracellular miR-223 expression was higher when the patients arrived at the clinic than it was 12 months later. [score:3]
Our observation that extracellular miR-223 expression was higher in patients who recovered than those who developed persistent pain, supports this hypothesis. [score:3]
Interestingly, miR-223 can inhibit NF-κβ activation and down-stream signalling including the activation of macrophages/immune cells [34, 36]. [score:3]
Linear regression adjusted for the sex, age and smoking, [beta = −2.97, p = 0.031, 95% CI (−5.67, −0.27)] Further analyses indicated that the change in the miR-223-3p expression (Additional file 2: Figure S1) from inclusion to 12 months were correlated with the change in pain (delta miR values versus delta VAS, two-sided Pearson correlation, r = 0.221, p = 0.029). [score:3]
Earlier observations show that miR-223 expressed in the myeloid lineage may be an important modulator of myeloid differentiation and inflammatory responses [33]. [score:3]
In particular, the NP expression of miR-223, which had an anti-nociceptive effect at the spinal level, was increased. [score:3]
Therefore, miR-223 transferred to recipient cells in the DRG or spinal cord could, as demonstrated in the present study, inhibit nociceptive signalling at the spinal level. [score:3]
Hence, dysregulation of miR-223 in the acute phase after disc herniation may be associated with persistent lumbar radicular pain. [score:2]
Dysregulation of miR-223 may predict chronic lumbar radicular pain. [score:2]
In this process, miR-223, similar to other miRs, can be exchanged between cells via exosomes (Additional file 3). [score:1]
The present animal data demonstrated that this process may involve release of small non-coding RNAs including miR-223 in ELVs. [score:1]
An anti-nociceptive effect of miR-223 at the spinal level was also demonstrated. [score:1]
Our findings suggest that miR-223, which can be released from the NP after disc herniation, attenuates the neuronal activity in the pain pathways. [score:1]
The present study suggests that miR-223 may be linked to the recovery rate in lumbar radicular pain patients. [score:1]
In activated macrophages, miR-223 reduces the production of IL-6 and NO [34]. [score:1]
The C-fiber responses were followed for 180 min after application of NP transplant covering 1–2 mm of the dorsal nerve roots, or 40 µL 0.6 mg/mL miR-223-3p in Invivofectamine (Invitrogen, Carlfbad, USA). [score:1]
In the patients, increased extracellular miR-223 was also verified in the acute phase after disc herniation. [score:1]
Interestingly, biologically active miR-223 [18] can be exchanged between cells via exosomes, which are small extracellular micro-vesicles that contain RNA and protein cargos [19]. [score:1]
Hence, more research is needed to determine the functional role of miR-223 in lumbar radicular pain patients. [score:1]
b, c IL-6 and miR-223 levels in the serum of patients with lumbar radicular pain at inclusion and 12 months. [score:1]
However, increased levels of the miR-223 after disc herniation was only observed in patients who recovered. [score:1]
miR-223-3p, miR760-5p and miR-145-5p were also found in the media fraction (Fig.   3). [score:1]
These observations suggests that disc herniation also involved changes in miR-223 release. [score:1]
Paired Students t test, **p < 0.01. d miR-223 at inclusion versus IL-6 at 12 months in the serum of patients with lumbar radicular pain. [score:1]
A two-sided Pearson correlation test was performed to examine the relationship between miR-223-3p at inclusion and IL-6 at 12 months and the delta miR values versus delta VAS values. [score:1]
In addition, high levels of miR-223 in the acute phase after disc herniation were associated with a decreased risk of chronic lumbar radicular pain. [score:1]
No significant association between miR-223-3p at inclusion versus IL-6 at 12 months (Fig.   5d) was demonstrated (Pearson’s correlation; rho = −0.04, p > 0.05). [score:1]
e miR-223 levels at inclusion in the recovery group versus the persistent pain group defined as reduction in VAS from inclusion to 12 months. [score:1]
Lumbar radicular pain Disc herniation Inflammation Immune response microRNA-223 miR-223 Experimental data suggest that lumbar disc herniation may induce sensitization of the primary afferent nerve fibers, even in the absence of nerve root compression [1– 5]. [score:1]
e Electrically evoked C-fiber responses in the dorsal horn neurons at baseline i. e., before and 180 min after the application of miR-223 onto the dorsal nerve roots; within subjects effects rmANOVA, p = 0.037. [score:1]
Moreover, miR-223 may be negatively correlated with inflammatory mediators [28], suggesting that miR-223 could be involved in a negative feedback loop that decreases the cytokines synthesis. [score:1]
Additional qPCR analysis of the ELV samples showed that miR-223-3p, miR760-5p and miR-145-5p were present in the exosome fraction (Fig.   4d). [score:1]
The serum analyses in patients demonstrated a significant decrease in IL-6 (Fig.   5b) and miR-223-3p (Fig.   5c) from inclusion to 12 months (paired Student’s t test, p = 0.005), which was not the case for miR-760-5p and miR-145-5p (data not shown). [score:1]
Significantly higher miR-223-3p levels at inclusion were observed in the recovery group than in the persistent pain group [beta = −2.97, p = 0.031, 95% CI (−5.67, −0.27)]. [score:1]
Representative western blot showing alix, tsg101 and CD-9. d Examples of miR-223, miR-760 and miR-145 qPCR amplification plot in the exosome fraction. [score:1]
In patients with rheumatoid arthritis, miR-223 appears to increase in response to anti-TNF treatment [28]. [score:1]
An increased release of small non-coding RNAs, including miR-223, miR-760 and miR-145, from NP in exosome-like vesicles was demonstrated. [score:1]
Application of miR-223-3p onto the spinal nerve roots decreased the C-fiber response in the dorsal horn neurones within 180 min (Fig.   4e). [score:1]
Although no clear relationship between miR-223 and IL-6 was observed, a correlation between the change in the miR-223 levels and change in the pain scores was demonstrated. [score:1]
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6
[+] score: 46
Despite extensive disagreement, several microRNAs showed concordant changes in expression across studies; these included the upregulation of miR-223 and miR-21 and the downregulation of miR-124 and miR-219, which were observed in most, if not all, of the examined studies. [score:9]
Conversely, changes in microRNA expression may reduce the activation of the inflammatory NF-κB Ρpathway; for example, this may have occurred via the decreased expression of miR-124 and miR-181b at 3 and 7 days after injury and the increased expression of miR-15, miR-223 and miR-146a (Table 8). [score:7]
Nakanishi et al. [5] observed similar changes in miR-223 and miR-124 expression, which were also observed by Liu et al. [6], and these studies also identified coincident expression changes in miR-21, miR-146a, and miR-17, among others. [score:5]
Expression changes respect to control/sham 1 dpo 7 dpo Name Liu Present Liu Present rno-miR-130b 1.42 NE rno-miR-146a 1.72 INC S rno-miR-15b 1.15 DEC NS rno-miR-17 1.74 INC NS rno-miR-18a 2.71 NE 3.41 NE rno-miR-200c 4.12 NE rno-miR-206 3.26 NE rno-miR-20a 1.69 NC rno-miR-20b-5p 1.83 NE rno-miR-21 1.37 INC S rno-miR-214 2.01 INC NS rno-miR-219-5p −1.82 DEC S rno-miR-221 1.1 NE rno-miR-223 3.58 INC S 3.4 INC S rno-miR-24-2* 2.41 DEC NS rno-miR-290 3.66 INC NS 2.96 DEC S rno-miR-378 1.31 INC NS rno-miR-410 −1.21 NE rno-miR-466b 3.05 DEC S rno-miR-541 1.11 INC S rno-miR-874 2,8 NEData restricted to microRNAs with significant changes in expression (2-fold or greater) according to Liu et al. [6]. [score:5]
Upregulation of miR-223 is associated with the presence of neutrophils [25], [78], [79], which transiently infiltrate the spinal cord early after injury [2]. [score:4]
MicroRNAs miR-21, miR-223, miR-146a, and miR-219-5p showed significant expression changes in our study (identified with both a t-test and a Rank Product test) as well as in other reports [6], [25]. [score:3]
Furthermore, the microRNAs miR-21 and miR-223 have previously been reported to be overexpressed in other nervous system array studies [5], [25]. [score:3]
SCI severity has been shown to determine the timing and degree of neutrophil infiltration [108] as well as the expression profile of miR-223 following SCI [25]. [score:3]
In parallel, the infiltration of immune cells, such as neutrophils and macrophages, may also explain the overexpression of miR-223 after spinal cord injury [25]. [score:3]
The Q-PCR analysis from animals sacrificed at 3 days postoperation revealed that miR-21 and miR-223 are significantly upregulated in injured animals compared to both control and sham animals. [score:3]
We validated the changes in the levels of the microRNAs miR-21, miR-223, miR-146a, miR-219-5p, miR-29c, miR-468, miR-145 and miR-107 using Q-PCR. [score:1]
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7
[+] score: 33
Our study showed that the expression of miR-223-3p was inversely related to the expression of E2F1 or STAT3 in esophageal tissue. [score:5]
In conclusion, our results demonstrated that exosomal miR-29a-3p might assist in the diagnosis of GERD, and increased expression of esophageal miR-223-3p was inversely associated with expression of E2F1 or STAT3 in esophageal tissue reflux esophagitis. [score:5]
Second, we identified that the expression of esophageal miR-223-3p in reflux esophagitis was significantly increased compared with control tissue, and expression gradually decreased during the acute to chronic phases of reflux esophagitis. [score:4]
Figure 6A–D shows the correlation between expression level of miR-223-3p and other mRNAs in esophageal tissue. [score:3]
MicroRNA-223 is deregulated in many inflammation-related disorders including a mouse inflammatory bowel disease mo del [19, 20]. [score:3]
Microarray analysis revealed an upregulation of miR-29a-3p, miR-128-3p, miR-223-3p and miR-3473 in reflux esophagitis (p < 0.05 compared to controls). [score:3]
There were no correlations between miR-223-3p and IL-1β or COX-2. Therefore, the data suggest that miR-223-3p may inversely regulate E2F1 or STAT3 (Figure 6E). [score:2]
The expression level of miR-223-3p on day 3 in reflux esophagitis was significantly higher compared with controls and gradually decreased from the acute phase to the chronic phase (Figure 4C). [score:2]
Several studies reported that miR-223 impacts several different cellular processes, including cell cycle regulation, invasiveness, hematopoietic differentiation and immune function. [score:2]
There was a trend for negative correlation between miR-223-3p and E2F1 (r = −0.41, p = 0.05) and a weak negative correlation between miR-223-3p and STAT3 (r = −0.35). [score:1]
The Relationship between miR-223-3p and mRNA in Esophageal Tissue. [score:1]
Haneklaus M. Gerlic M. O'Neill L. A. Masters S. L. miR-223: Infection, inflammation and cancerJ. [score:1]
There were no differences in miR-223-3p between control and reflux esophagitis during any phase (Figure 2C). [score:1]
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8
[+] score: 30
Four differentially expressed miRNAs in the lung had functions in cell differentiation, protein expression and apoptosis, including promotion of muscle differentiation (miR-206), regulation of cholangiocyte expression factor (miR-98), targeting pro-apoptotic and antiapoptotic proteins (miR-494), myeloid lineage development and promoting granulocytic differentiation, and suppression of erythrocytic differentiation (miR-223). [score:13]
The number of target genes predicted for each differentially expressed miRNA varied from 4 (miR-223) to 490 (miR-346*), with an average of 168 for up-regulated miRNAs and 96 for down-regulated miRNAs (Figure 2A and B). [score:11]
Some miRNAs such as miR-223, were found to be highly expressed in the lungs of the Wistar rats, potentially acting as immune regulators of the host immune response. [score:4]
MiR-223 has been shown to be an essential modulator of myeloid and to mediate the development of the myeloid lineage. [score:1]
It was found that miR-494, miR-365 and miR-451 were present in liver, miR-206, miR-468 and miR-691 in spleen, and miR-223, miR-98 and miR-206 in lung. [score:1]
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9
[+] score: 30
Our data showed that acupuncture at taichong acupoint regulated miR-339, miR-223, and miR-145 expression, while acupuncture at nonacupoint failed to affect these miRNAs' expression. [score:6]
Moreover, compared to acupuncture at nonacupoint, acupuncture at taichong point significantly upregulated the expression of miRNA-339, miR-223, and miR-145 in medullas of SHRs (Figure 3). [score:5]
The data showed that miR-339, miR-223, and miR-145 were significantly upregulated in medullas of SHRs treated with acupuncture at taichong point in contrast to the mo del group untreated with acupuncture (Figure 2). [score:4]
To validate the microarray profiling data, qRT-PCR was used to confirm the upregulated miRNAs including miRNA-339, miR-223, miR-145, and miR-451. [score:4]
miRNA-339, miR-223, and miR-145 are highly conserved and have multiple targets predicted for them in both humans and rats [39– 41]. [score:3]
Importantly, our RT-PCR assay has confirmed that miRNA-339, miR-223, and miR-145 were upregulated in SHRs treated with acupuncture at taichong acupoint in comparison with the nonacupoint group. [score:3]
While being compared to the normal control group (healthy SD rats), miR-339, miR-223, and miR-145 were significantly downregulated in mo del group. [score:3]
Similarly, miR-223 has been found to negatively regulate progenitor proliferation and granulocyte differentiation and activation [42]. [score:2]
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10
[+] score: 29
Both miR-375 and miR-223 play roles in regulating inflammation [52] but exhibited very different, sex-biased expression in the kidney, with miR-375 showing female-biased expression at 15 weeks of age (Table  2) and miR-223 showing male-biased expression at old age (Table  3 and Figure  7). [score:8]
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
The expression of three miRNAs associated with fibrosis (miR-142-5p, miR-150, miR-223) was correlated with histopathology fibrosis severity scores. [score:3]
Three of these six molecules exhibited a pattern of increasing expression with age (miR-223, miR-150, miR-142-5p). [score:3]
Significant age differences in the expression of miR-34a, miR-223, and miR-130b (Figure  7A,E,F) were confirmed by qPCR. [score:3]
Individual animal kidney fibrosis severity scores correlated positively and significantly (p < 0.05) with individual miR-142-5p (R = 0.526), miR-150 (R = 0.567), and miR-223 (R = 0.724) expression from those animals at 78 and 104 weeks of age. [score:3]
These miRNAs showed high representation in renal inflammation and nephritis pathways, and included miR-214, miR-130b, miR-150, miR-223, miR-142-5p, miR-185, and miR-296*. [score:1]
These six miRNAs are miR-130b, miR-296*, miR-223, miR-142-5p, miR-185, and miR-150. [score:1]
Old age -associated miRNAs showed enrichment in pathways related to endocrine system disorders (miR-129-1, miR-375, miR-223, miR-664, miR-29b, miR-34a), cancer (miR-223, miR-29b, miR-375, miR-96), and cellular movement/invasion of cells (miR-29b, miR-29c, miR-7a, miR-96, miR-34a, miR-375). [score:1]
Furthermore, miR-142-5p and miR-223, both male-biased DEMs (Figures  5 and 7), have been previously implicated in fibrosis pathways [53], highlighting agreement regarding the functional roles of these miRNAs. [score:1]
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11
[+] score: 28
Overexpression of miR-223 decreased the levels of GluR2 and NR2B, inhibited NMDA -induced calcium influx in hippocampal neurons, and protected the brain from neuronal cell death following transient global ischemia and excitotoxic injury[64] Rno-miR-185 miR-185 has been associated with inflammatory responses during brain ischemic stroke in mice and may provide underlying target for prevention and treatment of stroke[65] Rno-miR-329 Inhibition of miR-329 increased neovascularization and blood flow recovery after ischemia in mice subjected to double femoral artery ligation[60] Rno-miR-138hypoxia -induced miR-138 is an essential mediator of endothelial cell dysfunction via targeting S100A1 Ca [2+] sensor[81] We showed that transcription factors, Maf, Creb1 and Stat1, were the 3 principal hubs with high connectivity in the early phase IR-injury regulatory network, whereas Stat1, Lef1 and Bcl6 were the 3 principal hubs in the late phase IR-injury network. [score:12]
It has been shown that miR-223 was neuroprotective by targeting glutamate receptors in mice brain, since overexpression of miR-223 decreased the levels of GluR2 and NR2B, inhibited NMDA -induced calcium influx in hippocampal neurons, and protected the brain from neuronal cell death following transient global ischemia and excitotoxic injury [64]. [score:7]
Stroke patients and atherosclerosis subjects showed significantly lower miR-221 serum levels than healthy controls[80] Rno-miR-873 Late (7d) miR-873 was up-regulated after onset of focal cerebral ischemia in mice[63] Rno-miR-223 miR-223 targeted glutamate receptors in mice brain. [score:6]
For example, the top three miRNA-hubs in the early IR-injury regulatory network were rno-miR-495, rno-miR-214 and rno-miR-298, whereas rno-miR-873, rno-miR-223 and rno-miR-185 were hubs observed at the late phase post-IR injury. [score:2]
In contrast at 7d, rno-miR-873 (degree of 55), rno-miR-223 (degree of 48) and miR-410 (degree of 45) had the highest degrees of connectivity. [score:1]
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12
[+] score: 26
Other miRNAs from this paper: rno-mir-21, rno-mir-146a, rno-mir-155
Also, this upregulation of miR-223 may in part account for the unchanged levels of circulating IL-1 β in six months and its downregulation after 12 months [16]. [score:7]
Chronic ingestion of sucrose induced the upregulation of miR-21 and miR-223 in plasma and EVs. [score:4]
These results are opposed to others previously reported in obese [30, 31] and type 2 diabetic individuals [32], in whom downregulation of miR-223 was found. [score:4]
We found miR-223 upregulated in both plasma and plasma EVs from the sucrose group of rats. [score:4]
In the adipose tissue miR-223 suppresses proinflammatory activation of macrophages [34] and probably contributes to the results showing high levels of adiponectin in sucrose ingestion [6]. [score:3]
It has been recognized that miR-223 negatively regulates NLRP3 and therefore IL-1 β production [35]. [score:2]
Such is the case of miR-21, miR-146a, miR-155, and miR-223 [9– 11]. [score:1]
The relative abundance of miRNAs present in plasma EVs was miR-223 > miR-21 > miR-155 > miR-146a (Figure 3). [score:1]
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13
[+] score: 20
These selected miRNAs included the seven most strongly upregulated miRNAs (miR-330, miR-338, miR-223, miR-20a, miR-181a, miR-592, miR-212) in the Ago2 IP at 30 min, the only downregulated miRNA (miR-29b) in the Ago2 IP at 30 min, and the three most strongly upregulated miRNAs (miR-219, miR-384, let-7f) in the Ago2 IP at 120 min post-HFS (significant by t-test with Dunn–Bonferroni correction and 1-Way ANOVA with LSD test). [score:10]
miR-330 and miR-223 expression was unchanged or slightly decreased in input samples at 30 min post-HFS but enhanced in the Ago2 IP. [score:3]
Target gene list sizes for miRNAs with activity -dependent association with Ago2 for the 8 enhanced miRNAs were 97 (miR-20a), 156 (miR-219), 58 (miR-223), 114 (miR-29b), 30 (miR-330), 91 (miR-34a), 156 (miR-384), and 53 (miR-592) and for the 5 depleted miRNAs were 52 (let-7f), 55 (miR-338), 47 (miR-212), 255 (miR-19a), 32 (miR-326). [score:3]
When comparing miRNA Ago2/input expression ratios, eight miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330 miR-223, and miR-34a) exhibited increases relative to the contralateral dentate gyrus, whereas five miRNAs (miR-let7f, miR-338, miR-212, miR-19a, and miR-326) showed decreases in this ratio. [score:3]
Seven miRNAs (miR-384, miR-29b, miR-219, miR-592, miR-20a, miR-330, and miR-223) showed enhanced, NMDAR -dependent association with Ago2. [score:1]
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14
[+] score: 18
In this study, we showed that rno-miR-223-3p was upregulated whereas CaSR was downregulated in the kidney of stone-forming group, indicating that CaSR was a potential target gene of rno-miR-223-3p. [score:9]
Among the miRNAs differentially expressed in Liu's study, rno-miR-132-3p, rno-miR-146b-5p, rno-miR-223-3p, rno-miR-21-5p, and rno-miR-214-3p were upregulated, which was just the same as our findings. [score:6]
In addition, as predicted by the bioinformatics databases, SLC4A1 was the potential target gene of rno-miR-34b, rno-miR-146b, rno-miR-214, rno-miR-223, and rno-miR-351. [score:3]
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15
[+] score: 18
Other miRNAs from this paper: hsa-mir-223
miR-223, the mature form of Mir223, is a microRNA that is highly expressed in monocytes/macrophages and directly targets STAT3 to regulate its activation (Chen et al., 2012). [score:7]
Inducible microRNA-223 down-regulation promotes TLR-triggered IL-6 and IL-1β production in macrophages by targeting STAT3. [score:6]
When CAF-diet effects were compared to those of the STD diet, this translated into a moderate change in gene expression profile in circulating monocytes of the LEW rat, whereas a substantial set of genes was differentially modulated in WKY rats including microRNA 223 (Mir223) expression. [score:5]
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16
[+] score: 17
Of the 482 miRNAs that were expressed in both sham-operated animals and animals subjected to SAH, we found that 4 miRNAs (miR-30a, miR-143, miR-191*, and miR-223) showed statistically significant changes in expression between the experimental groups (Table  1). [score:5]
To confirm the differential expression of miR-30a, miR-143, miR-191*, and miR-223 in SAH and sham animals as well as the lack of differential expression of miR-145, additional qPCR assays were performed. [score:4]
The differential expression of miR-191* and miR-223 could not be confirmed. [score:3]
The other two miRNAs identified in the miRNA screen, miR-191* and miR-223, showed no significant differences in expression between the sham and the other groups (Figure  2). [score:3]
Fold change over sham for miR-30a (A), miR-143 (B), miR-191* (C), miR-223 (D), and miR-145 (E) at 0 h, 1 h, 6 h, and 24 h post-SAH. [score:1]
miR-145, miR-221, and miR-222 were selected based on their relationship with miR-143 and miR-223, respectively. [score:1]
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17
[+] score: 13
When compared to T cells from peripheral blood, qRT-PCR analyses of purified TCRαβ [+] blood T cells from the same rats indicated a similar expression pattern, with upregulation of miR-21, miR-99a, miR-223, miR-326, and miR-345-5p (Figure 6D), indicating that the GvHD grade during sampling of T cells may be crucial in terms of miRNA expression. [score:7]
We also observed upregulation of miR-223 in intestinal T cells (Figure 6C). [score:4]
The generated network depicted in Figure 7A demonstrates that miR-21, miR-223, and miR-326 may all interact in the same network of molecular responses related to T cell activation and migration. [score:1]
As input for the analysis, we chose miR-21, miR-99a, miR-223, miR-326, miR-345-5p, and miR-743b, and also genes involved in GvHD pathogenesis as well as T cell activation, proliferation, and migration. [score:1]
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18
[+] score: 13
MiR-223 and miR-133 regulate the expression of glucose transporter 4 in cardiomyocytes either by directly targeting GLUT4 3′UTR or indirectly targeting other protein-coding mRNA, e. g., KLF15 [35], [36]. [score:10]
MiR-223 up-regulation in cardiomyocytes causes the phosphatidylinositol-3-kinase (PI-3K) independent increase of glucose transport activity [36]. [score:3]
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19
[+] score: 13
Of the 30 miRNAs they found upregulated in traumatic spinal cord injury, miR-223, miR-214, miR-20b-5p, miR-17, miR-146a, miR-199a-3p, miR-221-3p, miR-146b, and miR-145 were also upregulated in our study, and among the 16 downregulated miRNAs in traumatic spinal cord injury, miR-34a and miR-338 were also downregulated after ventral combined with dorsal root avulsion in our study. [score:13]
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[+] score: 13
On day 2, miR-31, miR-223, miR-18a, and miR-18b were up-regulated, whereas miR-451 and miR-499-5p were down-regulated. [score:7]
Two of these aberrantly expressed miRNAs (miR-223, mir-499) have been reported to be associated with inflammation [23- 25]. [score:3]
miRNA Tissues in which miRNA is most highly expressed tissueDay 2(Fold change/Q-value)Day 7(Fold change/Q-value)Day 14(Fold change/Q-value) miR-31 Colon4.504/0.000 [#]5.923/0.000 [#]8.224/0.000 [#] miR-18a Small intestine2.136/0.013 [#] 1.016/0.507 0.904/0.612 miR-18b Small intestine2.045/0.000 [#] 1.502/0.023 1.314/0.000 miR-214 Distal colon 1.970/0.0002.992/0.000 [#]2.404/0.000 [#] miR-223 Spleen4.063/0.013 [#] n/a n/a miR-923 n/a 1.461/0.160 n/a2.232/0.000 [#] miR-711 n/a n/a n/a2.542/0. [score:3]
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[+] score: 10
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
Some of the differentially expressed miRNAs were previously reported (miR-223, miR-129, and miR-92) [4, 5], which support our results. [score:3]
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[+] score: 10
Other miRNAs from this paper: rno-mir-21, rno-mir-132, rno-mir-145, rno-mir-214, rno-mir-222
For example, miR-223 is highly expressed in neutrophils that are present in the spinal cord during the early phase of spinal cord injury [30]; miR-132 regulates dendritic spine morphology and synaptic physiology, contributes to the maturation of dendrites in newborn neurons in the adult hippocampus, and impacts the plasticity of visual cortex circuits [31], [32]; miR-21 is highly expressed in the spinal cord and DRGs following traumatic injury, thus promoting neurite outgrowth by down -regulating expression of Sprouty2 protein [18], [25]. [score:9]
Out of 26 miRNAs, miR-223, 132 and 21 have been previously reported to be associated with nervous system. [score:1]
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[+] score: 8
For instance, miR-223 was strongly up-regulated in hepatic IRI, whereas miR-122 and miR-146a were markedly down-regulated [11– 13]. [score:7]
Several studies have suggested the important roles of miRNAs in I/R injury, such as miR-122, miR-124, miR-146a, miR-223, miR-370 [11– 15]. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-100, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-9-2, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-184, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-205, mmu-mir-206, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-199a-2, hsa-mir-205, hsa-mir-181a-1, hsa-mir-214, hsa-mir-219a-1, hsa-mir-223, mmu-mir-302a, hsa-mir-1-2, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-184, hsa-mir-206, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-103-1, mmu-mir-103-2, rno-mir-338, mmu-mir-338, rno-mir-20a, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-100, mmu-mir-181a-1, mmu-mir-214, mmu-mir-219a-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-372, hsa-mir-338, mmu-mir-181b-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-100, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-145, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-184, rno-mir-199a, rno-mir-205, rno-mir-206, rno-mir-181a-1, rno-mir-214, rno-mir-219a-1, rno-mir-219a-2, hsa-mir-512-1, hsa-mir-512-2, rno-mir-1, mmu-mir-367, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, rno-mir-17-2, hsa-mir-1183, mmu-mir-1b, hsa-mir-302e, hsa-mir-302f, hsa-mir-103b-1, hsa-mir-103b-2, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-219b, hsa-mir-23c, hsa-mir-219b, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, mmu-mir-219b, mmu-mir-219c, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
For instance, a study analyzing miRNA expression profiles of ovarian adenocarcinomas demonstrated that two similarly expressed miRNAs (miR-9 and miR-223) regulate two independent targets of a common pathway involved in ovarian metastatis [38]. [score:8]
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[+] score: 8
On the other hand, the levels of expression in colostrum whey and mature milk whey of miR-29b, and miR-223 are different from those of bovines [4]. [score:3]
That is to say, in comparison between colostrum and mature milk whey by qPCR in bovine, there was no significantly difference in miR-29b between colostrum and mature milk, and miR-223 was significantly higher in colostrum whey than in mature milk whey. [score:1]
Our previous human milk whey study also showed that miR-150 and miR-223 were present at higher levels in serum than in whey [6]. [score:1]
However, in rat, miR-29b was significantly higher in d 9 milk whey than in d 2 colostrum whey, and there was no difference in miR-223 in colostrum whey and in mature milk whey. [score:1]
Comparison of whey and serum qPCR analyses using the same volumes of samples showed that only miR-192, miR-150, and miR-223 (apart from the tissue-specific miRNAs miR-451 and miR-122) were detected at higher levels in serum than in whey. [score:1]
Comparison of whey qPCR analyses using the same volumes of samples showed that levels of some miRNAs, such as let-7c, miR-29a, miR-29c, miR-192, miR-21, miR-146a, miR-150, miR-223, and miR-320, did not change during the lactation period (Fig. 6). [score:1]
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[+] score: 7
No differences in miRNA expression were found in kidneys of ischemic heart failure mice compared to control animals (S6 Table) and only small differences were observed between expression levels of miR-18a-5p, miR-30e-5p, miR-199a-3p and miR-223-3p in the LV of mice with ischemic heart failure compared to controls (S7 Table), however not reaching significance after Bonferroni correction for multiple testing. [score:3]
In addition to the cardiac specific miR-208a-3p and miR-499-5p, we found that the expression of let-7i-5p, miR-16-5p, miR-27a-3p, miR-199a-3p and miR-223-3p was significantly higher in the heart compared to the kidney, independent of the presence of ischemic heart failure (S4 Fig and S5 Table). [score:2]
In general, the rank order of the expression levels of the measured miRNAs was comparable in mice and rats, with the highest miRNA levels of miR-16-5p and miR-223-3p and the lowest levels of miR-199a-3p, miR-652-3p, miR-423-3p and miR-26b-5p (S1– S3 Figs). [score:1]
Indeed, the majority of miRNAs we previously identified in human plasma had similar sequences in both mice and rats, except for miR-223-3p (similar between humans and mice, different in rats) and miR-106a-5p (not present in rats and different in mice). [score:1]
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[+] score: 7
Recently Pulikkan et al. demonstrated that miR-223 targets and inhibits E2F1 which binds to the miR-223 promoter in AML blast cells and inhibits miR-223 transcription, generating negative feedback loop between these two molecules [46]. [score:7]
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[+] score: 7
For example, miR-223 regulates TLR-triggered IL-6 and IL-1β production by targeting Signal transducer and activator of transcription (STAT3) [19] and miR-146 exerts negative feedback regulation of TLRs and cytokine receptor signaling via targeting IL-1 receptor -associated kinase (IRAK)1 and TNF receptor -associated factor (TRAF)6 [20]. [score:7]
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[+] score: 7
miR-146a-5p, miR-155-5p, miR-147b, and miR-223-3p were downregulated, while miR-182-5p, miR-183-5p, and miR-9-3p were upregulated. [score:7]
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[+] score: 7
For liver cancer, one recent study reported that miR-21, miR-31, miR-122, miR-221, miR-222 were significantly up-regulated in HCC tissues, whereas miR-145, miR-146a, miR-200c, and miR-223 were found to be down-regulated [15]. [score:7]
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[+] score: 6
Treatment with triptolide enhanced expression of five miRNAs (rno-miR-146b-5p, rno-miR-20b-5p, rno-miR-142-3p, rno-miR-223-3p, and rno-miR-21-5p), while that of five other miRNAs (rno-miR-668, rno-miR-203-3p, rno-miR-382-5p, rno-miR-344b-3p, and rno-miR-30b-3p) was significantly downregulated (Tables 3 and 4, and Figure 8). [score:6]
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[+] score: 6
Downstream target networks for upstream regulators of responsive mouse genes: (A) IL12 complex, (B) mir-223, and (C) STAT1. [score:4]
The activated upstream regulators include factors related to inflammatory responses (IL6, the NF B-activating kinase IKBKB, NLRP3 inflammasome, and mir-223), interferon signaling and action (IFNAR, IFNG, IFNα/IFNβ, STAT1, IRF3, IRF5, IRF7), and TLR signaling associated with innate immune responses (TLR3, TLR4, TLR9, TICAM1, DDX58, MYD88) (Figures  4, 5, and Additional file 2: Figures S4 and S5). [score:2]
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[+] score: 6
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment. [score:6]
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[+] score: 5
Other miRNAs from this paper: rno-mir-27b
The molecular mechanism underpinning this preconditioning effect is that CXCR2 activation increases the expression of miR-223, which inhibits NF κB and subsequently miR-27b levels. [score:5]
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[+] score: 5
For example, it has been reported that miR-221 [15], miR-199a/b [16][17], miR-27b [18], miR-195 [11] and miR-34a/b/c [19] positively regulate cardiac hypertrophy, while miR-378 [9], miR-29 [20], miR-150 [11], miR-223 [21] and miR-1 [22] negatively regulate cardiac hypertrophy. [score:3]
MicroRNA-223 prevents cardiomyocyte hypertrophy by targeting cardiac troponin-I-interacting kinase. [score:2]
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[+] score: 4
miR-223 appears to be predominantly present in hematopoietic cells but interestingly has been shown to be highly expressed in neutrophils that are present in the spinal cord during the early phase of spinal cord injury [28]. [score:3]
miR-21, miR-223, miR-455-5p, miR-431 and miR-18 were significantly increased, while miR-138, miR-483 and miR-383 were significantly decreased following nerve transection. [score:1]
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37
[+] score: 4
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Brain stem let-7c-1, miR-17, miR-135b, miR-150, miR-199a, miR-218-1, miR-223, miR-329. [score:1]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
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[+] score: 4
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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
E [2] decreased miR-146a, miR 125a, miR-125b, let-7e, miR-126, miR-145, and miR-143 and increased miR-223, miR-451, miR-486, miR-148a, miR-18a, and miR-708 expression in mouse splenic lymphocytes [199]. [score:3]
AS to miR-223 blocked LPS -induced IFNγ secretion in splenocytes from E [2] treated mice. [score:1]
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[+] score: 4
In contrast, rno-miR-330-5p, rno-miR-223-5p and rno-miR-191a-3p exhibited the greatest down-regulations, which were approximately four-fold changes. [score:4]
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Lu MC Yu CL Chen HC Yu HC Huang HB Lai NS Increased miR-223 expression in T cells from patients with rheumatoid arthritis leads to decreased insulin-like growth factor-1 -mediated interleukin-10 productionClin Exp Immunol. [score:3]
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Other miRNAs from this paper: hsa-mir-223, hsa-mir-126, rno-mir-126a, rno-mir-126b
[5] Another microRNA (miR-223) was clearly shown to suppress endothelial inflammation and reactivity so as to prevent atherosclerosis-related leukocyte infiltration and inflammation. [score:3]
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Among these 21 differentially expressed miRNAs, 17 (miR-10b-5p, miR-223-3p, miR-208a-5p, miR-434-3p, miR-190a-5p, miR-30d-5p, miR-347, miR-493-5p, miR-29a-5p, miR-451-5p, miR-190b-5p, miR-466c-5p, miR-883-5p, miR-466b-1-3p, miR-21-3p, miR-3596c, miR3584-3p) were proven significant (P < 0.05) by qRT-PCR, one (miR-487b-3p) had a tendency to be significant (P = 0.06), and three (miR-138-2-3p, miR-1188-3p, miR-665) were not confirmed to be significant (Table  2). [score:3]
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Using the same human ESCC tissues in which we previously documented overexpression of miR-31, miR-21, miR-223 by ISH [28], Figure 4 shows these human ESCC tissues were also highly proliferative with numerous PCNA -positive nuclei (n = 12 cases). [score:3]
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In an attempt to discover whether the guinea pig Abcb1 isoform 1’s 3′UTR contains MREs, the reverse complement of several human ABCB1-specific miRs validated to reduce ABCB1 mRNA expression and ABCB1 activity (miR223 [24], miR508-5p [25], bta-miR145 [26], miR381 and miR-495 [27]) were searched via BLAST alignment for extrapolation to guinea pig; however, none were found. [score:3]
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Wang et al. proved that HRCR (heart-related circRNA) could protect the heart from pathological hypertrophy and heart failure by targeting miR-223 [28]. [score:3]
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In contrast, there was no significant difference in the serum and lung levels of miR-150-5p, miR-143-3p, and miR-223-3p of among the normal, IMD, and non-IMD rats (P > 0.05, Fig.   3c–h). [score:1]
Serum (g) and lung (h) levels of miR-223-3p in normal, IMD, and non-IMD rats. [score:1]
Fig. 3Validation of miR130a-3p, miR-150-5p, miR-143-3p, and miR-223-3p in serum and lung tissues by qRT-PCR. [score:1]
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Raw miRNA data were normalized using five endogenous miRNAs (U6-1, U6-2 miR-16, miR-223 and miR-1937b), and a total of 113 and 92 plasma circulating miRNAs were detected in four RYGB- and four SHAM-operated rats, respectively, 88 of which were common to both groups (Supplementary Table S1). [score:1]
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117.311572 28724745 8. Chen Y. Song Y. Huang J. Qu M. Zhang Y. Geng J. Zhang Z. Liu J. Yang G. Y. Increased circulating exosomal miRNA-223 is associated with acute ischemic strokeFront. [score:1]
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The eight circulating miRNAs, miR-29a, miR-34a, miR-375, miR-103, miR-107, miR-132, miR-142-3p and miR-144, and the two tissue-specific miRNAs, miR-199a-3p and miR-223, were identified to be significantly altered in T2D across a meta-analysis of controlled profiling studies [51]. [score:1]
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