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40 publications mentioning rno-mir-15b

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-15b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 121
Our analysis suggests a mechanistic mo del, using Bdnf and miR-15b expression levels in dying and surviving cells as an example, for how injury-dysregulated miRNAs could induce differential cell death in adjacent cells that are subjected to the same stressor: because of stochastic fluctuations in Bdnf expression in individual neurons, suppression of Bdnf expression by TBI -induced miRNAs, such as miR-15b, would push the cell below a critical threshold in some cells and result in cell death (Fig.   4). [score:10]
Although a consistent trend was observed - adding the LNA miR-15b inhibitor to the miR-15b mimic returned luciferase expression levels closer to that of control plasmids in every experiment - the noise and variability in Bdnf expression levels prevented the restored expression from reaching statistical significance (Supplementary Fig.   7B). [score:9]
High levels of miR-15b in dying neurons negatively correlate with a validated target, BdnfIPAs miRNA target filter showed that in dying neurons miR-15b has the largest number (166) of predicted gene targets among the approximately 2000 TBI-dysregulated genes that were validated by microarray analysis [4]. [score:8]
miR-15b -mediated suppression of random fluctuations in expression levels of pro-survival target genes, such as Bdnf, could lower the threshold for cell survival and result in neurodegeneration after TBI. [score:7]
Nevertheless, in aggregate, these data combined with the decreased Bdnf levels in laser captured dying neurons (microarray data) and the increased expression of miR-15b in dying neurons (ISH) and increased trends in expression of miR-15b (microfluidic qPCR) support the predicted miR-15b regulation of Bdnf. [score:6]
In comparison to a scrambled miRNA LNA probe (showing only background staining and serving as a negative control probe) and a U6 (small nuclear RNA probe which does not share homology with miRNA sequences available in miRBase) probe that labels all neurons (Supplementary Fig.   5A–C), we found that miR-15b expression is highly upregulated in many dying, FJ+ neurons in all hippocampal subfields (CA1, CA3, dentate gyrus [DG]) and in dying cortical neurons (Fig.   3A,B). [score:6]
IPAs miRNA target filter showed that in dying neurons miR-15b has the largest number (166) of predicted gene targets among the approximately 2000 TBI-dysregulated genes that were validated by microarray analysis [4]. [score:6]
One limitation of these experiments is that although we tried to measure miRNA expression in small numbers of laser captured neurons using microfluidic qPCR analysis, the noise and variability in the miRNA expression data prevented us from definitive conclusions other than that the trends were in the same direction, i. e. higher expression of miR-15b in dying neurons. [score:6]
Transfections (three separate experiments) were performed in triplicate by adding 10 ul of transfection complex containing 0.5 ul Lipofectamine 2000 (Invitrogen), 100 ng of Bdnf miRNA Target Sequence 3′UTR expression clone (GeneCopoeia), 60 nmol/L miR-15b mimic (Dharmacon), or 37 nmol/L antisense LNA oligo (Exiqon). [score:5]
Inset shows expression levels (from separate microarray experiments) of miR-15b in hippocampus of traumatic brain injured (TBI) rats and expression levels of Bdnf in pools of laser capture microdissected dying and surviving hippocampal pyramidal neurons after TBI. [score:5]
Although virtually all FJ+ neurons in the DG and cortex expressed high levels of miR-15b, we found that not all dying, FJ+ neurons in the CA1-CA3 subfields had high levels of miR-15b and conversely, we found miR-15b expressing neurons that were not FJ+; this supports our current hypothesis (see discussion) that gene dosage determines neuronal death, not any specific gene. [score:5]
Since the miR-15b seed binding site is among the most highly conserved (Supplementary Fig.   7A), we used a GeneCopoeia plasmid construct containing the Bdnf 3′ UTR and performed dual luciferase reporter assays to find further evidence that miR-15b directly regulates Bdnf expression. [score:4]
To validate its role in promoting neurodegeneration after TBI, we used in situ hybridization (ISH) with a locked nucleic acid (LNA), digoxigenin-labeled antisense probe to determine if miR-15b expression was increased in dying or surviving neurons in TBI brain sections. [score:3]
One of the predicted targets of miR-15b is Bdnf, a gene which is essential for cell survival, neuroplasticity, and cognitive functions [23]. [score:3]
High levels of miR-15b in dying neurons negatively correlate with a validated target, Bdnf. [score:3]
The deletion of the miR15/16 family is causally linked to chronic lymphocytic leukemia, suggesting that miR-15b has a tumor suppressor/pro-apoptotic function [21]. [score:3]
Experimental conditions included plasmid alone, plasmid + miR-15b mimic, and plasmid + miR-15b mimic and LNA inhibitor. [score:3]
Hullinger TG Inhibition of miR-15 protects against cardiac ischemic injuryCirc. [score:3]
Microfluidic analysis of laser captured neurons has never been reported; in this proof-of-principle experiment, although differences did not reach statistical significance due to the stochastic variability in the six 30 cell pools of dying or surviving neurons, we detected a trend in increased expression of miR-15b and miR-19a in dying neurons. [score:3]
Figure 3 In situ hybridization analysis of miR-15b expression using a digoxigen-labeled locked nucleic acid antisense miR-15b probe in frozen sections of the injured rat brain. [score:3]
miR-15b is highly expressed in many but not all dying, Fluoro-Jade -positive (FJ+) neurons in the hippocampal CA1-3 subfields, in all dying (FJ+) neurons of the dentate gyrus (DG) (A), and in all FJ+ neurons of the cortex (B). [score:3]
A paired t-test was used to compare the miR-15b mimic groups and miR-15b mimic plus inhibitor groups to BDNF plasmid alone groups. [score:3]
Conversely, in FJ+ but miR-15b negative neurons, cell death occurs due to the cumulative dysregulation of other miRNAs and genes. [score:2]
Using serial sections immediately adjacent (before and after) to the miR-15b ISH/FJC labeled slides, we identified dying, Fluoro-Jade positive neurons and adjacent surviving, Fluoro-Jade negative neurons and laser captured them from the ipsilateral (directly under the injury site) rat hippocampus. [score:2]
Bdnf has a large, 2.9 kb 3′UTR with multiple seed binding sites for several miRNAs differentially affected by TBI, miR-15b, miR-146b, miR-17-5p (all increased) and miR-181c (decreased). [score:1]
In situ hybridization for miR-15b Ten µm fresh frozen coronal sections were fixed in 10% formalin overnight at ambient room temperature. [score:1]
The miR-15b positive neurons that were FJ− may have had high pre-injury levels of prosurvival genes and therefore, the neurons did not reach the threshold needed to undergo cell death. [score:1]
Indeed, in animal mo dels of myocardial infarction, antagomirs to miR-15 reduced infarct size and enhanced cardiac function [31]. [score:1]
M. -A. M. developed the miR-15b in situ/Fluoro-Jade co-staining protocol. [score:1]
In preparation for the hybridization of the double-DIG LNA probe to miR-15b, hybridization buffer was diluted 1:1 in RNase free water. [score:1]
Frozen sections immediately adjacent to miR-15b ISH/FJC labeled slides were removed from the cryostat and placed at ambient temperature for approximately 30 sec then promptly fixed for 1 min in 75% ethanol; rinsed in RNase-free water (1 min); stained with 1% cresyl violet (20 sec); rinsed in RNase-free water (30 sec × 2); stained with. [score:1]
In situ hybridization for miR-15b. [score:1]
The high conservation of the miR-15/16 clusters among 44 vertebrate species, including humans and primates, suggests conservation of function [22] with implications for human TBI. [score:1]
Yue J Tigyi G Conservation of miR-15a/16-1 and miR-15b/16-2 clustersMamm. [score:1]
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2
[+] score: 119
Other miRNAs from this paper: rno-mir-16, rno-mir-30d, rno-mir-20b, rno-mir-15a
In order to identify the footprint of miR-15a, -15b and -16 on gene expression in a genome wide scale, putative miR-15b and -16 targets obtained from the miRWalk algorithm (771 predicted targets) were compared with the downregulated genes at 180 minutes after hyperosmotic exposure (721 genes). [score:9]
Overall, these findings implicate that signaling pathways activated by hyperosmotic hepatocyte shrinkage downregulate the expression of anti-apoptotic genes, which are either validated (Bcl2 and Ccnd1) or predicted (Mcl1) miR-15/16 targets. [score:8]
In order to identify additional putative targets of miR-15a, -15b and -16 that could be involved in regulation of cell death or survival we queried two different target prediction databases miRWalk and MicroCosm for miR-15b and miR-16 predicted targets. [score:8]
We found that the expression of miR-15a, miR-15b and miR-16 was significantly upregulated following perfusion of rat livers with hyperosmotic solution, whereas hypoosmotic perfusion had no significant effect on the expression level of these microRNAs (Fig. 1a-c). [score:8]
qPCR validation of the 18 putative targets of miR-15a, miR-15b and miR-16 detected as significantly downregulated by Affymetrix arrays in hyperosmotically perfused livers. [score:6]
Specifically, miR-15a was found to be significantly upregulated at both 60 minutes (5.3-folds, p = 0.0002) and 120 minutes (5.3-folds; p = 0.0001) compared to the preperfusion state (defined as T0), while miR-15b (1.7-folds; p = 0.006) and miR-16 (2.1-folds; p = 0.0078) were both found significantly upregulated at 60 minutes after perfusion of the livers with hyperosmotic solution. [score:6]
Importantly, we found that among the genes downregulated within 180 minutes of hyperosmotic perfusion, 18 genes were predicted target genes of miR-15b and miR-16 (Table 1 and Fig. 10). [score:6]
The expression of members of the miR-15 family is upregulated in response to hyperosmotic stimulation. [score:6]
Specifically, expression of miR-15a, miR-15b and miR-16 was found to be significantly upregulated in the livers of hyperosmotically perfused rats. [score:6]
Description of the miR-15b and miR-16 putative targets downregulated under hyperosmotic conditions. [score:6]
How to cite this article: Santosa, D. et al. Hyperosmotic stress activates the expression of members of the miR-15/107 family and induces downregulation of anti-apoptotic genes in rat liver. [score:6]
Specifically, statistical analysis with unpaired student’s t-test indicates that miR-15a and miR-16 were significantly downregulated, while miR-15b expression was unchanged after addition of apocynin (Fig. 3). [score:6]
ROS formation activates JNK 4 which may directly or indirectly regulate transcription factors being required for the regulation of apoptotic genes and the biogenesis of the miR-15/107 family. [score:5]
Fas apoptotic inhibitory molecule is a novel potential target of the miR-15 family. [score:5]
analyses further revealed that the seed sequences of the miR-15 family are around 2,2 kb downstream of the 3′UTR of Bcl2, potentially targeting this miRNA which leads to inhibition. [score:5]
Further studies are required to substantiate the link between hyperosmotic Egr1/Foxo3 regulation and miR-15/16 expression. [score:4]
Importantly, our analysis suggests that the transcription factors Foxo3 and Egr1 could be possible drivers of the hyperosmotic-specific activation of miR-15/16 expression. [score:3]
Moreover, these miRNAs, which are all members of the miR-15/107 family, serve key functions as they are known for repressing the expression of genes involved in cell division and metabolism 47. [score:3]
mRNA analysis of target genes of the miR-15 family under hyper- and normoosmotic conditions in perfused rat liver. [score:3]
ROS -mediated activation of JNK is required to activate the expression of miR-15a, miR-15b and miR-16. [score:3]
Applying this approach, two putative binding sites for miR-15b and -16 were identified in the 3′UTR of Faim at positions 493/513 (rno-miR-16) and 292/313 (rno-miR-15b and rno-miR-16), suggesting that Faim could be a novel target for miR-15/16. [score:3]
Notably, these miRNAs belong to the miR-15/107 family, which comprises 10 paralogous miRNAs sharing the same seed sequence AGCAGC 22. [score:1]
Transcription factors Foxo3a and Egr1 are potential candidates in the modulation of the miR-15 family. [score:1]
miR-15a, miR-15b and miR-16 are conserved between human, mouse and rat genome. [score:1]
Following, the expression of miR-15 family members was measured by miQPCR. [score:1]
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3
[+] score: 51
It was reported that miR-15 family members were upregulated in infarct region of pigs [15] but downregulated in both border and infarct zone of mice [17] in response to myocardial infarction, while they were found to be up-regulated in the overloaded heart in multiple species [19]. [score:10]
Roy et al reported that only miR-15b but no other family members was upregulated in mouse heart subjected to IR for 2 or 7 days [25], while in rats with cerebral IR for 24 h or 48 h, only miR-497 in brain tissue was significantly upregulated [26]. [score:7]
We noted that miR-15 family members may be upregulated, downregulated or unchanged in response to various cardiac stresses (Supplementary Material, Figure S1). [score:7]
Although miR-15 family members share similar structure and some common targets, they can also exert distinct role in the pathogenesis of cardiovascular disease. [score:5]
Anti-miR chemistries suppressing miR-15 in mice were reported to reduce myocardial infarct size [15], while inhibition of either miR-15a or miR-16 enhanced post-ischemic neovascularization [19]. [score:5]
The miR-15 family members including miR-15a, miR-15b, miR-16, miR-195, miR-424, and miR-497, show 5′-end sequence similarity and many common targets [16, 17]. [score:3]
MiR-15 and miR-16 were reported to induce apoptosis by inhibiting Bcl-2 [18]. [score:3]
Similar to our findings on miR-497, Hullinger et al has demonstrated that miR-15b, also a member of miR-15 family, aggravates myocardial IR injury by targeting Bcl-2 [15]. [score:3]
The expression heterogeneity of miR-15 family members was also supported by previous studies. [score:3]
The regulation of miR-15 family is spatial, temporal and dynamic [15, 17]. [score:2]
It was reported miR-195 increases cardiac hypertrophy [27] and worsens systolic dysfunction in mice with MI [17], while miR-15b, another member of the same miR-15 family, was found to attenuate myocardial fibrosis and hypertrophy in pressure-overloaded mice [19]. [score:1]
Recent studies have shown that the miR-15 family can worsen or alleviate myocardial ischemia and heart failure [13– 15]. [score:1]
The expressions of other members of miR-15 family in cardiomyocytes or heart subjected to AR or MI or pressure overload induced by transverse aortic constriction were also investigated. [score:1]
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4
[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
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5
[+] score: 21
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
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6
[+] score: 19
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]
Apoptosis may be stimulated by the downregulation of up to 7 protective microRNAs as well as the upregulation of the pro-apoptotic miR-15b microRNA at 3 days after injury. [score:7]
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]
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7
[+] score: 15
Furthermore, our findings that the expression of miR-21 and miR-15 was significantly lower in MSC-Exo compared to MSC, which are in line with previous reports that downregulation of miR-21 prevents hypertrophy [39] and inhibition of miR-15 prevents cardiac ischemic injury [40]. [score:7]
To further characterize the difference of miRNA expression between MSC-Exo and MSCs, the hierarchical cluster of miRNA expression was made, which indicated that the expression of several miRNAs (including miR-15) derived from MSC-Exo was significantly different from that of MSCs (Figure 3(b)). [score:5]
For example, the expression of miR-21 and miR-15, which regulate cardiac functions, was significantly lower in MSC-Exo compared to that in MSCs (Figure 4(a)). [score:3]
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8
[+] score: 15
Notably, 23 circulating miRNAs (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were significantly downregulated in DIO mice but upregulated in DIO + LFD mice. [score:7]
As shown in the Venn diagram in Fig.   7, notably, 23 of the 28 upregulated miRNAs in DIO + LFD mice (mmu-miR-16, mmu-let-7i, mmu-miR-26a, mmu-miR-17, mmu-miR-107, mmu-miR-195, mmu-miR-20a, mmu-miR-25, mmu-miR-15b, mmu-miR-15a, mmu-let-7b, mmu-let-7a, mmu-let-7c, mmu-miR-103, mmu-let-7f, mmu-miR-106a, mmu-miR-106b, mmu-miR-93, mmu-miR-23b, mmu-miR-21, mmu-miR-30b, mmu-miR-221, and mmu-miR-19b) were downregulated in the DIO mice. [score:7]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
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9
[+] score: 12
So we paid more attention to miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497, which are the targeted results for CX3CL1 in the Targetscan Database. [score:5]
In order to investigate whether some micro -RNA contained in the MVs played a role, we searched CX3CL1 in the TargetScan database (version 6.2) and identified six putative micro -RNA (miR-15a, miR-15b, miR-16, miR-195, miR-424 and miR-497) targets to CX3CL1 mRNA by matching the seed regions of each. [score:3]
Interestingly, the miR-16, miR-15b and miR-15a were profiled successfully both in hWJMSCs and hWJMSC-MVs by the real-time quantitative PCR method with a high concentration, and we think that these micro -RNAs contained in MVs may involve the modulation of CX3CL1 expression. [score:3]
The real-time quantitative PCR analysis indicated that there were relatively high levels of miR-15a, miR-15b and miR-16 contained in hWJMSC-MVs, but none or low levels of miR-195, miR-424 and miR-497 (Figure  7B). [score:1]
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10
[+] score: 11
However, miR-15b, miR-16, miR-20a, miR-20b [17], [18], miR-205 [23] and miR-195 [22] down-regulate angiogenesis by directly targeting VEGF. [score:7]
Recent studies also indicate that a panel of miRNAs (i. e., miR-10, miR-15b, miR-16, miR-20a, miR-20b, miR-27a, miR-126, miR-145, miR-195, miR-205, and miR-210) is involved in the regulation of VEGF expression in ECs and tumor cells [16]– [26]. [score:4]
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11
[+] score: 9
Both miR-1 and miR-15b target Bcl-2 down-regulation [47, 48] and thus, increase the cardiomyocyte susceptibility to apoptosis in the setting of ischemia and reperfusion injury. [score:6]
In addition, miR-1, miR-15 and miR-21 can directly influence the survival of cardiomyocytes. [score:2]
Thus, the finding that chronic losartan treatment significantly increased miR-1 and, particularly miR-15b of 9-fold, as well as decreased miR-21 by 50% in the left ventricle, suggests a novel mechanism of miRs in angiotensin receptor-modulated vulnerability of the heart in response to acute onset of ischemic injury. [score:1]
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12
[+] score: 8
MiR-15b and miR-16 were downregulated when HSCs were activated, and their overexpression induced HSCs apoptosis and cell cycle arrest through caspase and Bcl-2 signaling pathways [12]. [score:6]
MiR-195, an important member of the miR-15 family, plays a crucial role in regulating cell cycle progression and cell apoptosis [15]. [score:2]
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13
[+] score: 7
It has been shown that miR-29, miR-15 and miR-107 are upregulated; while miR-124, miR-34 and miR-153 are downregulated in patients with AD (Delay et al., 2012; Lau et al., 2013). [score:7]
[1 to 20 of 1 sentences]
14
[+] score: 6
Several endogenous miRNAs (including mmu-miR-15b, -92a, -19b, -532-3p, and -30b) portrayed a similar, stable pattern of expression and low standard deviation (<7.6%) among all samples. [score:3]
Shown are miR-15b normalized treated vs. [score:1]
Briefly, ΔC [T] values were obtained by subtracting the reference gene (mmu-miR-15b) C [T] from the C [T] for each miRNA of interest. [score:1]
Mmu-miR-15b was selected to be utilized as the endogenous reference for normalization based on its reported stability in serum [22], its observed low standard deviation in our sample set (< 4.9%), and lack of significant difference between the treatment groups, and across study time points (p≤0.05, Student’s t-test). [score:1]
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15
[+] score: 6
Our results indicated that the functions of miR-15b-5p and miR-335, which were upregulated in the rat liver following C. sinensis infection, include regulation of apoptosis [23, 24]. [score:5]
However, future experiments are required to further reveal the functions of miR-15b-5p and miR-335 during C. sinensis infection. [score:1]
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16
[+] score: 6
Other miRNAs from this paper: rno-mir-222, bta-mir-222, bta-mir-15b
It has been demonstrated that dietary supplementation of ARG or NCG affect microRNAs (miR-15b, miR-222) targeting VEGFA and endothelial NO synthase gene expressions in umbilical vein, consequently regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue [36]. [score:6]
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17
[+] score: 6
There were no significant changes in the expression of miR-15, miR-30, and miR-133a between healthy subjects and patients with burn injury. [score:3]
MiR-15, miR-133a, and miR-30 also had P [CT] > 0.75. [score:1]
We assessed the levels of let-7b, let-7e, miR-194, miR-15, miR-133a, miR-15, and miR-195 (as a non-specific control) by real-time PCR. [score:1]
MiR-195, let-7e, miR-15, miR-133a, and miR-30 did not show any significant difference between burn rats and sham rats (Figure 1A) (P>0.05). [score:1]
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18
[+] score: 5
Expression of microRNA-15b and the glycosyltransferase GCNT3 correlates with antitumor efficacy of Rosemary diterpenes in colon and pancreatic cancer. [score:3]
CA exerts antitumor activity by down -regulating miR-15b (Gonzalez-Vallinas et al., 2014), and increases miR-34a to exert an anti-apoptotic effect (Shan et al., 2015). [score:2]
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19
[+] score: 5
A second a group of miRNAs whose expression is higher in the vesicles-enriched pellets (i. e., Let-7a, miR-15b, -142-3p and -98, Fig. 5, right column) and a third group of miRNAs which presents comparable expressions in both groups (i. e., miR-15a, -16, -155, -21, -18a and RNU6, Fig. 5, middle column). [score:5]
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20
[+] score: 5
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
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[+] score: 4
In contrast, proapoptotic miRNAs are usually downregulated in cancer, and include miR-15, miR-16, the let-7 family and members of the miR-34 family. [score:4]
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22
[+] score: 4
The first documentation of a miRNA abnormality in cancer was reported by Croce and colleagues in 2002, who found that two miRNAs, miR-15 and miR-16, were lost or down-regulated in most patients with chronic lymphocytic leukaemia (CLL) [18]. [score:4]
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[+] score: 4
Overall, we speculate that microRNAs like miR-15b and miR-98 co-ordinate the regulation of the expression of E-cadherin, ZEB1 (TCF8), HMGA2 and SNAIL. [score:4]
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24
[+] score: 4
Among miRNAs that were present at higher levels in colostrum whey, let-7i, miR-148b-3p, miR-27b, and miR-125b-3p affect the function of antigen-presenting cells, and miR-15b, miR-24, miR-92a, miR-181a, miR-181c, and miR-181d affect T cell development and function [29], [30], [35]. [score:2]
The results for miR-15b, miR-27b, and miR-106b are in accordance with those for bovine [4]. [score:1]
On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-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-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
It has been reported that the expression of miR-143, let-7a, miR-15b is under negative control of follicle stimulating hormone (FSH) during follicular development [36] and may be involved in FSH -induced rat granulosa cell progesterone production [37]. [score:4]
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[+] score: 3
GRN expression is also under the post-transcriptional control of miR-107 (a member of a miRNA group also including miR-15, miR-16, miR-103, miR-195, miR-424, miR-497, miR-503, and miR-646), with implications for brain disorders (Wang et al., 2010). [score:3]
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[+] score: 3
For example, CSF exosomal miR-193b was proposed as a biomarker for Alzheimer's disease (Liu et al., 2014), CSF exosomal miR-15b and miR-21 as markers for gliomas (Baraniskin et al., 2012) and some miRNAs in CSF as biomarkers of stroke (Sørensen et al., 2014). [score:3]
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[+] score: 3
In addition, a number of miRNAs, including miR-16, miR-210, miR-15b, miR300-3p, miR-540, miR-325-5p and miR-487b, were observed to have target DEGs involved in cholesterol -associated metabolism, e. g. IDI1 and FDFT1. [score:3]
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[+] score: 3
However, there is no experimental evidence on the effect of miR-16 on cardiac ischemia, although a member of the miR-15 family miR-15a has been proven to participate in the regulation of myocyte proliferation and apoptosis [3, 31]. [score:2]
miR-16 located at 13q14, which is identified as miR-15 miRNA cluster that includes miR-15a, miR-15b, miR-16, miR-195, and miR-497 [25]. [score:1]
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[+] score: 3
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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Similarly, we found all members of the miR-15, miR-16, miR-18 and miR-133 families in our sequences, suggesting that all members belonging to these miRNA families are expressed in these three (heart, liver and thymus) tissues. [score:3]
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[+] score: 3
Hullinger TG Inhibition of miR-15 protects against cardiac ischemic injuryCirc. [score:3]
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[+] score: 3
We found that miRNAs with higher expression in WBCs includes different miRNA families: mir-15, mir-17, mir-181, mir-23, mir-27 and mir-29 families. [score:3]
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[+] score: 2
In recent studies, miRNAs, including miRNA-15b [14], miRNA-34a [15], miRNA-92a [16], and miRNA-320 [17] have been reported to be involved in the regulation of cardiomyocyte apoptosis after MI. [score:2]
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[+] score: 2
The other highly significant miRNAs displaying a steep decrease from younger to older animals (miR-301b, miR-130b, miR-20a, and miR-15b) are known to be involved in cancers (Attar et al. 2012; Funamizu et al. 2014; O’Donnell et al. 2005; Zhu et al. 2015), suggesting a role for these miRNAs in regulating MEC cell proliferation immediately after birth. [score:2]
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[+] score: 1
Recent evidence suggests that miRNAs are involved in apoptosis and other injuries in myocardial cells induced by H/R [23– 25]; miRNAs such as miR-1, miR-15b, and miR-21 have been implicated in modulating the survival and recovery of myocardial I/R injury due to their effects on key genes associated with apoptosis [26– 29]. [score:1]
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[+] score: 1
MicroRNA profiling identified several miRNAs that have been previously associated with cardiac hypertrophy such as miR-214, miR-23b, miR-15b, rno-miR-26b, rno-miR-221, rno-miR-222, rno-miR-107 [59], miR-23a, miR-208, rno-miR-133b, miR-19a and mi-r133a [60]. [score:1]
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[+] score: 1
Finally, there is mixed support for 7 of the miRNAs we reported (mir-129-1, miR-15b-3p, mir-204, miR-29c-3p, miR-301b-3p, miR-495, and mir-9a-2), with some studies showing changes consistent with our data, and other studies showing changes opposite those of our study (15, 31– 33, 38– 47). [score:1]
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[+] score: 1
A number of miRNAs, including miR-1 [15], miR-15b [16], miR-21 [17] and miR-145 [18], have been implicated in myocardial I/R injury due to their effects on key genes associated with apoptosis. [score:1]
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[+] score: 1
Several recent reports have highlighted the post-transcriptional repression of HMGA proteins by non-coding RNAs and, in particular, numerous miRNAs with this activity have been identified (let-7a, miR-15, miR-16, miR-26a, miR-34b, miR-196a2, miR-326, miR-432, miR-548c-3p, miR-570, miR-603) (53, 54). [score:1]
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[+] score: 1
For example, miR-105, miR-125b and miR-140 are involved in the inflammatory phase; miR-15a, miR-15b and miR-16 participate in the granulation phase; and miR-29 and miR-192 function in the remo deling phase [10]. [score:1]
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