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15 publications mentioning ssc-mir-34a

Open access articles that are associated with the species Sus scrofa and mention the gene name mir-34a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 60
Other miRNAs from this paper: ssc-mir-34c-1, ssc-mir-34c-2
For example, miR-34c inhibits lung cancer proliferation, migration and invasion by targeting PDGFRα/β [19]; miR-34a affects the growth of pulmonary artery smooth muscle cells in human by targeting PDGFRα [20]. [score:7]
Peng Y. Guo J. J. Liu Y. M. Wu X. L. MicroRNA-34A inhibits the growth, invasion and metastasis of gastric cancer by targeting PDGFR and MET expressionBiosci. [score:6]
Therefore, miR-34a may directly target PDGFRα and repressed IMF deposition through inhibiting the Erk signaling pathway. [score:6]
In addition, using mRNA TargetScan analysis, we found that PDGFRα may be targeted by miR-34a. [score:5]
Therefore, we presume that miR-34a may affect PDGFRα expression by targeting it during porcine IMF preadipocyte differentiation. [score:5]
The results showed that overexpression of miR-34a dramatically suppressed mRNA levels of PDGFRα and lipogenesis genes, including PPARg and FABP4 (Figure 6B), which was consistent with the protein level (Figure 6D,E–I). [score:5]
Using mRNA TargetScan analysis, we found that PDGFRα may be targeted by miR-34a. [score:5]
2.6. miR-34a Represses Lipogenesis through Targeting PDGFRα. [score:3]
The expressions of all genes were normalized to GAPDH, but U6 small RNA was internal reference when examined the level of miR-34a. [score:3]
Wang P. Xu J. Hou Z. L. Wang F. F. Song Y. L. Wang J. Zhu H. Jin H. B. miRNA-34a promotes proliferation of human pulmonary artery smooth muscle cells by targeting PDGFRACell Prolif. [score:3]
Overexpression efficiency of miR-34a mimics was high enough to carry out subsequent experiments (Figure 6A). [score:3]
Taken together, miR-34a represses lipogenesis in IMF preadipocytes through targeting PDGFRα. [score:3]
Mechanically, PDGFRα regulated by miR-34a and FoxO1 promotes adipogenensis in porcine intramuscular preadipocytes through activating Erk signaling pathway. [score:2]
Therefore, the experiment on PDGFRα regulated via miR-34a was performed. [score:2]
Preadipocytes were seeded in 12-well or 6-well plates, and miR-34a mimics or negative control (NC) (GenePharma, Shanghai, China) were transfected into cells at 80% density in 50 nM using X-tremeGENE siRNA Transfection Reagent (Roche) and Opti-MEM (Gibco) culture medium according to the manufacturer’s protocol and the culture medium was changed to fresh medium after 24 h. When the cells grew to confluence after transfection, adipogenic differentiation was initiated by switching to differentiation medium. [score:1]
So we transfect miR-34a mimics into porcine IMF preadipocyte. [score:1]
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2
[+] score: 33
In other cases, miR-34a expression has been found to be increased in human patients with liver disease and in a rat liver fibrosis mo del [43, 44]. [score:5]
Accordingly, our previous study showed that miR-34a and miR-708 are upregulated in Duroc pigs, which are more obese than Pietrain [42]. [score:4]
The same SNPs that regulated miRNA-34a also regulated mRNAs including FBXO6, KIF1B, GALP, LZIC, LOC100516739 and NMNAT1. [score:3]
Figure 3 depicts a Manhattan plot of miR-34a, miR-708 and miR-652 together with the top SNPs associated with their expression levels. [score:3]
The genetic regulated miRNAs miR-34a, miR-30e, miR-148-3p, miR-204, miR-181-5p, miR-143-5p and let-7g were also correlated with haematological and biochemical traits. [score:2]
This information links miR-34a to IP and TCHO, providing evidence of a functional link between IP, energy metabolism, genetic regulation of miRNA 34a and GALP. [score:2]
Based on the synteny between the human and pig genome and the discovery of other transcripts in this region regulated with the same SNPs, we expected miR-34a to be cis-eQTL. [score:2]
The SNPs that significantly associated with miR-34a were also associated with KIF1B and FBXO6, which have a cis-eQTL. [score:1]
Human miR-34a is located on chromosome 1 at 9.15 Mb, a region syntenic to SSC6 position 64–65 Mb. [score:1]
miR-34a is an obesity -associated miRNA that attenuates metabolic hormone function [39, 40]. [score:1]
miR-34a was negatively correlated with IP (r = 0.35, p = 2.26 × 10 [−7]). [score:1]
Twelve out of 61 SNPs associated with miR-34a. [score:1]
We found that SNPs around miR-708 and miR-34a were also associated with the mRNA transcripts in the vicinity. [score:1]
Genetic links between mRNA and miRNA were also shown using pleiotropic association analyses of miR-34a with GALP, LZIC, FBXO6 and KIF1B with 376 SNPs on SSC6 (FDR < 5%). [score:1]
Of note, miR-34a has not yet been annotated in the porcine genome. [score:1]
Interestingly, SNPs associated with transcripts located on SSC6 at 55–65 Mb also associated with transcript levels of miR-34a. [score:1]
We found that IP was correlated with a number of miRNAs including miR-34a and miR-194, which are both abundant in the liver. [score:1]
Two miRNA (miR-708-5p and miR-34a) are highly associated with SNPs in surrounding regions (cis-eQTL). [score:1]
For example, miR-34a correlated with IP, and TCHO or miR-204, miR-15a, miR-16b correlated with TG. [score:1]
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3
[+] score: 31
Since our in vitro study has shown that overexpressing miR-34 inhibits muscle development, we believe the miR-34c overexpression experiment alone would be sufficient to demonstrate the role of miR-34c in vivo. [score:8]
A previous study indicated miR-34a inhibits mouse smooth muscle cell proliferation by directly targeting Notch1 [26]. [score:6]
Another miR-34 family member miR-34c also has been shown to inhibit rat vascular smooth muscle cell proliferation [27]. [score:3]
The full-length blot images are presented in Supplementary Figure  1. Overexpressing miR-34c inhibits PSCs proliferation in vitroFirst, we investigated the role of miR-34 in PSCs proliferation. [score:3]
But, the role of miR-34 plays in pig skeletal muscle development has not been reported. [score:2]
Through the dual-luciferase reporter assay, we found N1ICD decreased the pGL3-basic-miR-34 upstream recombinant vector relative luciferase activity, but this inhibition was abolished by the mutated CSL-N1ICD complex binding site (GTGGGAA) (Fig.   6F). [score:2]
In human, three miR-34 precursors are produced from two transcriptional units, miR-34a precursor is transcribed from chromosome 1, and miR-34b and miR-34c precursors are co-transcribed from a region on chromosome 11 [23]. [score:1]
The miR-34 family members (miR-34a, miR-34b, and miR-34c) were discovered computationally [20] and later verified by experiment 21, 22. [score:1]
As shown in Fig.   6E the miR-34 upstream of its genomic site (about 4600 bp) is inserted into the pGL3-basic vector. [score:1]
So we constructed the pGL3-basic-miR-34 upstream recombinant vector (pGL3-basic-miR-34 upstream). [score:1]
But only miR-34a and miR-34c are found in pig 24, 25. [score:1]
N1ICD with pGL3-basic-miR-34 upstream recombinant vector relative or pGL3-basic-miR-34 upstream (mut) recombinant vector were transfected into HEK-293T cells respectively. [score:1]
Lanes 1–7 represent DL 10000, pGL3-basic, double digested pGL3-basic, double digested miR-34 upstream of its genomic site, pGL3-basic-miR-34 upstream recombinant vector, double digested pGL3-basic-miR-34 upstream recombinant vector, DL5000, respectively. [score:1]
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4
[+] score: 28
Other miRNAs from this paper: ssc-mir-193a, ssc-mir-574, ssc-mir-129a, ssc-mir-126, ssc-let-7d
From the 119 miRNAs highly expressed (>80 reads) in MLN, 8 miRNAs were DE, five up-regulated (mir-126-3p, mir-126-5p, let-7d-3p, mir-129a, mir-let-7b-3p) and three down-regulated (mir-193a-5p, mir-574-5p and mir-34a) (Table  3). [score:9]
Differential expression of miRNAs in MLN is high due to the PCV2 infection; from the most represented miRNAs in both tissues (CN > 80): mir-126-3p, mir-126-5p, mir-let-7d-3p, miR-129-2-3p and mir-let-7b-3p were up-regulated in MLN of PCV2 infected animals, while miR-193a-5p, miR-574-5p and miR-34a-5p were down-regulated. [score:9]
miR-34a-5p is down-regulated in MLN and this regulatory role was predicted to be involved in several immunological pathways and the MAPK signalling pathway. [score:5]
In this case, target prediction analysis revealed that miR-34a-5p targets KLRK1, killer cell lectin-like receptor subfamily K, member 1, which binds to a diverse family of ligands that include MHC class I chain-related A and B proteins and UL-16 binding proteins, where ligand-receptor interactions can result in the activation of NK and T cells [39]. [score:5]
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5
[+] score: 26
This pattern included the two created target sites for ssc-miR-34a and ssc-miR-34c, both predicted by TargetScan and PACMIT in SLA-1 (Figure 3 A); the disrupted target site for ssc-miR-148a in HSPA1A predicted by PACMIT and TargetSpy (Figure 3 B); the ssc-miR-133b (TargetScan and PACMIT), ssc-miR-133a-3p (TargetScan) and ssc-miR-323 (TargetSpy) created target sites in RNF5 (Figure 3 C); and the disrupted site for ssc-miR-2320 predicted by TargetSpy in SLA-1 (Figure 3D). [score:19]
For example, both TargetScan and PACMIT predicted that the DSP in the ABCF1 3′-UTR created a new ssc-miR-34a/c target site while disrupting the ssc-miR-885-3p predicted target site (Table S4). [score:7]
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6
[+] score: 13
LCN2 has target sites for miR-34a and miR-1285, which are both upregulated in the liver. [score:6]
MiR-34a (FC 2.4; p value 1.0x10 [-3]) was the most upregulated miRNA. [score:4]
MiR-34a is also upregulated in the liver of obese mice [70]. [score:3]
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7
[+] score: 12
miR-21 and miR-34a have been also shown to regulate the cell cycle progression by targeting relevant G1-to-S transit proteins. [score:4]
In the present study, we found that only miR-15a but not other miRNAs including miR-16, miR-21, and miR-34a, exhibited significant upregulation in the synchronized PCV2-infected PK15 cells. [score:4]
Synchronized PK15 cells were mock infected or infected with PCV2 at an MOI of 1. At 24 h postinfection, expression levels of miR-15a and miR-16 as well as miR-21 and miR-34a were assayed by qRT-PCR. [score:2]
Therefore, we further determined the expression levels of miR-21 and miR-34a in the synchronized PCV2-infected PK15 cells and found that no obvious changes were observed as compared to that in the mock-infected cells (Fig. 4). [score:2]
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8
[+] score: 11
A study on the expression profile of novel miRNAs in 11 pig tissues, including brain, liver, heart, muscle, colon, kidney, lung, spleen, stomach, cervix and fibroblasts, indicated that ssc-miR-15b, ssc-miR-23a, ssc-miR-23b, ssc-miR-24, ssc-miR-29a, ssc-miR-30b, ssc-miR-145, and ssc-miR-152 are expressed in all tissues; ssc-miR-210 is mainly expressed in the liver, spleen, and stomach; ssc-miR-34a and ssc-miR-130a are mainly expressed in the lungs; and ssc-miR-140 is highly expressed in the cervix. [score:11]
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9
[+] score: 10
Secondly, targets for a sub-set of down-regulated miR (miR-15, miR-16, miR-27, miR-29, miR-34 and miR-106), of which 44 targets were identified based on our previous criteria were predicted (see Additional file 4). [score:8]
These miR have been implicated in multiple cellular processes including cell growth (miR-24), apoptosis (miR-16, miR-24 and miR-29), and cell cycle regulation in normal (miR-16) and cancerous cells (miR-24, miR-27, miR-29 and miR-34) [9, 40- 46]. [score:2]
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10
[+] score: 8
miR-34a is an inhibitor of beige and brown fat formation that functions by suppressing adipocyte FGF21 signaling and SIRT1 function [37], and our observations indicated that miR-34a was down-regulated in the H group. [score:8]
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11
[+] score: 6
In addition to tissue-specific ageing, it is increasingly evident that many miRNA regulate gene expressions in well-known ageing pathways, most notably in the p53 tumor suppressor pathway (miR-34, miR-29 and miR-217, etc. ) [score:6]
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12
[+] score: 6
However, we did not detect differential expression of other previously identified miRNAs (miR-223, miR-150, miR-92a), although miR-10b, miR-20a, miR-30a-5p, miR-34a, miR-17—5p, miR-16, miR-146b, and miR-155-5p expression was significantly different. [score:5]
Many immune-related miRNAs have been identified in innate and adaptive immune systems, including the miR-17—92 cluster, miR-221, miR-10, miR-196b, miR-126, miR-155, miR-150; miR-181a, miR-326, miR-142-3p, miR-424, miR-21, miR-106a, miR-223, miR-146; the let-7 family, miR-9, and miR-34 [6]. [score:1]
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13
[+] score: 4
Among these, miR-363, miR-423 and miR-34 were the top three upregulated miRNAs in Duroc pigs with fold change ranging from 3.29 to 1.68. [score:4]
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14
[+] score: 3
Other miRNAs from this paper: ssc-mir-107
Ssc-miR-34a and Ssc-miR-107 were selected as endogenous controls, which were confirmed to be stably expressed in the PBMC [24]. [score:3]
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15
[+] score: 3
MiR-34a, -134 and -134-5p, enriched in endothelial cells, were revealed to be highly expressed in PBMCs of the AMI patients than that in the stable angina patients [10, 19]. [score:2]
Abbreviations: CECs = circulating endothelial cells, other abbreviations as in Fig 3. Studies have found that elevated miRNAs during ACS come from several origins: skeletal muscle miRNAs (miR-1 [8], -133a [9], and -133b), cardiac-specific miRNAs (miR-208a [9], -208b, -499, and -499-5p [8]), pancreatic miRNAs (miR-375), liver-specific miRNAs (miR-122), brain-enriched miRNAs (miR-34a, -124, -134, and -134-5p [10]) [8– 10], and endothelium-enriched miRNAs (miR-221-3p [11], -126, and -423 [12]). [score:1]
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