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2 publications mentioning chi-mir-130b

Open access articles that are associated with the species Capra hircus and mention the gene name mir-130b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 286
Pan et al. found that overexpressed miR-130b in HeLa-229 cells can be packaged into macrovesicles and shuttled into recipient primary cultured porcine adipocytes to reduce fat deposition by suppressing its target gene PPAR-α, involving in regulation of fat deposition[48]. [score:8]
The results showed that ectopic overexpression of miR-130b strongly up-regulated the mRNA expression of ACSL, CPT, ACOX1, HSL and ATGL (Fig 4). [score:8]
Our results showed that miR-130b significantly suppressed the luciferase activity, suggesting that miR-130b could function through the 3′UTR of PGC-1α to inhibit the reporter gene expression. [score:7]
Our results showed that mRNA of PGC-1α was down regulated by overexpression of miR-130b, and up regulated by inhibition of miR-130b (Fig 5A). [score:7]
In support of these findings, profiling of fat metabolism related gene expression in GMECs in which miR-130b was inhibited or overexpressed indicated that miR-130b could involve in lipid metabolism signaling pathways. [score:7]
These findings demonstrated that miR-130b directly interacted with the predicted target site of the PGC-1α mRNA and negatively regulated its expression, which at least partially explains the functional role of miR-130b during lactation. [score:7]
In this study, we constructed a miRNA library which included not only 267 Capra hircus primary miRNAs and 793 Bos Taurus primary miRNAs from miRBase but also the sequencing results via Solexa sequencing, with which we screened a series of potential miRNAs involved in regulation of milk metabolism and found that miR-130b had the highest inhibitory effect on adipogenesis at least partly via targeting PGC-1α gene. [score:6]
To prove that miR-130b could directly target this site, we synthesized a 3’UTR segment of PGC-1α containing the predicted miR-130b target site (or a mutated seed site) and cloned into the psi-CHECK2 vector, for constructing a 3'-UTR reporter plasmid. [score:6]
To confirm that PGC-1α is a real target of miR-130b, we first cloned 3′UTR of PGC-1α containing the putative miRNA regulatory element (MRE) for miR-130b into a luciferase reporter plasmid to determine whether miR-130b could have inhibitory effect. [score:6]
On the other hand, cells transfected with miR-130b inhibitor displayed marked down-regulation of several fat metabolism-related genes, such as SCD, DGAT1, LPL, CD36, SLA27A6 (Solutecarrier family 27 transporter,sub -family A,member6), SREBP1 and PPARγ (Fig 4). [score:6]
Interestingly, we also found that miR-130b could be down-regulated by knockdown of PGC-1α via PGC-1α-siRNA (Fig 5D), the significance and mechanism of which is needed further studies. [score:5]
GMECs were transfected with miR-130b mimic or inhibitor for 48h, the mRNA expression of ACSL, CPT, ACOX1, HSL, ATGL, SCD, DGAT1, LPL, CD36, SLA27A6, SREBP1 and PPARγ were quantified by RT-qPCR (n = 6). [score:5]
In addition, we made a mutation of the potential binding site for miR-130b in the 3’UTR, and this mutation abrogated the suppressive effect ofmiR-130b on the 3′UTR of PGC-1α. [score:5]
Values are presented as means ± standard errors, *, P<0.05; **, P<0.01 A: GMECs were transfected with miR-130b mimic or inhibitor for 48h, PGC-1α expression level was quantified by RT-qPCR (n = 4). [score:5]
A: NC mimic treatment, B: miR-130b mimic treatment, C: NC inhibior treatment, D: miR-130b inhibior treatment. [score:5]
Our results show that miR-130b express abundantly in the mammary gland of goat and is one of the miRNAs with most significantly differential expression in different periods. [score:5]
Meanwhile, we found that overexpression of miR-130b suppressed fat droplet formation, using oil red O staining (Fig 3). [score:5]
GMECs were transfected with miR-130b mimic or inhibitor for 48h, the mRNA expression of ACSL, CPT, ACOX1, HSL, ATGL, SCD, DGAT1, LPL, CD36, SLA27A6, SREBP1 and PPARγ were quantified by RT-qPCR. [score:5]
Both miR-130b mimic and inhibitor were used in the research, miR-130b level was 30 times higher in miR-130b mimic transfected group than the negative control, oppositely, with 90% decrease in miR-130b inhibitor group (Fig 2A and 2B). [score:5]
0142809.g005 Fig 5A: GMECs were transfected with miR-130b mimic or inhibitor for 48h, PGC-1α expression level was quantified by RT-qPCR (n = 4). [score:5]
B and E: Target site of miR-130b in PGC-1α 3’UTR and the construction of the luciferase (Luc) expression vector fused with the PGC-1α 3’UTR. [score:5]
0142809.g004 Fig 4GMECs were transfected with miR-130b mimic or inhibitor for 48h, the mRNA expression of ACSL, CPT, ACOX1, HSL, ATGL, SCD, DGAT1, LPL, CD36, SLA27A6, SREBP1 and PPARγ were quantified by RT-qPCR (n = 6). [score:5]
It was found in goat that the 3’-UTR of PGC-1a was targeted by miR-130b targets. [score:5]
To understand the exact function and molecular mechanism of miR-130b in mediating milk fat metabolism, we firstly carried out some function experiment, including detection of lipid contents and fat droplet formation, in the condition of miR-130b overexpression and inhibition. [score:5]
Among these miRNAs, miR-130b is one of the most down-regulated (Fig 1A and 1B). [score:4]
0142809.g002 Fig 2A: miR-130bmimic treatment (60nM); B: miR-130b inhibitor treatment (60nM); C: Triglyceride levels in cells transfected with miR-130b mimic or inhibitor; Triglyceride levels were compared with that of control (n = 6). [score:4]
A: miR-130bmimic treatment (60nM); B: miR-130b inhibitor treatment (60nM); C: Triglyceride levels in cells transfected with miR-130b mimic or inhibitor; Triglyceride levels were compared with that of control (n = 6). [score:4]
The down regulation of miR-130b increases PGC-1α and PPAR-γexpression levels in DCMECs. [score:4]
Take these findings together, we hypothesize miR-130b could target and regress PGC-1α, which combine to PPARγ to regulate a large number of downstream genes, involving in milk fat metabolism. [score:4]
Fig 2D showed that there were no significant difference in proliferation of GMEC between control group and experimental group (miR-130b mimic or inhibitor), indicating miR-130b didn’t impact the process of goat mammary development. [score:4]
Cells were transfected with either the scramble or miR-130b mimic (60nM) or inhibitor (60nM) (Invitrogen, USA) using Lipofectamine TM RNAiMAX (Invitrogen, USA) according to manufacturer’s instructions. [score:3]
0142809.g003 Fig 3Changes in the lipid contents of GMECs transfected with miR-130b mimic (60nM) or miR-130b inhibitor (60nM). [score:3]
C: miR-130b expression in various tissues of milk goats. [score:3]
C: Western blot analysis of PGC-1α expression in the miR-130b mimic and NC treatment experiments. [score:3]
After a 6h recovery period in medium, cells then transfected either with scramble or miR-130b mimic or inhibitor using Lipofectamine TM RNAi MAX according to the manufacturer’s protocol. [score:3]
Moreover, fat droplet formation increased in miR-130b inhibited group (Fig 3). [score:3]
Whether the expression of some fat metabolism-related genes are changed by miR-130b? [score:3]
Therefore we further measured the content of cellular triglyceride and fat droplets in GMECs, in which miR-130b was overexpressed or inhibited. [score:3]
Fat droplet detection after transecting with miR-130b mimic or inhibitor in GMEC. [score:3]
Changes in the lipid contents of GMECs transfected with miR-130b mimic (60nM) or miR-130b inhibitor (60nM). [score:3]
Eun Kyung Lee pointed out that miR-130 influenced PPAR-α expression and adipocyte differentiation, and highlighted the potential flame for people to understand, prevent, and manage human obesity through microRNAs [21]. [score:3]
MiR-130b regulates expression of genes related to fat metabolism in GMECs. [score:3]
MiR-130b targeted PGC-1α 3’UTR directly. [score:3]
GMECs were transfected with either the scramble or the miR-130b mimic or inhibitor. [score:3]
Next, we tested the miR-130b expression in different tissue of milk goats. [score:3]
D: GMECs were transfected with siRNA of PGC-1α for 48h later, miR-130b expression levels was quantified by RT-qPCR (n = 6). [score:3]
Wang identified miR-130b as a potential biomarker for overweight and metabolic syndrome, and discovered a novel mechanism linking obesity and obesity-related metabolic diseases, which involved circulating miRNA -based adipose-muscle crosstalk. [score:3]
Many genes were the potential targets of miR-130b, based on the 3’-UTR complementary prediction, such as PGC-1α. [score:3]
Furthermore, we next predicted miR-130b targeted genes with bioinformatics software and selected a group of genes potentially associated with the milk fat metabolism for subsequent analysis. [score:3]
miR-130b is majorly expressed in muscle and breast tissues (Fig 1C), supporting that miR-130b may play an important role in milk fat metabolism process. [score:3]
White bars, negative control; black bars, miR-130b mimic or inhibitor. [score:3]
miR-130b suppresses Lipid metabolism in GMECs. [score:3]
org/) for prediction analysis to identify target genes of miR-130b. [score:3]
0142809.g006 Fig 6Diagram summarizing our findings miR-130b inversely target both PGC-1α and PPAR-γ in DCMECs. [score:3]
Interestingly, the lipid accumulation and triglyceride content were significantly increased by miR-130b mimic and repressed by miR-130b inhibitor, suggesting that miR-130b may be related to milk fat metabolism and secretion. [score:3]
On the other hand, triglyceride content increased significantly when miR-130b inhibited (Fig 2C). [score:3]
In brief, epithelial cells transfected with either scramble or miR-130b mimic or inhibitor were washed three times in phosphate buffer solution (PBS) and then fixed in 10% paraformaldehyde for 1h. [score:3]
The miR-130b expression level were detected in heart, liver, Spleen, Lung, Kidney, Muscle, Mammary gland, Stomach and Sebum. [score:3]
miR-130b has been reported to be involved in diseases, such as obesity, and lipid metabolism in adipose tissue, indicating its role in the process of lactation. [score:3]
Diagram summarizing our findings miR-130b inversely target both PGC-1α and PPAR-γ in DCMECs. [score:3]
Our findings revealed that miR-130b plays a crucial role in milk fat metabolism and suppresses milk fat synthesis in goat mammary gland. [score:3]
PGC-1α was identified as a target of miR-130b in GMECs. [score:3]
MiR-130b specifically target PGC-1α in GMEC. [score:2]
WT, Luc reporter vector with the WT PGC-1α 3’UTR (1958 to 1981); MU, Luc reporter vector with the mutation at miR-130b site in PGC-1α 3’UTR. [score:2]
All these results supported our hypothesis that miR-130b regulates fat metabolism in GMECs. [score:2]
miR130b regulation fat metabolism in GMEC. [score:2]
showed that miR-130b mimic reduced the relative luciferase activity of the reporter with a wild-type 3’UTR but not the one with mutations in the seed sequences (Fig 5B and 5E). [score:2]
Since miR-130b didn’t involve the development of goat mammary gland, we next explored its role in milk fat metabolism. [score:2]
However, there is still much unknown about the exact mechanism, for example how the change of PGC-1α and PPAR-γ regulated by miR-130b impact lipid accumulation. [score:2]
To figure out the functional role of miR-130b in goat mammary gland, we used GMECs obtained from individual lactation milk goats as the research mo del. [score:1]
However, all these researches have little exploration about the functional and mechanism role of miR-130b in lactation process. [score:1]
The sequence of miR-130b: 5’- CAGUGCAAUGAUGAAAGGGCAU-3’, and the sequence of siRNA: sense: 5’- GCCAACACUCAGCUAAGUUTT-3’, antisense: 5’- AACUUAGCUGAGUGUUGGCTT-3’, was performed as described previously with modification [27]. [score:1]
Above we have proved the crucial role of miR-130b in the process of milk fat metabolism. [score:1]
Several reports have studied the function of miR-130b in fat metabolism. [score:1]
The sequence of miR-130b: 5’- CAGUGCAAUGAUGAAAGGGCAU-3’, and the sequence of siRNA: sense: 5’- GCCAACACUCAGCUAAGUUTT-3’, antisense: 5’- AACUUAGCUGAGUGUUGGCTT-3’, Oil red O staining was performed as described previously with modification [27]. [score:1]
MiR-130b regulates milk fat synthesis. [score:1]
Taken together, our results have unraveled an important role of miR-130b in triglyceride accumulation and unsaturated fatty acid acceleration in GMECs for the first time. [score:1]
Therefore we could focused on the miR-130b in subsequent studies. [score:1]
Furthermore, we detected the protein level of PGC-1α after miR-130b mimic treatment via western blotting, which was consistent with mRNA level (Fig 5C). [score:1]
The effect of miR-130b mimics on PGC-1α protein expression was evaluated by western blot analysis in GMECs. [score:1]
Our study suggests that miR-130b plays a significant role in milk fat accumulation in goats. [score:1]
Moreover, as shown in Fig 5E, goat PGC-1α indeed has a potential binding site for miR-130b in the 3’-UTR. [score:1]
To this end, we investigated the effect of elevated expression of miR-130b with miRNA mimic on milk fat synthesis in goat mammary gland epithelial cells (GMEC). [score:1]
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[+] score: 7
Lee E. K. Lee M. J. Ab delmohsen K. Kim W. Kim M. M. Srikantan S. Martindale J. L. Hutchison E. R. Kim H. H. Marasa B. S. miR-130 suppresses adipogenesis by inhibiting peroxisome proliferator-activated receptor gamma expression Mol. [score:7]
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