A Novel Function of MicroRNA 130a-3p in Hepatic Insulin Sensitivity and Liver Steatosis

Xiao, Fei; Yu, Junjie; Liu, Bin; Guo, Yinlong; Li, Kai; Deng, Jiali; Zhang, Jin; Wang, Chunxia; Chen, Shanghai; Du, Ying; Lu, Yingli; Xiao, Yuzhong; Zhang, Zhou; Guo, Feifan

doi:10.2337/db13-1689

Cited by 76 publications

(53 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of miR-130a-3p were first studied in mice and were later verified in studies with human embryonic stem cells. It appears to be a vertebrate-specific miRNA and is widely developed in angiogenesis, cell cycle, and so on [15]. It has been reported that down-regulation of miR-130-3p can promote cisplatin resistance in ovarian cancer cells [16].…”

Section: Introductionmentioning

confidence: 99%

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

View full text Add to dashboard Cite

The aim of the present study was to explore the mechanism through which miR-130a-3p affects the viability, proliferation, migration, and invasion of nasopharyngeal carcinoma (NPC). Tissue samples were collected from the hospital department. NPC cell lines were purchased to conduct the in vitro and in vivo assays. A series of biological assays including MTT, Transwell, and wound healing assays were conducted to investigate the effects of miR-130a-3p and BACH2 on NPC cells. MiR-130a-3p was down-regulated in both NPC tissues and cell lines, whereas BACH2 was up-regulated in both tissues and cell lines. MiR-130a-3p overexpression inhibited NPC cell viability, proliferation, migration, and invasion but promoted cell apoptosis. The converse was true of BACH2, the down-regulation of which could inhibit the corresponding cell abilities and promote apoptosis of NPC cells. The target relationship between miR-130a-3p and BACH2 was confirmed. The epithelial–mesenchymal transition (EMT) pathway was also influenced by miR-130a-3p down-regulation. In conclusion, miR-130a-3p could bind to BACH2, inhibit NPC cell abilities, and promote cell apoptosis.

show abstract

Section: Introductionmentioning

confidence: 99%

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Further, Xiao et al reported that miR130a-3p affects insulin resistance in hepatic cells by targeting the growth factor receptor-bound protein 10 (GRB10), an adapter protein that regulates receptor tyrosine kinase signaling cascades, and confirmed their finding in a mouse model [143]. Mice overexpressing miR-130a-3p had improved glucose clearance, and concomitant over-expression of GRB10 could overcome this beneficial outcome.…”

Section: Micrornas and Insulin Resistancementioning

confidence: 90%

MicroRNAs in obesity-associated disorders

Abente

Mahadevan

Ramachandran

et al. 2016

Archives of Biochemistry and Biophysics

View full text Add to dashboard Cite

“…A recent study shows that miR-130a-3p is aberrantly reduced in livers of a mouse model with nonalcoholic fibrosing steatohepatitis, and the overexpression of miR-130a-3p inhibits hepatic stellate cells (HSC) activation and proliferation and promotes HSC apoptosis (26). Moreover, miR-130a-3p has been proven regulation of liver steatosis, glucose homeostasis and insulin sensitivity (10,21). miR-301a-3p, as an oncogene, has been reported to be upregulated in several malignant tumors (27,28).…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs (miRs) are endogenous, noncoding, short, single-stranded RNAs (18-25 nucleotides) that are evolutionarily highly conserved, believed to regulate the translation of target messenger RNAs (mRNAs) by binding to its 3'-untranslated regions (3'-UTRs) and verified to play a role in controlling a variety of biological processes (10). Recently, several studies have highlighted the significance of miRs in maintaining glucose metabolism-associated cell dysfunction (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

“…Recently, several studies have highlighted the significance of miRs in maintaining glucose metabolism-associated cell dysfunction (11)(12)(13). For example, miR-130a-3p has been shown to mediate insulin sensitivity (10), and miR-24-3p, miR-146a-5p, miR-194-5p, miR-197-3p, miR-301a-3p and miR-375 are correlated with residual beta cell function in children with new-onset type 1 diabetes mellitus (T1DM) (12). Moreover, miR-27a, miR-34a, miR-195 and miR-218 promote podocyte injury (6,(14)(15)(16), in contrast to that miR-29a, miR-30a and miR-217 protect against high glucose-induced podocyte injury (9,17,18).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

Jiang

Wang²,

Liu

et al. 2017

Exp Ther Med

View full text Add to dashboard Cite

Abstract. Tumor necrosis factor (TNF)-α has been reported to be important in glomerulonephritis, which is closely associated with podocyte dysfunction and apoptosis. However, the precise mechanisms by which TNF-α expression are regulated remain unclear. The purpose of the present study was to investigate the role of microRNA (miR)-130a-3p/301a-3p in the post-transcriptional control of TNF-α expression and high glucose (HG)-induced podocyte dysfunction. Mice MPC5 podocytes were incubated with HG and transfected with miR-130a-3p/301a-3p mimics or inhibitors, reactive oxygen species (ROS) levels were measured by flow cytometry assay, and the mRNA and protein levels were assayed by using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and verified using a dual luciferase reporter assay. It was observed that miR-130a-3p/301a-3p was a novel regulator of TNF-α in mouse podocytes. miR-130a-3p/301a-3p mimics inhibited TNF-α 3'-untranslated region luciferase reporter activity, in addition to endogenous TNF-α protein expression. Furthermore, forced expression of miR-130a-3p or miR-301a-3p resulted in the downregulation of ROS and malondialdehyde (MDA) and the upregulation of superoxide dismutase (SOD) 1 in the presence of HG. Inhibition of TNF-α level prevented a remarkable reduc tion in SOD activity and a marked increase in ROS and MDA levels in HG-treated podocytes. Furthermore, TNF-α loss-of-function significantly reversed HG-induced podocyte apoptosis. These data demonstrated a novel up-stream role for miR-130a-3p/301a-3p in TNF-α-mediated podocyte dysfunction and apoptosis in the presence of HG. IntroductionGlomerular podocytes are highly differentiated cells that play a key role in maintaining the integrity of the glomerular filtration barrier (1). In glomerular diseases, podocyte damage leads to increased glomerular barrier pore size, allowing the passage of proteins or other mediators to the tubular lumen, which results in proteinuria and progressive loss of kidney function (2). Accumulating evidence indicates that hyperglycemia contributes to podocyte lesions (3). Clinical data demonstrate that podocyte integrity is impaired, and the decreased podocyte number is confirmed in individuals with type 1 (T1DM) and 2 diabetes mellitus (T2DM) (4,5). In cultured podocytes, high glucose induces apoptosis, epithelial-mesenchymal transition (EMT), mitochondrial fission and autophagy through different signaling pathways (6-9). However, the underlying molecular mechanisms of high glucose-induced MPC5 podocytes dysfunction remain to be fully elucidated.MicroRNAs (miRs) are endogenous, noncoding, short, single-stranded RNAs (18-25 nucleotides) that are evolutionarily highly conserved, believed to regulate the translation of target messenger RNAs (mRNAs) by binding to its 3'-untranslated regions (3'-UTRs) and verified to play a role in controlling a variety of biological processes (10). Recently, several studies have h...

show abstract

A Novel Function of MicroRNA 130a-3p in Hepatic Insulin Sensitivity and Liver Steatosis

Cited by 76 publications

References 39 publications

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

MiR-130a-3p inhibits the viability, proliferation, invasion, and cell cycle, and promotes apoptosis of nasopharyngeal carcinoma cells by suppressing BACH2 expression

MicroRNAs in obesity-associated disorders

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

Contact Info

Product

Resources

About