MicroRNA-30c promotes human adipocyte differentiation and co-represses<i>PAI-1</i>and<i>ALK2</i>

Karbiener, Michael; Neuhold, Claudia; Opriessnig, Peter; Prokesch, Andreas; Bogner‐Strauß, Juliane Gertrude; Scheideler, Marcel

doi:10.4161/rna.8.5.16153

Cited by 120 publications

(84 citation statements)

References 59 publications

(85 reference statements)

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“…The higher miR-26b and -30b levels that we observed in IS subjects may stimulate adipogenesis and terminal adipocyte differentiation; in primary human adipocyte culture, miR-26b is upregulated during differentiation, miR26b knock-down inhibits differentiation, and miR-26b overexpression enhances brite adipogenesis (23). Similarly, miR-30 family members contribute to thermogenesis (20), are upregulated during adipocyte differentiation (12), and their expression can directly impact adipogenesis (22,46). miR-145.…”

Section: Discussionmentioning

confidence: 90%

Integrative mRNA-microRNA analyses reveal novel interactions related to insulin sensitivity in human adipose tissue

Kirby

Walton

Finlin

et al. 2016

Physiological Genomics

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Section: Discussionmentioning

confidence: 90%

Integrative mRNA-microRNA analyses reveal novel interactions related to insulin sensitivity in human adipose tissue

Kirby

Walton

Finlin

et al. 2016

Physiological Genomics

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“…In differentiating adipocytes, miR-30c is up-regulated and silences ALK-2 expression (Karbiener et al 2011); miR-148b and miR-365 target the 3 0 -untranslated region of ALK-2 mRNA (Mura et al 2012); down-regulation of ALK-2 mRNA by miR-148a is relevant for the cancer stem-cell population in hepatocellular carcinoma (Li et al 2015); in the liver, BMP signaling is coordinated with the homeostasis of iron; and, after depletion of iron levels, miR-130a expression is up-regulated causing ALK-2 silencing and decrease in BMP-6 signaling, leading to down-regulation of the BMP target gene hepcidin, which produces the liver hormone that regulates iron homeostasis (Zumbrennen-Bullough et al 2014).…”

Section: Control Of Tgf-b Receptor Expression By Micrornasmentioning

confidence: 99%

Signaling Receptors for TGF-β Family Members

Heldin

Moustakas

2016

Cold Spring Harb Perspect Biol

552

498

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Transforming growth factor b (TGF-b) family members signal via heterotetrameric complexes of type I and type II dual specificity kinase receptors. The activation and stability of the receptors are controlled by posttranslational modifications, such as phosphorylation, ubiquitylation, sumoylation, and neddylation, as well as by interaction with other proteins at the cell surface and in the cytoplasm. Activation of TGF-b receptors induces signaling via formation of Smad complexes that are translocated to the nucleus where they act as transcription factors, as well as via non-Smad pathways, including the Erk1/2, JNK and p38 MAP kinase pathways, and the Src tyrosine kinase, phosphatidylinositol 3 0 -kinase, and Rho GTPases.

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“…Many miRNAs have been reported to be involved in the regulation of adipogenic differentiation, such as miR-143, miR-17-92, miR-130, miR-138, miR-17-5p, miR-106a, miR-210, miR-709, miR-137, and miR-302 [36][37][38][39][40][41][42][43][44]. However, few miRNAs have been reported in association with obesity and the positive regulation of adipogenesis [45]. Therefore, future studies are warranted to understand the exact role of obesity-associated miRNAs in the adipogenic differentiation of AMSCs.…”

Section: Introductionmentioning

confidence: 99%

Obesity-Associated MiR-342-3p Promotes Adipogenesis of Mesenchymal Stem Cells by Suppressing CtBP2 and Releasing C/EBPα from CtBP2 Binding

Wang

et al. 2015

Cell Physiol Biochem

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Background/Aims: The elucidation of the molecular mechanism of adipocyte differentiation in mesenchymal stem cells is of essential importance for the development of treatments for metabolic diseases, such as obesity and diabetes. Methods: The expression levels of miR-342-3p and carboxy-terminal binding protein 2 (CtBP2) were regulated by oligonucleotide transfection. Adipogenic differentiation was induced by adipogenic medium containing indomethacin, dexamethasone and 3-isobutyl-1-methylxanthine on day 12, as determined by Oil Red O staining and triglyceride concentration assay to assess intracellular lipid accumulation. The induction of adipocyte-specific transcription factors and markers was detected by qRT-PCR and western blot. The regulation of CtBP2 expression by miR-342-3p was determined by western blot, qRT-PCR, luciferase reporter assay, ChIP assay and functional experiments. Results: We revealed that miR-342-3p was enriched in the adipose tissue of obese mice, and its expression was significantly elevated during adipogenic differentiation in both human mesenchymal stem cells (hMSCs) and 3T3L1 cells. Using gain- and loss-of-function assays, we demonstrated that the overexpression of miR-342-3p markedly promoted the differentiation of hMSCs into an adipogenic lineage. Adipogenesis was significantly blocked by miR-342-3p downregulation. We identified and validated that CtBP2 was a direct target of miR-342-3p in this process. The effects of the inhibition of CtBP2 were similar to those of miR-342-5p overexpression on adipogenic differentiation, promoting the release of C/EBPα from CtBP2 binding. Conclusion: miR-342-3p is a powerful enhancer of the adipogenesis of human adipose-derived MSCs that acts by inhibiting CtBP2 and releasing the key adipogenic regulator C/EBPα from CtBP2 binding, subsequently activating the expression of adipogenic transcription factors and markers.

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MicroRNA-30c promotes human adipocyte differentiation and co-repressesPAI-1andALK2

Cited by 120 publications

References 59 publications

Integrative mRNA-microRNA analyses reveal novel interactions related to insulin sensitivity in human adipose tissue

Integrative mRNA-microRNA analyses reveal novel interactions related to insulin sensitivity in human adipose tissue

Signaling Receptors for TGF-β Family Members

Obesity-Associated MiR-342-3p Promotes Adipogenesis of Mesenchymal Stem Cells by Suppressing CtBP2 and Releasing C/EBPα from CtBP2 Binding

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