当前位置： SCI文献检索 > ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS期刊下所有文献 > MicroRNA-130a has pro-fibroproliferative potential in hypertrophic scar by targeting CYLD.

MicroRNA-130a has pro-fibroproliferative potential in hypertrophic scar by targeting CYLD.

Abstract：

:Hypertrophic scars are dermal fibrosis diseases that protrude from the surface of the skin and irregularly extend to the periphery, seriously affecting the appearance and limb function of the patient. In this study, we found that microRNA-130a (miR-130a) was increased in hypertrophic scar tissues and derived primary fibroblasts, accompanied by up-regulation of collagen1/3 and α-SMA. Inhibition of miR-130a in hypertrophic scars fibroblasts suppressed the expression of collagen1/3 and α-SMA as well as the cell proliferation. Bioinformatics analysis combined with luciferase reporter gene assay results indicated that CYLD was a target gene of miR-130a, and the miR-130a mimic could reduce the level of CYLD. In contrast to miR-130a, the expression of CYLD was downregulated in hypertrophic scars and their derived fibroblasts. Overexpressing CYLD inhibited the expression of collagen 1/3 and α-SMA, slowed cell proliferation, and inhibited Akt activity. As expected, further study showed that the overexpression of CYLD could prevent the pro-fibroproliferative effects of miR-130a. Consistent with the in vitro results, the inhibitor of miR-130a effectively ameliorated excessive collagen deposition in bleomycin-induced skin fibrosis mouse model. Taken together, our results indicate that miR-130a promotes collagen secretion, myofibroblast transformation and cell proliferation by targeting CYLD and enhancing Akt activity. Therefore, the miR-130a/CYLD/Akt pathway may serve as a novel entry point for future skin fibrosis research.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Zhang J,Zhou Q,Wang H,Huang M,Shi J,Han F,Cai W,Li Y,He T,Hu D

doi

10.1016/j.abb.2019.07.003

subject

Has Abstract

pub_date

2019-08-15 00:00:00

pages

152-161

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(19)30175-4

journal_volume

671

pub_type

杂志文章

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