Long non-coding RNA H19 acts as a microRNA-194 sponge to inhibit the apoptosis and promote the proliferation of hypertrophic scar fibroblasts
Autor: | Rongjun Xia, Shengjin Yu, Lijuan Lin, Bo Liu, Linlin Zheng |
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Rok vydání: | 2021 |
Předmět: |
Cicatrix
Hypertrophic MAP Kinase Signaling System Physiology Apoptosis p38 Mitogen-Activated Protein Kinases Cell Line Receptor IGF Type 1 Hypertrophic scar Text mining Physiology (medical) microRNA medicine Humans Cell Proliferation Pharmacology biology business.industry General Medicine Fibroblasts biology.organism_classification medicine.disease P38 MAPK Signaling Pathway Long non-coding RNA Cell biology MicroRNAs Sponge embryonic structures RNA Long Noncoding Hypertrophic scars business |
Zdroj: | Canadian Journal of Physiology and Pharmacology. 99:1288-1297 |
ISSN: | 1205-7541 0008-4212 |
Popis: | The effects of long non-coding RNAs (lncRNAs) on the proliferation of hypertrophic scars have been described, however, the underlying mechanisms are not well characterized. The present study aimed to investigate the mechanisms of lncRNA H19 in hypertrophic scars. The effects of the lncRNA H19 on the proliferation and apoptosis of hypertrophic scar fibroblasts (HSFs) were analyzed using 5′-ethynyl-2′-deoxyuridine staining, flow cytometry, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT). The results revealed H19 promoted the proliferation and inhibited the apoptosis in HSF. In addition, the binding associations between H19 and microRNA-194 (miR-194), and miR-194 and insulin-like growth factor I receptor (IGF1R) were identified using bioinformatics screening and verified using dual-luciferase assays. Furthermore, the effects of the IGF1R knockdown on H19-induced HSF phenotypes and regulation over the p38 MAPK pathway were determined. Mechanistically, miR-194 was identified as the downstream effector of the H19-mediated phenotypes of HSFs through its ability to directly target IGF1R, thus modulating the p38 MAPK signaling pathway. In conclusion, the findings suggested that H19 may inhibit the apoptosis and promote the proliferation of HSFs through the miR-194/IGF1R/p38 MAPK signaling axis, thereby contributing to the progression of hypertrophic scars. These findings may provide novel targets for the treatment of hypertrophic scars. |
Databáze: | OpenAIRE |
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