血管生成
基因敲除
细胞周期
细胞凋亡
细胞生长
化学
小RNA
细胞生物学
流式细胞术
癌症研究
分子生物学
生物
生物化学
基因
作者
Kun Miao,Fang Xie,JinGui Lin
标识
DOI:10.18388/abp.2020_6295
摘要
Previous studies have shown that miR-221-3p plays an important role in vascular remodeling, but it is unclear whether it contributes to angiogenesis after burn injury. The purpose of this study was to investigate the effect of miR-221-3p on angiogenesis in HUVECs after burn injury and to reveal its underlying molecular mechanism.The burn HUVECs model was established by heat treatment. Plasmid or oligonucleotide transfection altered the expression of miR-221-3p and CDKN1B in HUVECs. MTT, colony formation, Transwell, flow cytometry, and tube formation experiments were applied to assess the proliferation, migration, apoptosis, cell cycle, and tube formation capacity of HUVECs. miR-221-3p, CDKN1B, Ki-67, and PCNA expression was assessed by RT-qPCR or Western blot. The dual-luciferase reporter assay verified the targeting relationship between miR-221-3p and CDKN1B.miR-221-3p was lowly expressed and CDKN1B was highly expressed in burn HUVECs. Overexpression of miR-221-3p promoted the proliferation, migration, and tube formation ability of burn HUVECs and inhibited apoptosis and the proportion of cells in the G0/G1 phase, whereas overexpression of CDKN1B had the opposite effect. Knockdown of miR-221-3p further inhibited the angiogenic capacity of burn HUVECs, but this effect was reversed by knockdown of CDKN1B. Mechanistically, miR-221-3p targeted CDKN1B.miR-221-3p improves the angiogenesis of burn HUVECs by targeting CDKN1B expression, and the miR-221-3p/CDKN1B axis may serve as a potential molecular target for future burn therapy.
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