LncRNA HOX转录反义RNA通过miR-126-5pAkt轴介导高血糖诱导的肾小管上皮细胞损伤

IF 3.1 Q3 GERIATRICS & GERONTOLOGY Aging Medicine Pub Date : 2023-09-27 DOI:10.1002/agm2.12266
Qiong Jiang, Ting Yang, Yan Zou, Mingjie He, Qingchun Li, Xiaohui Chen, Aimin Zhong
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引用次数: 0

摘要

目的:探讨HOX转录物反义RNA (HOTAIR)在高糖诱导肾小管上皮细胞损伤中的作用。结果:在高糖诱导的HK-2细胞中,HOTAIR表达上调,导致细胞增殖受到抑制。同时,HOTAIR上调促凋亡蛋白Bax和cleaved caspase-3的表达,下调抗凋亡蛋白Bcl-2的表达。荧光素酶报告基因检测显示HOTAIR可以靶向miR-126-5p。此外,我们发现PI3K/Akt信号通路是miR-126-5p的下游靶点。HOTAIR的下调减轻了细胞凋亡,而miR-126-5p的进一步抑制导致HK-2细胞凋亡。结论:HOTAIR通过miR-126-5p/PI3K/Akt信号通路,在高糖诱导的HK-2细胞损伤中发挥调节作用,具体影响细胞凋亡和细胞活力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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LncRNA HOX transcript antisense RNA mediates hyperglycemic-induced injury in the renal tubular epithelial cell via the miR-126-5pAkt axis

Objective: To investigate the involvement of HOX transcript antisense RNA (HOTAIR) in the injury of renal tubular epithelial cells induced by high glucose.

Results: In high glucose-induced HK-2 cells, the expression of HOTAIR was upregulated, resulting in suppressed cell proliferation. Meanwhile, HOTAIR upregulates the expression of pro-apoptotic proteins Bax and cleaved caspase-3, while downregulating the expression of the anti-apoptotic protein Bcl-2. Luciferase reporter assays revealed that HOTAIR could target miR-126-5p. Additionally, it was found that the PI3K/Akt signaling pathway serves as a downstream target of miR-126-5p. Knockdown of HOTAIR relieved apoptosis, whereas further inhibition of miR-126-5p led to apoptosis in HK-2 cells.

Conclusions: HOTAIR plays a regulatory role in mediating high glucose-induced injuries in HK-2 cells, specifically affecting apoptosis and cell viability, via the miR-126-5p/PI3K/Akt signaling pathway.

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来源期刊
Aging Medicine
Aging Medicine Medicine-Geriatrics and Gerontology
CiteScore
4.10
自引率
0.00%
发文量
38
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