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 2.2 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

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,抑制细胞增殖。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,我们还发现PI3K/Akt信号通路是miR‐126‐5p的下游靶点。HOTAIR的下调减轻了凋亡,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,特别是影响细胞凋亡和细胞活力。
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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
Abstract 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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