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长链非编码RNA HOX转录本反义RNA通过miR-126-5p/Akt轴介导高血糖诱导的肾小管上皮细胞损伤。

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

作者信息

Jiang Qiong, Yang Ting, Zou Yan, He Mingjie, Li Qingchun, Chen Xiaohui, Zhong Aimin

机构信息

Jiangxi Provincial Key Laboratory of Nephrology Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College Nanchang China.

出版信息

Aging Med (Milton). 2023 Sep 27;6(4):427-434. doi: 10.1002/agm2.12266. eCollection 2023 Dec.

Abstract

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

摘要

探讨HOX转录本反义RNA(HOTAIR)在高糖诱导的肾小管上皮细胞损伤中的作用。在高糖诱导的HK-2细胞中,HOTAIR表达上调,导致细胞增殖受抑。同时,HOTAIR上调促凋亡蛋白Bax和裂解的caspase-3的表达,而下调抗凋亡蛋白Bcl-2的表达。荧光素酶报告基因检测显示HOTAIR可靶向miR-126-5p。此外,发现PI3K/Akt信号通路是miR-126-5p的下游靶点。敲低HOTAIR可减轻细胞凋亡,而进一步抑制miR-126-5p则导致HK-2细胞凋亡。HOTAIR通过miR-126-5p/PI3K/Akt信号通路在介导高糖诱导的HK-2细胞损伤中发挥调节作用,尤其影响细胞凋亡和细胞活力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7ef/10792317/cd5fb2cc632d/AGM2-6-427-g004.jpg

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