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LncRNA136131 通过靶向 miR-378a-3p/Rab10 轴抑制急性肾损伤肾小管上皮细胞凋亡。

LncRNA136131 suppresses apoptosis of renal tubular epithelial cells in acute kidney injury by targeting the miR-378a-3p/Rab10 axis.

机构信息

Department of Nephrology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.

Department of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

出版信息

Aging (Albany NY). 2022 Apr 28;14(8):3666-3686. doi: 10.18632/aging.204036.

DOI:10.18632/aging.204036
PMID:35482482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9085219/
Abstract

The pathogenesis of acute kidney injury (AKI) is not fully understood. To date, the exact role and regulatory mechanism of long non-coding RNA (lncRNA)136131 in AKI remains unclear. Here, we demonstrate that lncRNA136131 in BUMPT cells is induced by antimycin A. Furthermore, after incubating BUMPT cells in antimycin for two hours, lncRNA136131 prevented BUMPT cell apoptosis and cleaved caspase-3 expression. Mechanistically, lncRNA136131 sponged miR-378a-3p and then increased the expression of Rab10 to suppress apoptosis. Finally, I/R-induced decline of renal function, tubular damage, renal tubular cells apoptosis, and the upregulation of cleaved caspase-3 were aggravated by lncRNA136131 siRNA. In contrast, this effect was attenuated by the overexpression of lncRNA136131. In conclusion, lncRNA136131 protected against I/R-induced AKI progression by targeting miR-378a-3p/Rab10 and may be utilized as a novel target for AKI therapeutics.

摘要

急性肾损伤 (AKI) 的发病机制尚未完全阐明。迄今为止，长链非编码 RNA (lncRNA)136131 在 AKI 中的确切作用和调节机制仍不清楚。在这里，我们证明 BUMPT 细胞中的 lncRNA136131 是由安密妥星诱导的。此外，在安密妥星孵育 BUMPT 细胞两小时后，lncRNA136131 可防止 BUMPT 细胞凋亡并降低 cleaved caspase-3 的表达。在机制上，lncRNA136131 可以与 miR-378a-3p 结合，然后增加 Rab10 的表达以抑制细胞凋亡。最后，lncRNA136131 siRNA 加重了 I/R 诱导的肾功能下降、肾小管损伤、肾小管细胞凋亡和 cleaved caspase-3 的上调，而 lncRNA136131 的过表达则减弱了这一作用。总之，lncRNA136131 通过靶向 miR-378a-3p/Rab10 来保护 I/R 诱导的 AKI 进展，可能作为 AKI 治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/021d26dede58/aging-14-204036-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/b116530c7106/aging-14-204036-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/1ea654873d9e/aging-14-204036-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/ba9c525bdc83/aging-14-204036-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/80896abd7a63/aging-14-204036-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/2341549f5e75/aging-14-204036-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/5591ce87c9f5/aging-14-204036-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/021d26dede58/aging-14-204036-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/b116530c7106/aging-14-204036-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/d4a219af5a32/aging-14-204036-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/48a98fbf7c5a/aging-14-204036-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/1ea654873d9e/aging-14-204036-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/ba9c525bdc83/aging-14-204036-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/80896abd7a63/aging-14-204036-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/2341549f5e75/aging-14-204036-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/5591ce87c9f5/aging-14-204036-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b44b/9085219/021d26dede58/aging-14-204036-g009.jpg

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