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长链非编码 RNA ENSMUST00000171502 通过靶向 miR-130b-3p/Mybl-1 轴诱导 HIF-1α 减轻缺血性急性肾损伤。

LncRNA ENSMUST00000171502 Induced by HIF-1α Ameliorates Ischemic Acute Kidney Injury via Targeting the miR-130b-3p/Mybl-1 Axis.

机构信息

Department of Emergency, Second Xiangya Hospital, Central South University, Changsha 410011, China.

Emergency Medicine and Difficult Diseases Institute, Second Xiangya Hospital, Central South University, Changsha 410011, China.

出版信息

Cells. 2022 Nov 23;11(23):3747. doi: 10.3390/cells11233747.

DOI:10.3390/cells11233747
PMID:36497007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9735850/
Abstract

Numerous studies have suggested that long non-coding RNA (lncRNA) affects the progression of ischemic acute kidney injury (IAKI). However, little information is currently available concerning the mechanisms of lncRNA171502 involved in IAKI. We applied an RT-qPCR assay for the expression of lncRNA171502 and miRNA-130b-3p, immunoblotting for the detection of Mybl-1-myeloblastosis oncogene-like 1 (Mybl-1) and cleaved caspase-3 (CC3) expression, and flow cytometry (FCM) for the evaluation of apoptosis. Initially, lncRNA171502 was induced by HIF-1α in the mouse proximal tubular (BUMPT) cell line and C57BL/6J mice during ischemic injury. Secondly, ischemic injury-induced BUMPT cell apoptosis was markedly relieved following the overexpression of lncRNA171502. However, this effect was enhanced by the knockdown of lncRNA171502. Mechanistically, lncRNA171502 could sponge miRNA-130b-3p and would subsequently upregulate the expression of Mybl-1 to drive the apoptotic process. Lastly, the overexpression of lncRNA171502 alleviated the development of IAKI by targeting miRNA-130b-3p/Mybl-1 pathways. In summary, the HIF-1α/lncRNA171502/miRNA-130b-3p/Mybl-1 axis prevented the progression of IAKI and might serve as a potential therapeutic target.

摘要

大量研究表明，长链非编码 RNA（lncRNA）影响缺血性急性肾损伤（IAKI）的进展。然而，目前关于 lncRNA171502 参与 IAKI 的机制知之甚少。我们应用 RT-qPCR 法检测 lncRNA171502 和 miRNA-130b-3p 的表达，免疫印迹法检测 Mybl-1-myeloblastosis 癌基因样 1（Mybl-1）和 cleaved caspase-3（CC3）的表达，流式细胞术（FCM）评估细胞凋亡。首先，在缺氧诱导因子 1α（HIF-1α）诱导的小鼠近端肾小管（BUMPT）细胞系和 C57BL/6J 小鼠中诱导 lncRNA171502 的表达。其次，过表达 lncRNA171502 明显减轻缺血性损伤诱导的 BUMPT 细胞凋亡。然而，lncRNA171502 的敲低增强了这种作用。从机制上讲，lncRNA171502 可以海绵化 miRNA-130b-3p，并随后上调 Mybl-1 的表达，从而驱动凋亡过程。最后，lncRNA171502 通过靶向 miRNA-130b-3p/Mybl-1 通路缓解 IAKI 的发展。总之，HIF-1α/lncRNA171502/miRNA-130b-3p/Mybl-1 轴阻止了 IAKI 的进展，可能成为一个有潜力的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/0953f58fb71c/cells-11-03747-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/b07139368790/cells-11-03747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/eab890390aa8/cells-11-03747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/86c5764a23cd/cells-11-03747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/d82c66e48799/cells-11-03747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/94637d97d7e4/cells-11-03747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/163b604843ce/cells-11-03747-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/e9f1c81ef19b/cells-11-03747-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/1432a551a6cd/cells-11-03747-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/3baeed226a26/cells-11-03747-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/0953f58fb71c/cells-11-03747-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/b07139368790/cells-11-03747-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/eab890390aa8/cells-11-03747-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/86c5764a23cd/cells-11-03747-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/d82c66e48799/cells-11-03747-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/94637d97d7e4/cells-11-03747-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/163b604843ce/cells-11-03747-g006a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/e9f1c81ef19b/cells-11-03747-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/1432a551a6cd/cells-11-03747-g008a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/3baeed226a26/cells-11-03747-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/03ad/9735850/0953f58fb71c/cells-11-03747-g010.jpg

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