LncRNA 148400 Promotes the Apoptosis of Renal Tubular Epithelial Cells in Ischemic AKI by Targeting the miR-10b-3p/GRK4 Axis

Xingjin Li; Zhifen Wu; Jurong Yang; Dongshan Zhang

doi:10.3390/cells11243986

LncRNA 148400 Promotes the Apoptosis of Renal Tubular Epithelial Cells in Ischemic AKI by Targeting the miR-10b-3p/GRK4 Axis

Cells. 2022 Dec 9;11(24):3986. doi: 10.3390/cells11243986.

Authors

Xingjin Li^{1

2

3}, Zhifen Wu⁴, Jurong Yang⁴, Dongshan Zhang^{1

2

3}

Affiliations

¹ Department of Emergency Medicine, Second Xiangya Hospital, Central South University, Changsha 410011, China.
² Emergency Medicine and Difficult Diseases Institute, Second Xiangya Hospital, Central South University, Changsha 410011, China.
³ Department of Nephrology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
⁴ Department of Nephrology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing 401120, China.

Abstract

Although recent studies have reported that long non-coding RNA (lncRNA) is involved in the development of ischemic acute kidney injury (AKI), the exact function and regulatory mechanism of lncRNAs in ischemic AKI remain largely unknown. Herein, we found that ischemic injury promoted the expression of lncRNA 148400 in mouse proximal tubule-derived cell line (BUMPT) and C57BL/6J mice. Furthermore, the lncRNA148400 mediates ischemic injury-induced apoptosis of BUMPT cells. Mechanistically, lncRNA 148400 sponged miR-10b-3p to promote apoptosis via GRK4 upregulation. Finally, knockdown of lncRNA 148400 alleviated the I/R-induced deterioration of renal function, renal tubular injury, and cell apoptosis. In addition, cleaved caspase-3 is increased via targeting the miR-10b-3p/GRK4 axis. Collectively, these results showed that lncRNA 148400/miR-10b-3p/GRK4 axis mediated the development of ischemic AKI.

Keywords: AKI; GRK4; apoptosis; lncRNA148400; miR−10b−3p.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Acute Kidney Injury* / genetics
Acute Kidney Injury* / metabolism
Acute Kidney Injury* / pathology
Animals
Apoptosis / genetics
Apoptosis / physiology
Epithelial Cells* / metabolism
Epithelial Cells* / pathology
Ischemia / genetics
Ischemia / metabolism
Kidney Tubules, Proximal* / blood supply
Kidney Tubules, Proximal* / metabolism
Kidney Tubules, Proximal* / pathology
Mice
Mice, Inbred C57BL
MicroRNAs / genetics
MicroRNAs / metabolism
RNA, Long Noncoding* / genetics

Substances

MicroRNAs
RNA, Long Noncoding
MIRN10 microRNA, mouse
GRK4 protein, mouse

Grants and funding

The study was supported in part by a grant from National Natural Science Foundation of China (81870475). Changsha Science and Technology Bureau project (kq2001039). Key Project of Hunan provincial science and technology innovation (2020SK1014). Department of Science and Technology of Hunan Province project of International Cooperation and Exchanges (2020WK2009). Fundamental Research China Hunan Provincial Science and Technology Department (2021SK4004). The Chongqing Talent Program Project (cstc2021ycjh-bgzxm0090).