2. Academic Validation
  3. MiR-132-3p activation aggravates renal ischemia-reperfusion injury by targeting Sirt1/PGC1alpha axis

MiR-132-3p activation aggravates renal ischemia-reperfusion injury by targeting Sirt1/PGC1alpha axis

  • Cell Signal. 2023 Jul 9;110801. doi: 10.1016/j.cellsig.2023.110801.
Chenglong Li 1,  Shangting Han 2,  Jiefu Zhu 3,  Fan Cheng 4
Affiliations

Affiliations

  • 1 Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
  • 2 Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China; Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
  • 3 Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China; Department of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China. Electronic address: jiefuzhu@whu.edu.cn.
  • 4 Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China. Electronic address: urology1969@aliyun.com.
PMID: 37433399 DOI: 10.1016/j.cellsig.2023.110801
Abstract

The pathogenesis of renal ischemic diseases remains unclear. In this study, we demonstrate the induction of microRNA-132-3p (miR-132-3p) in ischemic acute kidney injury (AKI) and cultured renal tubular cells under oxidative stress. miR-132-3p mimic increased Apoptosis in renal tubular cells and enhanced ischemic AKI in mice, whereas miR-132-3p inhibition offered protective effects. We analyzed miR-132-3p target genes through bioinformatic analysis and SIRT1 was predicted as the target gene of miR-132-3p. Luciferase MicroRNA target reporter assay further verified SIRT1 as a direct target of miR-132-3p. In cultured tubular cells and mouse kidneys, IRI and H2O2 treatment repressed SIRT1 and PGC-1α/NRF2/HO-1 expression, whereas anti-miR-132-3p preserved SIRT1 and PGC-1α/NRF2/HO-1 expression. In renal tubular, SIRT1 Inhibitor suppressed PGC1-1α/NRF2/HO-1 expression and aggravated tubular Apoptosis. Together, the results suggest that miR-132-3p induction aggravates ischemic AKI and oxidative stress by repressing SIRT1 expression, and miR-132-3p inhibition offers renal protection and may be a potential therapeutic target.

Keywords

Acute kidney injury; Oxidative stress; Renal ischemic-reperfusion injury; Sirt1; miR-132-3p.

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