ESTROGEN RECEPTOR ALPHA PROTECTS KIDNEYS AGAINST ISCHEMIA/REPERFUSION INJURY IN MICE

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ESTROGEN RECEPTOR ALPHA PROTECTS KIDNEYS AGAINST ISCHEMIA/REPERFUSION INJURY IN MICE

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Co-author 1

You Ri Park youri0212@naver.com Kyungpook National University Anatomy Daegu Korea (Republic of) *

Co-author 2

Yong Kwon Han pig891001@hanmail.net Kyungpook National University Anatomy Daegu Korea (Republic of) - Cardiovascular Research Institute Anatomy Daegu Korea (Republic of)

Co-author 3

Se Young Jang vocjsy@knu.ac.kr Kyungpook National University Hospital Internal Medicine Daegu Korea (Republic of) -

Co-author 4

Kwon Moo Park kmpark@knu.ac.kr Kyungpook National University Anatomy Daegu Korea (Republic of) - Cardiovascular Research Institute Anatomy Daegu Korea (Republic of)

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Introduction

Female is more resistant to ischemia/reperfusion (I/R) injury than male, depending on sex hormones. However, the role of the estrogen receptor (ER) and underlying molecular mechanisms on the female’s resistance to I/R injury remain to be defined. Here, we investigate the role of ERα on proximal tubule cells on kidney I/R injury.

Methods

Proximal tubule specific Esr1 gene-deleted (PT-ERα KO) and wild-type (PT-ERα WT) female mice were generated by crossing Esr1f/f with PEPCK-cre mice. Mice were subjected to either bilateral ischemia (BIR) or sham-operation. Some mice were subjected to 17β-estradiol (E2) administration for 14 days or ovariectomy (OVX) before BIR. Kidney damage was evaluated functionally and histologically; plasma creatinine (PCr), blood nitrogen urea (BUN), and Periodic acid-Schiff (PAS). In addition, ferroptosis was evaluated by long-chain-fatty-acid CoA ligase 4 (ACSL4) and glutathione peroxidase 4 (GPx4) and lipid peroxidation.

Results

BIR induced kidney damage in both groups, along with greater kidney damage in PT-ERα KO compared with wild-types; as reflected by greater increase of PCr and BUN, tubule damage, and ferroptosis. Administration of E2 protected kidneys in both PT-ERα WT and PT-ERα KO against BIR. This protection was milder in PT-ERα KO mice compared with PT-ERα WT mice. OVX exacerbated I/R-induced kidney damages in both PT-ERα WT and PT-ERα KO mice, without significant differences between groups. I/R induced ACSL4 increase, GPx4 decrease, lipid peroxidation, and TUNEL-positive cells in both groups, with inductions of them in PT-ERα KO than PT-ERα WT mice. These indicate greater ferroptosis was occurred in PT-ERα KO than PT-ERα WT mice.

Conclusion

Taken together, our findings have demonstrated that estrogen-ERα protects the kidneys from I/R.

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