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Cited 2 time in webofscience Cited 2 time in scopus
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LPS-Induced Acute Kidney Injury Is Mediated by Nox4-SH3YL1

Authors
Yoo, Jung-YeonCha, Dae RyongKim, BorimAn, Eun JungLee, Sae RomCha, Jin JooKang, Young SunGhee, Jung YeonHan, Jee YoungBae, Yun Soo
Issue Date
20-10월-2020
Publisher
CELL PRESS
Keywords
AKI; cytokine; H2O2, LPS; inflammation; Nox4; sepsis; SH3YL1; TLR4; tubular damage
Citation
CELL REPORTS, v.33, no.3
Indexed
SCIE
SCOPUS
Journal Title
CELL REPORTS
Volume
33
Number
3
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/52425
DOI
10.1016/j.celrep.2020.108245
ISSN
2211-1247
Abstract
Cytosolic proteins are required for regulation of NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (Nox) isozymes. Here we show that Src homology 3 (SH3) domain-containing YSC84-like 1 (SH3YL1), as a Nox4 cytosolic regulator, mediates lipopolysaccharide (LPS)-induced H2O2 generation, leading to acute kidney injury. The SH3YL1, Ysc84p/Lsb4p, Lsb3p, and plant FYVE proteins (SYLF) region and SH3 domain of SH3YL1 contribute to formation of a complex with Nox4-p22(p)(hox) Interaction of p22(p)(hox) with SH3YL1 is triggered by LPS, and the complex induces H2O2 generation and pro-inflammatory cytokine expression in mouse tubular epithelial cells. After LPS injection, SH3YL1 knockout mice show lower levels of acute kidney injury biomarkers, decreased secretion of pro-inflammatory cytokines, decreased infiltration of macrophages, and reduced tubular damage compared with wild-type (WT) mice. The results strongly suggest that SH3YL1 is involved in renal failure in LPS-induced acute kidney injury (AKI) mice. We demonstrate that formation of a ternary complex of p22(p)(hox)-SH3YL1-Nox4, leading to H2O2 generation, induces severe renal failure in the LPS-induced AKI model.
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