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Hepatic ischemia/reperfusion injury disrupts the homeostasis of kidney primary cilia via oxidative stress

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Author(s)
Sang Jun HanHee-Seong JangSung Young SeuHee-Jung ChoYoon Jin HwangJee In KimKwon Moo Park
Publication Year
2017
Keyword
Acute kidney injuryDeciliationLiver ischemiaPrimary ciliaReactive oxidative species
Abstract
Acute kidney injury (AKI) is a major complication of hepatic surgeries. The primary cilium protrudes to the lumen of kidney tubules and plays an important role in renal functions. Disruption of primary cilia homeostasis is highly associated with human diseases including AKI. Here, we investigated whether transient hepatic ischemia induces length change and deciliation of kidney primary cilia, and if so, whether reactive oxygen species (ROS)/oxidative stress regulates those. HIR induced damages to the liver and kidney with increases in ROS/oxidative stress. HIR shortened the cilia of kidney epithelial cells and caused them to shed into the urine. This shortening and shedding of cilia was prevented by Mn(III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP, an antioxidant). The urine of patient undergone liver resection contained ciliary proteins. These findings indicate that HIR induces shortening and deciliation of kidney primary cilia into the urine via ROS/oxidative stress, suggesting that primary cilia is associated with HIR-induced AKI and that the presence of ciliary proteins in the urine could be a potential indication of kidney injury.
Department
Dept. of Molecular Medicine (분자의학)
Publisher
School of Medicine (의과대학)
Citation
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol.1863(7) : 1817-1828, 2017
Type
Article
ISSN
0925-4439
DOI
10.1016/j.bbadis.2017.05.004
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/41271
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