Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5500954 | Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease | 2017 | 34 Pages |
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.
Keywords
AKImedullary thick ascending limbmTALALTOSOMROSASTAspartate aminotransferaseacute kidney injuryAlanine aminotransferasehepatic ischemiaLiver ischemiacollecting ductBUNMDCK cellsMadin-Darby canine kidney cellsproximal tubuleblood urea nitrogenPCRPrimary ciliaplasma creatinineReactive oxidative species
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Authors
Sang Jun Han, Hee-Seong Jang, Sung Young Seu, Hee-Jung Cho, Yoon Jin Hwang, Jee In Kim, Kwon Moo Park,