Hepatic ischemia/reperfusion injury disrupts the homeostasis of kidney primary cilia via oxidative stress.
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.
['Han|Sang Jun|SJ|', 'Jang|Hee-Seong|HS|', 'Seu|Sung Young|SY|', 'Cho|Hee-Jung|HJ|', 'Hwang|Yoon Jin|YJ|', 'Kim|Jee In|JI|', 'Park|Kwon Moo|KM|']
D058186:Acute Kidney Injury D000818:Animals D000975:Antioxidants D002923:Cilia D006706:Homeostasis D008099:Liver D008297:Male D008665:Metalloporphyrins D051379:Mice D018384:Oxidative Stress D015427:Reperfusion Injury
Primary cilia Acute kidney injury Deciliation Liver ischemia Reactive oxidative species