title: Unilateral nephrectomy elongates primary cilia in the remaining kidney via reactive oxygen species.
abstract: The length of primary cilia is associated with normal cell and organ function. In the kidney, the change of functional cilia length/mass is associated with various diseases such as ischemia/reperfusion injury, polycystic kidney disease, and congenital solitary kidney. Here, we investigate whether renal mass reduction affects primary cilia length and function. To induce renal mass reduction, mice were subjected to unilateral nephrectomy (UNx). UNx increased kidney weight and superoxide formation in the remaining kidney. Primary cilia were elongated in proximal tubule cells, collecting duct cells and parietal cells of the remaining kidney. Mn(III) Tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP), an antioxidant, reduced superoxide formation in UNx-mice and prevented the elongation of primary cilia. UNx increased the expression of phosphorylated ERK, p21, and exocyst complex members Sec8 and Sec10, in the remaining kidney, and these increases were prevented by MnTMPyP. In MDCK, a kidney tubular epithelial cell line, cells, low concentrations of H2O2 treatment elongated primary cilia. This H2O2-induced elongation of primary cilia was also prevented by MnTMPyP treatment. Taken together, these data demonstrate that kidney compensation, induced by a reduction of renal mass, results in primary cilia elongation, and this elongation is associated with an increased production of reactive oxygen species (ROS).
authors.affiliation: Department of Anatomy and BK 21 Project, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
authors.forename: Sang Jun
authors.initials: SJ
authors.lastname: Han
authors.affiliation: Department of Anatomy and BK 21 Project, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
authors.forename: Hee-Seong
authors.initials: HS
authors.lastname: Jang
authors.affiliation: Department of Molecular Medicine and MRC, Keimyung University School of Medicine, Daegu 705-717, Republic of Korea.
authors.forename: Jee In
authors.initials: JI
authors.lastname: Kim
authors.affiliation: Department of Medicine, Medical University of South Carolina, Charleston, South Carolina, USA.|Department of Medicine, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, USA.
authors.forename: Joshua H
authors.initials: JH
authors.lastname: Lipschutz
authors.affiliation: Department of Anatomy and BK 21 Project, Kyungpook National University School of Medicine, Daegu 700-422, Republic of Korea.
authors.forename: Kwon Moo
authors.initials: KM
authors.lastname: Park
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D002923:Cilia / Q000187:drug effects / Q000378:metabolism; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D015870:Gene Expression; D006861:Hydrogen Peroxide / Q000378:metabolism; D007668:Kidney / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D007684:Kidney Tubules / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D008565:Membrane Proteins; D008665:Metalloporphyrins / Q000494:pharmacology; D051379:Mice; D009392:Nephrectomy; D009929:Organ Size; D017382:Reactive Oxygen Species / Q000378:metabolism*; D033921:Vesicular Transport Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; C000606329:EXOC5 protein, mouse; D008565:Membrane Proteins; D008665:Metalloporphyrins; C502230:Mn(III) 5,10,15,20-tetrakis(N-methylpyridinium-2-yl)porphyrin; D017382:Reactive Oxygen Species; C489608:Sec8l1 protein, mouse; D033921:Vesicular Transport Proteins; D006861:Hydrogen Peroxide; D048049:Extracellular Signal-Regulated MAP Kinases