title: Kidney injury molecule-1 (KIM-1) mediates renal epithelial cell repair via ERK MAPK signaling pathway.
abstract: The expression of kidney injury molecule-1 (KIM-1), a very promising sensitive and specific urinary biomarker for acute renal injury, is markedly upregulated in injured and regenerating renal proximal tubular epithelial cells following ischemic or toxic insults, suggesting a possible role for this molecule in renal repair process. In the present study, we report that expression of KIM-1 facilitates renal tubular epithelial cell repair by promoting cell migration and proliferation. KIM-1 expression also enhances ERK MAPK activation, and the modulatory effect of KIM-1 on cellular repair process is likely mediated via ERK MAPK signaling pathway.
authors.affiliation: Division of Nephrology, Department of Medicine, VA Loma Linda Healthcare System (111 N) and Loma Linda University School of Medicine, 11201 Benton Street, Loma Linda, CA, 92357, USA. zhiwei.zhang@va.gov.
authors.forename: Zhiwei
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Division of Gastroenterology, Department of Medicine, VA Loma Linda Healthcare System and Loma Linda University School of Medicine, Loma Linda, CA, USA.
authors.forename: Cindy X
authors.initials: CX
authors.lastname: Cai
mesh_terms: D002460:Cell Line; D002465:Cell Movement; D049109:Cell Proliferation; D004847:Epithelial Cells / Q000378:metabolism* / Q000473:pathology; D000072596:Hepatitis A Virus Cellular Receptor 1 / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000378:metabolism* / Q000473:pathology; D020935:MAP Kinase Signaling System
chemical_list: C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1
keywords: Cell migration; Cell proliferation; Cellular repair; ERK MAPK; Kidney injury molecule-1 (KIM-1)