Induction of CD14 in tubular epithelial cells during kidney disease

Jeremiah Morrissey, Guangjie Guo, Ruth Mccracken, Timothy Tolley, Saulo Klahr

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

Analysis of gene expression in a mouse model of unilateral ureteral obstruction (UUO) revealed significant induction of CD14 mRNA in kidneys with obstructed ureters. Immunocytochemical analysis indicated that CD14 was upregulated in tubular epithelial cells and this upregulation was not attributable to infiltration of the kidneys by mononuclear cells. This induction of CD14 mRNA was found to occur in BALB/C, C57BL/6, C3H/HeN, and C3H/HeJ mice during UUO. Ischemia/reperfusion of kidneys also induced CD14 mRNA. Mice lacking either of the rumor necrosis factor-α receptor (TNFR) genes were also studied; the induction of CD14 was blunted in TNFR1-knockout mice but not in TNFR2-knockout mice. Apoptosis of tubular cells in lipopolysaccharide-resistant CH3/HeJ mice was significantly (P < 0.05) less than that in lipopolysaccharide-responsive CH3/HeN mice during UUO. These results suggest that CD14 is acutely induced in tubular epithelial cells in two mouse models of renal injury. This induction is regulated by tumor necrosis factor-α, through TNFR1. CD14 may participate in the apoptosis of tubular epithelial cells on a more chronic basis by activating a pathway that is absent or deficient in C3H/HeJ mice.

Original languageEnglish
Pages (from-to)1681-1690
Number of pages10
JournalJournal of the American Society of Nephrology
Volume11
Issue number9
StatePublished - 2000

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