title: Induction of CD14 in tubular epithelial cells during kidney disease.
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 tumor necrosis factor-alpha receptor (TNFR) genes were also studied; the induction of CD14 was blunted in TNFR 1-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-alpha, 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.
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Jeremiah
authors.initials: J
authors.lastname: Morrissey
authors.affiliation: Department of Cell Biology and Physiology, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Guangjie
authors.initials: G
authors.lastname: Guo
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Ruth
authors.initials: R
authors.lastname: McCracken
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Timothy
authors.initials: T
authors.lastname: Tolley
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri.
authors.forename: Saulo
authors.initials: S
authors.lastname: Klahr
mesh_terms: D000818:Animals; D017209:Apoptosis; D001483:Base Sequence / Q000235:genetics; D004847:Epithelial Cells / Q000276:immunology / Q000473:pathology / Q000502:physiology; D005786:Gene Expression Regulation; D007150:Immunohistochemistry; D007438:Introns / Q000235:genetics; D007674:Kidney Diseases / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D007684:Kidney Tubules / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D018950:Lipopolysaccharide Receptors / Q000032:analysis* / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics; D008969:Molecular Sequence Data; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha