Tumor necrosis factor-α induces the aberrant expression of mucus core protein-2 in non-neoplastic biliary epithelial cells via the upregulation of CDX2 in chronic cholangitis

2008 ◽  
Vol 38 (10) ◽  
pp. 1006-1017 ◽  
Author(s):  
Hiroko Ikeda ◽  
Motoko Sasaki ◽  
Shusaku Ohira ◽  
Akira Ishikawa ◽  
Yasunori Sato ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Core Protein ◽  
Aberrant Expression ◽  
Biliary Epithelial Cells ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Induction of CD14 in Tubular Epithelial Cells During Kidney Disease

2000 ◽  
Vol 11 (9) ◽  
pp. 1681-1690 ◽  
Author(s):  
JEREMIAH MORRISSEY ◽  
GUANGJIE GUO ◽  
RUTH MCCRACKEN ◽  
TIMOTHY TOLLEY ◽  
SAULO KLAHR
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Knockout Mice ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Ischemia Reperfusion ◽  
Tubular Epithelial Cells ◽  
Factor Α ◽  
Cd14 Mrna ◽  
Necrosis Factor

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-α 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-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.

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