Adhesion of epithelial cells to fibronectin or collagen I induces alterations in gene expression via a protein kinase C-dependent mechanism

2001 ◽  
Vol 189 (1) ◽  
pp. 79-90 ◽  
Author(s):  
Kirby Lam ◽  
Lianfeng Zhang ◽  
Kenneth M. Yamada ◽  
Robert M. Lafrenie
1998 ◽  
Vol 107 (3) ◽  
pp. 213-219 ◽  
Author(s):  
Jizhen Lin ◽  
Youngki Kim ◽  
Steven K. Juhn

Tumor necrosis factor α (TNF-α), originally defined by its antitumoral activity, is now recognized as a polypeptide mediator of inflammatory and cellular immune response. Recent studies have demonstrated that TNF-α exists in the fluid of otitis media with effusion and, therefore, suggested its possible role in the pathogenesis of mucus hypersecretion. In this study, the effects of TNF-α on mucous glycoprotein (MGP) secretion from cultured chinchilla middle ear epithelial cells were examined, and TNF-α was found to stimulate MGP secretion in a time- and concentration-dependent manner. The action of TNF-α on MGP secretion was significantly and dose-dependently inhibited by TNF-α monoclonal antibody; this finding is suggestive of its specificity on MGP secretion. The addition of the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperidine (H-7) to the culture significantly blocked TNF-α-induced MGP secretion, while the calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) did not. This suggests that TNF-α stimulates MGP secretion via a protein kinase C—dependent mechanism.


2006 ◽  
Vol 97 (6) ◽  
pp. 1317-1327 ◽  
Author(s):  
Dezheng Zhao ◽  
Yanai Zhan ◽  
Huiyan Zeng ◽  
Mary P. Moyer ◽  
Christos S. Mantzoros ◽  
...  

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