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MUCOSAL BIOLOGY

Tumor necrosis factor- stimulates gastric epithelial cell proliferation

¹Division of Gastroenterology, Department of Medicine, Taipei Veterans General Hospital and National Yang-Ming University, School of Medicine, Taiwan, ²Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong

Submitted 1 March 2004 ; accepted in final form 29 June 2004

TNF- is a cytokine produced during gastric mucosal injury. We examined whether TNF- could promote mucosal repair by stimulation of epithelial cell proliferation and explored further the underlying mechanisms in a rat gastric mucosal epithelial cell line (RGM-1). TNF- treatment (1–10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells. TNF- treatment significantly increased cytosolic phospholipase A₂ and cyclooxygenase-2 (COX-2) protein expression and PGE₂ level but did not affect the protein levels of EGF, basic fibroblast growth factor, and COX-1 in RGM-1 cells. The mRNA of TNF receptor (TNF-R) 2 but not of TNF-R1 was also increased. Dexamethasone dose dependently inhibited the stimulatory effect of TNF- on cell proliferation, which was associated with a significant decrease in cellular COX-2 expression and PGE₂ level. A selective COX-2 inhibitor 3-(3-fluorophenyl)-4-[4-(methylsulfonyl)phenyl]-5,5-dimethyl-⁵H-furan-2-one (DFU) by itself had no effect on basal cell proliferation but significantly reduced the stimulatory effect of TNF- on RMG-1 cells. Combination of dexamethasone and DFU did not produce an additive effect. PGE₂ significantly reversed the depressive action of dexamethasone on cell proliferation. These results suggest that TNF- plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF- receptor and activation of the arachidonic acid/PG pathway.

cyclooxygenase; dexamethasone; phospholipase A₂; prostaglandin E₂

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