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Article: Tumor necrosis factor-α stimulates gastric epithelial cell proliferation

TitleTumor necrosis factor-α stimulates gastric epithelial cell proliferation
Authors
KeywordsProstaglandin E 2
Cyclooxygenase
Dexamethasone
Phospholipase A 2
Issue Date2005
Citation
American Journal of Physiology - Gastrointestinal and Liver Physiology, 2005, v. 288, n. 1 51-1, p. G32-G38 How to Cite?
AbstractTNF-α is a cytokine produced during gastric mucosal injury. We examined whether TNF-α 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-α treatment (1-10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells. TNF-α treatment significantly increased cytosolic phospholipase A2 and cyclooxygenase-2 (COX-2) protein expression and PGE 2 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-α 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-α on RMG-1 cells. Combination of dexamethasone and DFU did not produce an additive effect. PGE 2 significantly reversed the depressive action of dexamethasone on cell proliferation. These results suggest that TNF-α plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF-α receptor and activation of the arachidonic acid/PG pathway.
Persistent Identifierhttp://hdl.handle.net/10722/207488
ISSN
2015 Impact Factor: 3.297
2015 SCImago Journal Rankings: 1.936

 

DC FieldValueLanguage
dc.contributor.authorJiing, Chyuan Luo-
dc.contributor.authorShin, Vivianyvonne-
dc.contributor.authorYing, HuaYang-
dc.contributor.authorWu, William Ka Kei-
dc.contributor.authorYi, NiYe-
dc.contributor.authorSo, Wallace Hau Leung-
dc.contributor.authorChang, Fullyoung-
dc.contributor.authorChi, Hincho-
dc.date.accessioned2014-12-31T01:01:46Z-
dc.date.available2014-12-31T01:01:46Z-
dc.date.issued2005-
dc.identifier.citationAmerican Journal of Physiology - Gastrointestinal and Liver Physiology, 2005, v. 288, n. 1 51-1, p. G32-G38-
dc.identifier.issn0193-1857-
dc.identifier.urihttp://hdl.handle.net/10722/207488-
dc.description.abstractTNF-α is a cytokine produced during gastric mucosal injury. We examined whether TNF-α 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-α treatment (1-10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells. TNF-α treatment significantly increased cytosolic phospholipase A2 and cyclooxygenase-2 (COX-2) protein expression and PGE 2 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-α 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-α on RMG-1 cells. Combination of dexamethasone and DFU did not produce an additive effect. PGE 2 significantly reversed the depressive action of dexamethasone on cell proliferation. These results suggest that TNF-α plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF-α receptor and activation of the arachidonic acid/PG pathway.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Gastrointestinal and Liver Physiology-
dc.subjectProstaglandin E 2-
dc.subjectCyclooxygenase-
dc.subjectDexamethasone-
dc.subjectPhospholipase A 2-
dc.titleTumor necrosis factor-α stimulates gastric epithelial cell proliferation-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpgi.00093.2004-
dc.identifier.pmid15256360-
dc.identifier.scopuseid_2-s2.0-10844280063-
dc.identifier.volume288-
dc.identifier.issue1 51-1-
dc.identifier.spageG32-
dc.identifier.epageG38-

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