Endogenous TNF-alpha modulates the proliferation of rat mesangial cells and their prostaglandin E2 synthesis

Détails

ID Serval
serval:BIB_A1947F6EFFAE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Endogenous TNF-alpha modulates the proliferation of rat mesangial cells and their prostaglandin E2 synthesis
Périodique
Microvascular Research
Auteur(s)
Benador  N. M., Grau  G. E., Ruef  C., Girardin  E. P.
ISSN
0026-2862
Statut éditorial
Publié
Date de publication
09/1995
Peer-reviewed
Oui
Volume
50
Numéro
2
Pages
154-61
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep
Résumé
Mesangial cells (MC) are one cellular source of tumor necrosis factor alpha (TNF) within the kidney as shown by experimental stimulation with endotoxin. TNF was shown to increase MC synthesis of prostaglandins E2 (PGE2) which down regulate MC proliferation. The involvement of endogenous TNF as an autocrine factor to control MC proliferation is unknown. This role was evaluated in vitro by addition of anti-TNF immunoglobulins and soluble TNF receptor-I (sTNF-RI) on rat MC. Anti-TNF immunoglobulins and sTNF-RI induced a dose-dependent increase of cell proliferation when the cells were quiescent in 0.5% FCS P = 0.002). No effect was found when the cells were growing in 10% FCS (P = 0.113). Incubation of MC with anti-TNF immunoglobulins resulted in a dose-dependent decrease of PGE2 release. In order to investigate if the effect of TNF on MC proliferation was mediated by the decrease of PGE2 release, PGE2 was added to the culture medium at concentrations of 0.1 to 10 micrograms/ml in conjunction with anti-TNF immunoglobulins. PGE2 did not modify the proliferation induced by anti-TNF immunoglobulins. We conclude that anti-TNF immunoglobulins and sTNF-RI promoted MC DNA synthesis and influenced their PGE2 release by blocking the endogenous TNF. The mechanism of action on DNA synthesis was not mediated by PGE2. This indicates that endogenous TNF has a substantial role in the control of resting mesangial cells.
Mots-clé
Animals Antibodies/pharmacology Cell Division/drug effects Cells, Cultured Dinoprostone/*biosynthesis Glomerular Mesangium/*metabolism Male Rats Rats, Sprague-Dawley Receptors, Tumor Necrosis Factor/metabolism Tumor Necrosis Factor-alpha/antagonists & inhibitors/*metabolism
Pubmed
Web of science
Création de la notice
15/01/2008 14:28
Dernière modification de la notice
20/08/2019 15:07
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