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Tumor necrosis factor inhibits collagen and fibronectin synthesis in human dermal fibroblasts
Author(s) -
Mauviel A.,
Daireaux M.,
Rédini F.,
Galera P.,
Loyau G.,
Pujoi J.-P.
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80283-7
Subject(s) - fibronectin , chemistry , tumor necrosis factor alpha , prostaglandin e , intracellular , prostaglandin e2 , prostaglandin , cell culture , fibroblast , type i collagen , cyclooxygenase , extracellular matrix , dermal fibroblast , microbiology and biotechnology , biochemistry , endocrinology , biology , in vitro , enzyme , genetics
Tumor necrosis factor (TNF) caused inhibition of collagen production by confluent cultures of human dermal fibroblasts in a dose‐dependent manner. Concomitant increase of prostaglandin E 2 release was observed as a result of TNF‐induced cell activation. However, a blockade of the cyclooxygenase pathway of arachidonate metabolism by indomethacin did not abrogate the inhibitory effect of TNF on collagen synthesis, suggesting that this effect could be independent of prostaglandin metabolism. Gel electrophoresis of the newly synthesized macromolecules from the culture media showed that both type I and type III collagens as well as fibronectin were affected by the inhibition. Electrophoresis of cell layer‐associated proteins demonstrated that the reduction in amounts of collagen and fibronectin in the medium did not result from an intracellular accumulation of these macromolecules. Production of procollagens was reduced in parallel to that of collagens, suggesting that the effect of TNF is exerted before the processing steps of procollagens. These results clearly show that TNF could play a role in modulation of matrix deposition by fibroblasts during inflammatory processes.