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Transforming growth factor β1, insulin and prostaglandin E 1 enhance prostaglandin F 2α mitogenic action in Swiss 3T3 cells via separate events
Author(s) -
de Alzaga Maria Gomez,
Goin Mercedes,
Ortiz Marcela,
de Asua Luis Jimenez
Publication year - 1994
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(94)01223-7
Subject(s) - endocrinology , medicine , activator (genetics) , prostaglandin , protein kinase c , transforming growth factor beta , growth factor , alpha (finance) , beta (programming language) , dna synthesis , insulin , transforming growth factor , prostaglandin e2 , biology , chemistry , microbiology and biotechnology , signal transduction , receptor , biochemistry , dna , construct validity , nursing , computer science , patient satisfaction , programming language
Transforming growth factor β1 (TGFβ1) had no mitogenic effect in Swiss 3T3 cells, but could increase prostaglandin F 2α (PGF2α)‐induced DNA synthesis. Insulin, but not prostaglandin E 1 (PGE1), further enhanced PGF2α action at low TGFβ1 concentrations. TGFβ1 also acted concertedly with the protein kinase C (PKC) activator 1‐oleoyl‐2‐acetylglycerol to induce mitogenesis. Thus, it appears that TGFβ1 and insulin act via separate signals, while TGFβ1 and PGE1 might share a common pathway not involving TGFβ1‐mediated prostaglandin synthesis. These results suggest that TGFβ1 might elicit various signalling mechanisms to enhance PGF2α‐triggered events.