Transforming growth factor beta regulates the levels of different fibronectin isoforms in normal human cultured fibroblasts

Abstract

Fibronectin (FN) polymorphism is caused by alternative splicing patterns in at least three regions of the primary transcript of a single gene. Using a monoclonal antibody (Mab) specific for an FN segment (ED-A), that can be included or omitted from the molecule depending on the pattern of splicing, we have examined whether transforming growth factor beta (TGF-beta) and dexamethasone, which are both known to increase the level of total FN, regulate the levels of different FN isoforms. We found that, while dexamethasone does not significantly change the ratio between the total FN and the ED-A containing FN, TGF-beta preferentially increases the expression of the FN isoform containing the ED-A sequence.