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Induction of fibronectin gene expression by transforming growth factor beta‐1 is attenuated in bronchial epithelial cells by ADP‐ribosyltransferase inhibitors
Author(s) -
Beckmann Joe D.,
Illig Mary,
Romberger Debra,
Rennard Stephen I.
Publication year - 1992
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041520208
Subject(s) - fibronectin , microbiology and biotechnology , transforming growth factor , biology , gene expression , northern blot , transforming growth factor beta , cell culture , western blot , cell , gene , biochemistry , genetics
Transforming growth factor‐β (TGF‐β) exerts several effects on cultured airway epithelial cells including inhibition of proliferation and stimulation of fibronectin gene expression. ADP‐ribosylation is one potential regulatory mechanism of gene expression by TGF‐β. We tested this possibility by exposing cultured bovine bronchial epithelial cells to the chemical inhibitor of ADP‐ribosyl transferase enzymes, 3‐aminobenzamide (3‐AB) and, for comparison, 3‐aminobenzoic acid (3‐ABA), which is structurally similar to 3‐AB but which does not inhibit ADP‐ribosyl transferases. Exponential cell growth rate (1.2 doublings/day) or cellular morphology observed by phase contrast microscopy were not affected by 3 mM 3‐AB or 3‐ABA. Neither compound antagonized inhibition of cell division or induction of squamous morphology by TGF‐β1. In contrast, the sixfold stimulation of fibronectin production by exposure of cells to 30 pM TGF‐β1 for 48 h was reduced by 50% in the presence of 3 mM 3‐AB, whereas 3 mM 3‐ABA had no effect. The antagonistic effect was augmented by administration of 3‐AB 24 h prior to induction by TGF‐β1. Northern blot hybridization analyses demonstrated that 3‐AB, but not 3‐ABA, attenuated the induction of fibronectin mRNA by TGF‐β1 by up to 50%. These observations may implicate a role of cellular ADP‐ribosylation in the regulation of some gene expression by TGF‐β. © 1992 Wiley‐Liss, Inc.