Induction of fibronectin gene expression by transforming growth factor beta‐1 is attenuated in bronchial epithelial cells by ADP‐ribosyltransferase inhibitors

Joe D. Beckmann, Mary Illig, Debra Romberger, Stephen I. Rennard

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)274-280
Number of pages7
JournalJournal of Cellular Physiology
Volume152
Issue number2
DOIs
Publication statusPublished - Aug 1992

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ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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