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

Research output: Contribution to journalArticle

5 Citations (Scopus)

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
StatePublished - Jan 1 1992

Fingerprint

Transforming Growth Factor beta1
Fibronectins
Gene expression
Transforming Growth Factors
Epithelial Cells
Gene Expression
Acids
Transferases
Phase-Contrast Microscopy
Gene Expression Regulation
Cell growth
Regulator Genes
Northern Blotting
Cell Division
Microscopic examination
Cells
Messenger RNA
Enzymes
Growth

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Induction of fibronectin gene expression by transforming growth factor beta‐1 is attenuated in bronchial epithelial cells by ADP‐ribosyltransferase inhibitors. / Beckmann, Joe D.; Illig, Mary; Romberger, Debra; Rennard, Stephen I.

In: Journal of Cellular Physiology, Vol. 152, No. 2, 01.01.1992, p. 274-280.

Research output: Contribution to journalArticle

@article{4bed020e49dc49a5b0df0db99c204eb1,
title = "Induction of fibronectin gene expression by transforming growth factor beta‐1 is attenuated in bronchial epithelial cells by ADP‐ribosyltransferase inhibitors",
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. {\circledC} 1992 Wiley‐Liss, Inc.",
author = "Beckmann, {Joe D.} and Mary Illig and Debra Romberger and Rennard, {Stephen I.}",
year = "1992",
month = "1",
day = "1",
doi = "10.1002/jcp.1041520208",
language = "English (US)",
volume = "152",
pages = "274--280",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Induction of fibronectin gene expression by transforming growth factor beta‐1 is attenuated in bronchial epithelial cells by ADP‐ribosyltransferase inhibitors

AU - Beckmann, Joe D.

AU - Illig, Mary

AU - Romberger, Debra

AU - Rennard, Stephen I.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0026682484&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026682484&partnerID=8YFLogxK

U2 - 10.1002/jcp.1041520208

DO - 10.1002/jcp.1041520208

M3 - Article

VL - 152

SP - 274

EP - 280

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

IS - 2

ER -