TY - JOUR
T1 - Modulation of fibronectin production of bovine bronchial epithelial cells by transforming growth factor-beta.
AU - Romberger, D. J.
AU - Beckmann, J. D.
AU - Claassen, L.
AU - Ertl, R. F.
AU - Rennard, S. I.
PY - 1992/8
Y1 - 1992/8
N2 - Regulation of airway repair after injury is poorly understood but is thought to be important in the development of airway diseases such as chronic bronchitis and asthma. There is evidence that fibronectin (Fn), an extracellular matrix glycoprotein, has a role in repair processes. In addition, transforming growth factor-beta (TGF-beta) is also likely involved in would healing and is known to influence extracellular matrix constituents in other cell systems. We postulated that TGF-beta may effect airway repair by modulating Fn production from airway epithelial cells. To examine this hypothesis, we studied the effect of TGF-beta 1 on Fn production by bovine bronchial epithelial cells in culture. Fn, released into the media of cultures exposed to TGF-beta 1, increased in a dose- and time-responsive fashion. Fn in the cell layer also increased in response to TGF-beta 1. De novo protein synthesis was demonstrated by an increase in [35S]methionine incorporation into Fn immunoprecipitated from media of TGF-beta-treated cultures. TGF-beta 1 also induced an increase in expression of Fn mRNA from cultured bronchial epithelial cells, suggesting that TGF-beta modulates Fn production of these cells, at least in part, through modulation of Fn gene expression. These data support a role for TGF-beta in airway repair through modulation of Fn production by airway epithelium.
AB - Regulation of airway repair after injury is poorly understood but is thought to be important in the development of airway diseases such as chronic bronchitis and asthma. There is evidence that fibronectin (Fn), an extracellular matrix glycoprotein, has a role in repair processes. In addition, transforming growth factor-beta (TGF-beta) is also likely involved in would healing and is known to influence extracellular matrix constituents in other cell systems. We postulated that TGF-beta may effect airway repair by modulating Fn production from airway epithelial cells. To examine this hypothesis, we studied the effect of TGF-beta 1 on Fn production by bovine bronchial epithelial cells in culture. Fn, released into the media of cultures exposed to TGF-beta 1, increased in a dose- and time-responsive fashion. Fn in the cell layer also increased in response to TGF-beta 1. De novo protein synthesis was demonstrated by an increase in [35S]methionine incorporation into Fn immunoprecipitated from media of TGF-beta-treated cultures. TGF-beta 1 also induced an increase in expression of Fn mRNA from cultured bronchial epithelial cells, suggesting that TGF-beta modulates Fn production of these cells, at least in part, through modulation of Fn gene expression. These data support a role for TGF-beta in airway repair through modulation of Fn production by airway epithelium.
UR - http://www.scopus.com/inward/record.url?scp=0026904335&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026904335&partnerID=8YFLogxK
U2 - 10.1165/ajrcmb/7.2.149
DO - 10.1165/ajrcmb/7.2.149
M3 - Article
C2 - 1497903
AN - SCOPUS:0026904335
SN - 1044-1549
VL - 7
SP - 149
EP - 155
JO - American journal of respiratory cell and molecular biology
JF - American journal of respiratory cell and molecular biology
IS - 2
ER -