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Published ahead of print on January 10, 2003, doi:10.1165/rcmb.2002-0074OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 1, July 2003, 12-18

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Submitted on May 28, 2002
Revised on January 8, 2003

Effects of TGF-{beta} and Budesonide on MAPK activation and apoptosis in airway epithelial cells

Girolamo Pelaia1, Giovanni Cuda1, Alessandro Vatrella2, Donatella Fratto1*, Rosa Daniela R Grembiale1, Pierosandro Tagliaferri1, Rosario Maselli1, Francesco Saverio F Costanzo1, and Serafino Antonio S Marsico2

1 Department of Experimental and Clinical Medicine, University, Catanzaro, Italy, 2 Department of Cardiothoracic and Respiratory Sciences, Second University of Naples, Naples, Italy

* To whom correspondence should be addressed. E-mail: pelaia{at}unicz.it.

Airway epithelial cells play a central role in the inflammatory, apoptotic and remodeling processes associated with asthma. Within this context, a key function is exerted by transforming growth factor-{beta} (TGF-{beta}), whose biological effects are mediated at least in part by mitogen-activated protein kinases (MAPKs). The aim of our study was to investigate, in primary cultures of human bronchial epithelial cells (HBEC), the effects of TGF-{beta} (10 ng/ml) on both MAPK activation and apoptosis, in the presence or absence of a pretreatment with budesonide (10-8 M). MAPK activation was detected by Western blotting, using anti-phospho-MAPK monoclonal antibodies, which specifically recognize the phosphorylated, active forms of these enzymes. Apoptosis was assayed by caspase-3 activation and fluorescence microscopy using annexin-V (An-V) and propidium iodide (PI) as markers of cell death. Our results show that TGF-{beta} induced a marked (about 9-fold) increase in p38 MAPK phosphorylation and also dramatically enhanced cell death, that was completely prevented by specific MAPK inhibitors. Both MAPK activation and apoptosis were effectively inhibited by budesonide (BUD), thereby suggesting that the powerful anti-apoptotic action of inhaled glucocorticoids may be very important for their protective role against epithelial injury, which represents a key pathogenic event in asthma.




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