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Transforming growth factor-β1 in asthmatic airway smooth muscle enlargement: is fibroblast growth factor-2 required?

Authors

  • Y. Bossé,

    1. The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, BC, Canada
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  • J. Stankova,

    1. Department of Pediatrics, Immunology Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada
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  • M. Rola-Pleszczynski

    1. Department of Pediatrics, Immunology Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada
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Correspondence:
Dr. Ynuk Bossé, UBC iCAPTURE Centre, St. Paul's hospital, 1081, Burrard St. Room 166, Vancouver BC, Canada V6Z 1Y6.
E-mail: ybosse@mrl.ubc.ca

Summary

Enlargement of airway smooth muscle (ASM) tissue around the bronchi/bronchioles is a histopathological signature of asthmatic airway remodelling and has been suggested to play a critical role in the increased lung resistance and airway hyperresponsiveness seen in asthmatic patients. The pleiotropic cytokine, TGF-β1, is believed to contribute to several aspects of asthmatic airway remodelling and is known to influence the growth of many cell types. Increased TGF-β1 expression/signalling and ASM growth have been shown to occur concurrently in animal models of asthma. Abundant studies further substantiate this association by showing that therapeutic strategies that reduce or prevent TGF-β1 overexpression/signalling lead to a parallel decrease or prevention of ASM enlargement. Finally, recent findings have supported a direct link of causality between TGF-β1 overexpression/signalling and the overgrowth of ASM tissue. To follow-up on these in vivo studies, many investigators have pursued detailed investigation of ASM in cell culture conditions, assessing the direct role of TGF-β1 on cellular proliferation and/or hypertrophy. Inconsistencies among the in vitro studies suggest that the effect of TGF-β1 on ASM cell proliferation/hypertrophy is contextual. A hypothesis focusing on fibroblast growth factor-2 is presented at the end of this review, which could potentially reconcile the apparent discrepancy between the conflicting in vitro findings with the consistent in vivo finding that TGF-β1 is required for ASM enlargement in asthma.

Cite this as: Y. Bossé, J. Stankova and M. Rola-Pleszczynski, Clinical & Experimental Allergy, 2010 (40) 710–724.

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