Back to Search
Start Over
Proapoptotic Bid is required for pulmonary fibrosis
- Source :
- Proceedings of the National Academy of Sciences of the United States. March 21, 2006, Vol. 103 Issue 12, p4604, 6 p.
- Publication Year :
- 2006
-
Abstract
- The molecular mechanisms of pulmonary fibrosis are poorly understood. Previous reports indicate that activation of TGF-[beta]1 is essential for the development of pulmonary fibrosis. Here, we report that the proapoptotic Bcl-2 family member Bid is required for the development of pulmonary fibrosis after the intratracheal instillation of bleomycin. Mice lacking Bid exhibited significantly less pulmonary fibrosis in response to bleomycin compared with WT mice. The attenuation in pulmonary fibrosis was observed despite similar levels of inflammation, lung injury, and active TGF-[beta]1 in bronchoalveolar lavage fluid 5 days after the administration of bleomycin in mice lacking Bid and in WT controls. Bleomycin induced similar levels cell death in vitro in alveolar epithelial cells isolated from WT and [bid.sup.-/-] mice. By contrast, alveolar epithelial cells from [bid.sup.-/-] mice were resistant to TGF-[beta]1-induced cell death. These results indicate that Bcl-2 family members are critical regulators for the development of pulmonary fibrosis downstream of TGF-[beta]1 activation. apoptosis | Bcl-2 | TGF-[beta]
Details
- Language :
- English
- ISSN :
- 00278424
- Volume :
- 103
- Issue :
- 12
- Database :
- Gale General OneFile
- Journal :
- Proceedings of the National Academy of Sciences of the United States
- Publication Type :
- Academic Journal
- Accession number :
- edsgcl.144352453