期刊
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
卷 31, 期 3, 页码 344-350出版社
AMER THORACIC SOC
DOI: 10.1165/rcmb.2003-0420OC
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资金
- NHLBI NIH HHS [P01 HL 46902, HL 10332] Funding Source: Medline
Uncontrolled elastase activity is involved in the development of several types of lung disease. Previous reports demonstrated that growth factors are liberated from pulmonary matrix storage sites by elastase; however, release of these entities in vivo is not well defined. In the present study, we investigated the release of fibroblast growth factor-2 (FGF-2) and transforming growth factor-beta (TGF-beta), after intratracheal instillation of porcine pancreatic elastase into mice. We found that elastase promoted a time-dependent release of FGF-2 and TGF-beta, from the lung into bronchoalveolar lavage (BAL) fluid. A large fraction of the TGF-beta(1) in BAL fluid was in the active form (similar to 60%), suggesting that elastase might participate 9in the activation of TGF-beta(1) from its latent form. Analysis of the levels of FGF-2 and TGF-beta(1) in mouse blood indicated that the growth factors in BAL fluid were not entirely derived from blood. Moreover, elastase treatment of pulmonary fibroblasts cultures caused the release of TGF-beta(1), suggesting that the TGF-beta(1) in BAL fluid could have come from lung cells/matrix. Additional in vitro studies also indicated that TGF-beta(1) plays a role in upregulating elastin mRNA levels. These data suggest that elastase releases growth factors from lung that participate in elastolytic injury responses.
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