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Transforming growth factor beta within fibrotic scleroderma lungs.
L W Moreland1, K T Goldsmith, W J Russell
1Department of Medicine, University of Alabama School of Medicine, Birmingham 35294.
The American Journal of Medicine
|December 11, 1992
Summary
Transforming growth factor beta (TGF beta) protein levels were lower in fibrotic scleroderma lungs compared to normal lungs, despite similar gene expression. Cellular components did not determine TGF beta protein concentration.
Area of Science:
- Pulmonary Medicine
- Immunology
- Cell Biology
Background:
- Transforming growth factor beta (TGF beta) is implicated in pulmonary fibrosis.
- Investigating TGF beta in scleroderma-associated lung fibrosis is crucial.
Purpose of the Study:
- To measure TGF beta protein and gene expression in the alveolar epithelial lining fluid (ELF) of fibrotic scleroderma lungs.
- To compare TGF beta levels and gene expression in sclerotic lungs versus normal lungs.
Main Methods:
- Bronchoalveolar lavage (BAL) was used to collect ELF from patients.
- TGF beta protein was analyzed using Western blot and radioreceptor assays.
- Gene expression was assessed in BAL mononuclear cells via Northern blot.
Main Results:
- A 24-kd TGF beta 1 protein was detected in both normal and scleroderma subjects.
- TGF beta protein concentration was significantly lower in scleroderma subjects (177 pM) compared to normal subjects (705 pM).
- TGF beta 1 gene expression levels did not significantly differ between the groups.
Conclusions:
- Both normal and fibrotic lungs express TGF beta 1 at the alveolar surface.
- Contrary to expectations, TGF beta protein and gene expression were not elevated in fibrotic scleroderma lungs.
- Cellular components in ELF do not appear to be the primary drivers of TGF beta protein concentration.