Journal
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
Volume 41, Issue 1, Pages 85-92Publisher
AMER THORACIC SOC
DOI: 10.1165/rcmb.2007-0401OC
Keywords
carbon monoxide; heme oxygenase-1; lung fibrosis; small proline-rich protein; alpha-smooth muscle actin
Funding
- National Institutes of Health [1RO1HL087122-01A1]
- Veterans Administration
- Parker B. Francis Family Foundation
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL087122] Funding Source: NIH RePORTER
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Carbon monoxide (CO) is a biologically active molecule produced in the body by the stress-inducible enzyme, heme oxygenase. We have previously shown that CO suppresses fibrosis in a murine bleomycin model. To investigate the mechanisms by which CO opposes fibro-genesis, we performed gene expression profiling of fibroblasts treated with transforming growth factor-beta(1) and CO. The most highly differentially expressed categories of genes included those related to muscular system development and the small proline-rich family of proteins. We confirmed in vitro, and in an in vivo bleomycin model of lung fibrosis, that CO suppresses alpha-smooth muscle actin expression and enhances small proline-rich protein-1a expression. We further show that these effects of CO depend upon signaling via the extracellular signal-regulated kinase pathway. Our results demonstrate novel transcriptional targets for CO and further elucidate the mechanism by which CO suppresses fibrosis.
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