Abstract
Background: The Fra-1/AP-1 transcription factor regulates the expression of genes controlling various processes including migration, invasion, and survival as well as extracellular remodeling. We recently demonstrated that loss of Fra-1 leads to exacerbated bleomycin-induced pulmonary fibrosis, accompanied by enhanced expression of various inflammatory and fibrotic genes. To better understand the molecular mechanisms by which Fra-1 confers protection during bleomycin-induced lung injury, genome-wide mRNA expression profiling was performed.Results: We found that Fra-1 regulates gene expression programs that include: 1) several cytokines and chemokines involved in inflammation, 2) several genes involved in the extracellular remodeling and cell adhesion, and 3) several genes involved in programmed cell death.Conclusion: Loss of Fra-1 leads to the enhanced expression of genes regulating inflammation and immune responses and decreased the expression of genes involved in apoptosis, suggesting that this transcription factor distinctly modulates early pro-fibrotic cellular responses.
| Original language | English (US) |
|---|---|
| Article number | 381 |
| Journal | BMC Genomics |
| Volume | 14 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jun 7 2013 |
Funding
We acknowledge the Core Genomics Facility at UIC for performing microarray analysis on service charge basis. We thank Dr. Erwin F. Wagner (Spanish National Cancer Research Centre, Madrid, Spain) for providing the mice bearing a “Floxed” Fra-1 allele. This study was supported by grants from the NIH (RO1 ES11863, RO1 HL66109, and R21 ES18998) and Flight Attendents Medical Research Institute (FAMRI) to SPR. We thank Debbie McClellan for her help in editing the manuscript.
ASJC Scopus subject areas
- Genetics
- Biotechnology