Expression profiling of genes regulated by Fra-1/AP-1 transcription factor during bleomycin-induced pulmonary fibrosis

BMC Genomics

Research Article

Wei Zhang¹  Narsa M Reddy¹  Subbiah Rajasekaran¹  Sekhar P Reddy¹ 

[1] Division of Developmental Biology and Basic Research, Department of Pediatrics, University of Illinois at Chicago, 830 S. Wood Street, 60612, Chicago, IL, USA;

关键词: Idiopathic Pulmonary Fibrosis;    Pulmonary Fibrosis;    Bleomycin;    Matrin;    ADAM Gene;   

DOI  :  10.1186/1471-2164-14-381

 received in 2013-02-25, accepted in 2013-05-31,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundThe 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.ResultsWe 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.ConclusionLoss 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.

【 授权许可】

Unknown   
© Rajasekaran et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.