Welcome to CDC stacks | Mesothelial Cell Autoantibodies Upregulate Transcription Factors Associated with Fibrosis - 47533 | CDC Public Access
Stacks Logo
Advanced Search
Select up to three search categories and corresponding keywords using the fields to the right. Refer to the Help section for more detailed instructions.
Clear All Simple Search
Advanced Search
Mesothelial Cell Autoantibodies Upregulate Transcription Factors Associated with Fibrosis
  • Published Date:
    Jan 2017
  • Source:
    Inhal Toxicol. 29(1):10-17.

Public Access Version Available on: January 01, 2018 information icon
Please check back on the date listed above.
  • Pubmed ID:
  • Pubmed Central ID:
  • Description:
    Amphibole asbestos exposure is associated with the production of mesothelial cell autoantibodies (MCAA). These MCAA have been linked with pleural fibrotic disease in the asbestos exposed community of Libby, Montana, and induce collagen deposition by cultured mesothelial cells. However, the exact intracellular mechanism by which these autoantibodies cause an increase in collagen deposition remains unknown. This study sought to gain insight into the transcription factors involved in the collagen production after human mesothelial cells are exposed to MCAA. In this study, transcription factor activation profiles were generated from human mesothelial cells (Met5A) treated with serum from Libby subjects, and were compared to cells treated with serum cleared of IgG, and therefore containing no MCAA. Analysis of those profiles indicated C/EBP-beta and hypoxia inducible factor 1 alpha (HIF-1α) are significantly increased in the nucleus, indicating activation, due to MCAA exposure compared to controls. Inhibition of either of these transcription factors significantly reduced collagen 1 deposition by these cells following exposure to MCAA. These data suggest autoantibodies are directly involved in type I collagen deposition and may elucidate potential therapeutic targets for autoantibody mediated fibrosis.

  • Document Type:
  • Collection(s):
  • Funding:
    P20 GM103408/GM/NIGMS NIH HHS/United States
    R01 TS000099/TS/ATSDR CDC HHS/United States
    R15 ES021884/ES/NIEHS NIH HHS/United States
  • Supporting Files:
    No Additional Files
No Related Documents.
You May Also Like: