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Regulation of stromelysin‐2 in inflammation
Author(s) -
Chen Ann J,
Birkland Timothy P.,
Chen Peter,
Altemeier William A.,
Parks William C.,
McGuire John K.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.830.2
Subject(s) - inflammation , matrix metalloproteinase , biology , immunology , transcription factor , metalloproteinase , gene , cancer research , genetics
Specific members of the matrix metalloproteinases (MMPs) family are key mediators of inflammation. Our preliminary data suggest stromelysin‐2 (MMP‐10) also functions to moderate inflammation. Stromelysin‐2 is not found in healthy tissue but is highly induced in injured epithelium. However pathways controlling stromelysin‐2 up‐regulation in inflammatory processes are not known. Data We found high levels of stromelysin‐2 gene expression in various models of lung injury, including mice challenged with Pseudomonas aeruginosa, influenza, and bleomcyin. We found mice lacking stromelysin‐2 had increased lung injury and higher mortality in response to P. aeruginosa . Bioinformatic analysis of the five kilobase region upstream of the gene identified several binding regions essential to stromelysin‐2 gene regulation. Conclusion We conclude that increased expression of stromelysin‐2 is a generalized protective host response in inflammation. We report several transcription factor binding sites responsible for the regulation of stromelysin‐2 in inflammation. This research is supported by grants from the American Lung Association and the National Institute of Health (HL029594, HL077555).