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The Role of Scleraxis in Neutrophil Activation
Author(s) -
Awotunde Olanike,
Nillas Andrea,
Hammad Samar,
Reaves Titus A.
Publication year - 2017
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.31.1_supplement.182.2
Subject(s) - microbiology and biotechnology , inflammation , immunology , innate immune system , immune system , fibrosis , biology , chemistry , pathology , medicine
Scleraxis is a transcription factor in the basic helix loop helix (BHLH) family, and originally shown to regulate embryonic tissue into tendon and endothelium in blood vessels. More recently scleraxis has been linked to activation of fibroblasts and cardiac fibrosis. Organ fibrosis follows inflammation and is characterized by dysregulated and excessive production/release of extracellular matrix proteins—principally collagen. Within fibrotic organs there are a variety of immune cells. In particular, polymorphonuclear leukocytes (PMN) are components of the innate immune system and are first responder cells present in high numbers in organs undergoing fibrosis. PMN have two basic functions, they migrate to areas of inflammation/injury and destroy pathogenic organisms. Activated PMN release myeloperoxidase ((MPO), heme protease that is toxic to pathogens and is dependent on the leukocyte specific integrin CD11b) from their primary granules. We hypothesize that scleraxis is involved in the activation of PMN. Immunocytochemistry, flow cytometry, and Western blot analysis shows that PMN express scleraxis. Antibodies against scleraxis had minimal effects on cell attachment of PMN to fibrinogen, but induced substantial release of MPO. Taken together these results highlight scleraxis as a potential treatment protein for inflammatory conditions involving PMN. Support or Funding Information NIH 4R25HL092611‐09 and National Science foundation (RII), 3T34GM008663‐20S1