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Leukocyte Mechanosensitivity to Fluid Shear Stress Depends on the Subtypes of CD18 Integrins
Author(s) -
Zhang Xiaoyan,
Zhan Dongying,
Shin Hainsworth Y.
Publication year - 2012
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.26.1_supplement.680.7
Subject(s) - cd18 , integrin , cd11a , microbiology and biotechnology , cell adhesion , chemistry , platelet , cleavage (geology) , shear stress , proteases , biophysics , receptor , immunology , biology , cell , biochemistry , materials science , enzyme , paleontology , fracture (geology) , composite material
Fluid shear stress cleaves CD18 integrins on neutrophils, hypothetically to avert their adhesion to other cells such as platelets. Since lymphocytes and monocytes also express CD18 integrins (mainly LFA‐1 and Mac‐1) but in a cell type specific fashion, we examined whether shear‐induced CD18 cleavage is different among the three leukocyte subsets and if this shear response prevents leukocyte‐platelet adhesion. We exposed mixed leukocyte populations to shear stress (2.5 – 10 dyn/cm 2 ; 1 – 10 min) to assess cell and receptor subtype‐specific CD18 cleavage. Shear stress cleaved Mac‐1 on neutrophils and monocytes, but LFA‐1 on lymphocytes devoid of surface Mac‐1. Furthermore, neutrophils exposed to shear after treatment with cysteine protease inhibitor E‐64 (which blocks CD18 cleavage) exhibited elevated platelet adhesion and an impaired CD18 cleavage response relative to naïve cells. But, neither monocytes nor lymphocytes exhibited increases in platelet adhesion or impaired CD18 cleavage after E64 treatment. Shear‐induced CD18 cleavage and its impact on platelet adhesion thus appear to be cell type‐specific contingent on their differential expression of CD18 integrins and proteases. In terms of neutrophils, our data further support fluid shear mechanotransduction as an anti‐inflammatory measure under physiologic conditions. Funded by the NSF‐KY EPSCoR, and AHA.