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P‐selectin and MAC‐1 mediate monocyte rolling and adhesion to ECM‐bound platelets under flow conditions
Author(s) -
Kuijper P. H. M.,
Torres H. I. Gallardo,
Houben L. A. M. J.,
Lammers JW. J.,
Zwaginga J. J.,
Koenderman L.
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.64.4.467
Subject(s) - monocyte , platelet , adhesion , integrin , integrin alpha m , microbiology and biotechnology , cd18 , cell adhesion molecule , immunology , biology , chemistry , biochemistry , flow cytometry , receptor , organic chemistry
Accumulation of monocyte‐derived foam cells in focal areas of the atherosclerotic (A.S.‐) lesion is one of the key events in early atherogenesis. Using a flow model for the damaged vessel wall, we examined the ability of ECM‐bound platelets to induce monocyte tethering and adhesion. Whereas ECM‐proteins alone induced monocyte adhesion only at low shear stresses (<100 mPa), ECM‐bound platelets induced monocyte rolling and adhesion at shear stresses up to 240 mPa. Studies with specific antibodies showed that monocyte adhesion to platelets was mainly mediated by P‐selectin and monocyte PSGL‐1 (maximum inhibition 90%). β 2 ‐Integrin blocking CD18 and CD11b antibodies partly inhibited the arrest of rolling cells. Antibodies against other adhesion molecules such as LFA‐1, PECAM‐1, and β 1 ‐integrins had no effect. Even sparsely adhered platelets (~10% coverage of the surface) already strongly supported monocyte tethering. In conclusion, activated platelets present on ECM are a powerful adhesive substrate for monocyte recruitment under flow conditions. J. Leukoc. Biol . 64: 467–473; 1998.