Clustering the adhesion molecules VLA‐4 (CD49d/CD29) in Jurkat T cells or VCAM‐1 (CD106) in endothelial (ECV 304) cells activates the phosphoinositide pathway and triggers Ca2+ mobilization

European Journal of Immunology - Tập 27 Số 6 - Trang 1530-1538 - 1997
Isabelle Ricard1, M Payet2, Gilles Dupuis1
1Department of Biochemistry, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Canada
2Department of Physiology and Biophysics, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Canada

Tóm tắt

AbstractLigation of very late antigen (VLA)‐4 (α4β1 integrin) with a cross‐linked anti‐α4 subunit monoclonal antibody (mAb) triggered a biphasic Ca2+ response in Jurkat cell populations and in peripheral human lymphocytes. Cross‐linking vascular cell adhesion molecule (VCAM)‐1 (the counter‐receptor of VLA‐4) in ECV 304 endothelial cells generated a biphasic Ca2+ response. Tumor necrosis factor‐α‐primed human umbilical cord vascular endothelial cells also responded to the cross‐linked mAb with a biphasic Ca2+ profile. Ligated VLA‐4 (Jurkat cells) or VCAM‐1 (ECV 304) stimulated the production of myo‐inositol 1,4,5‐trisphosphate. ECV 304 cells induced a biphasic Ca2+ response in Fura2‐loaded Jurkat cells, whereas a transient response was observed when Jurkat cells were added to Fura2‐loaded ECV 304 cells. The Ca2+ responses in these experiments involved VLA‐4/VCAM‐1 interactions since they were significantly reduced (∼ 80%) by prior treatment of the target cells with the relevant noncross‐linked mAb. Close contact between the cells triggered mutual Ca2+ signaling as shown by spectrofluorimetric and confocal microscopy time‐dependent recordings. Fibronectin and its CS‐1 fragment (V25) triggered a sustained Ca2+ response in Jurkat cells (confocal microscopy). Our results suggest that the VLA‐4 and VCAM‐1 adhesion molecules can transduce a signal that involves activation of the phosphoinositide pathway and the mobilization of Ca2+.

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European Journal of Immunology

Tập 27 Số 6

1530-1538

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