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A role for adhesion and degranulation-promoting adapter protein in collagen-induced platelet activation mediated via integrin α(2) β(1)

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Jarvis, G. E., Bihan, D., Hamaia, S., Pugh, N., Ghevaert, C. J. G., Pearce, A. C., Hughes, C. E. orcid id iconORCID: https://orcid.org/0000-0002-9790-5820, Watson, S. P., Ware, J., Rudd, C. E. and Farndale, R. W. (2012) A role for adhesion and degranulation-promoting adapter protein in collagen-induced platelet activation mediated via integrin α(2) β(1). Journal of Thrombosis and Haemostasis, 10 (2). pp. 268-277. ISSN 1538-7933 doi: 10.1111/j.1538-7836.2011.04567.x

Abstract/Summary

Platelet aggregation and phosphorylation of phospholipase Cγ2 induced by collagen were attenuated in ADAP(-/-) platelets. However, aggregation and signaling induced by collagen-related peptide (CRP), a GPVI-selective agonist, were largely unaffected. Platelet adhesion to CRP was also unaffected by ADAP deficiency. Adhesion to the α(2) β(1) -selective ligand GFOGER and to a peptide (III-04), which supports adhesion that is dependent on both GPVI and α(2) β(1), was reduced in ADAP(-/-) platelets. An impedance-based label-free detection technique, which measures adhesion and spreading of platelets, indicated that, in the absence of ADAP, spreading on GFOGER was also reduced. This was confirmed with non-fluorescent differential-interference contrast microscopy, which revealed reduced filpodia formation in ADAP(-/-) platelets adherent to GFOGER. This indicates that ADAP plays a role in mediating platelet activation via the collagen-binding integrin α(2) β(1). In addition, we found that ADAP(-/-) mice, which are mildly thrombocytopenic, have enlarged spleens as compared with wild-type animals. This may reflect increased removal of platelets from the circulation.

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Item Type Article
URI https://reading-clone.eprints-hosting.org/id/eprint/44574
Item Type Article
Refereed Yes
Divisions Life Sciences > School of Biological Sciences > Biomedical Sciences
Publisher Wiley
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