Objective. This study characterized the activation of platelet integrin aⅡbβ3 induced by two anti-human platelet te-traspanin monoclonal antibodies(mAbs),HI117 and SJ9A4. Methods. Using 125I-labeled human fibdnogen(Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured as indication of activation of platelet integrin αⅡbβ3 by the two mAbs. Results. H1117 and SJ9A4( 10μg/ml and 20μg/ml) induced evident specific Fg binding to human platelets, sug-gesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin t Ⅱ 1β3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by sphingosing, aspirin, apyrase, and/or PGI2. Conclusion. The anti-platelet tetraspanin(CD9)mAbe,HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 act-vation independent of Fc-receptors. Three signaling pathways,i.e.thromboxane,secreted ADP, and cAMP pathways may be involved in the process, with protein kimse C activation presumably being the comtmon step of the three pathways.

Objectives　To characterize the activation of platelet integrin αⅡbβ3 induced by two anti-human platelet tetraspanin monoclonal antibodies (mAbs), HI117 and SJ9A4, and investigate their potential mechanism of action. Methods　Using 125　　I-labeled human fibrinogen (Fg), specific Fg binding to human platelets induced by HI117 and SJ9A4 was measured. Results　HI117 and SJ9A4 (10?μg/ml and 20?μg/ml) induced specific Fg binding to human platelets, suggesting that the two mAbs evoked activation of platelet integrin αⅡbβ3. Further study indicated that HI117 and SJ9A4 induced integrin αⅡbβ3 activation independent of platelet Fc-receptors, and that HI117 and SJ9A4-induced integrin αⅡbβ3 activation was inhibited by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI2. Conclusions　Anti-platelet tetraspanin (CD9) mAbs, HI117 and SJ9A4, can induce platelet integrin αⅡbβ3 activation independent of Fc-receptors. Three signaling pathways, namely thromboxane, secreted ADP, and cAMP pathways, may be involved in the process, with protein kinase C activation presumably being the common step of the three pathways.