Anti-human platelet tetraspanin (CD9) monoclonal antibodies induce platelet integrin αⅡbβ3 activation in a Fc receptor-independent fashion
10.3760/j.issn:0366-6999.2001.01.003
- VernacularTitle:抗人血小板Tetraspanin (CD9)单克隆抗体以不依赖Fc受体的方式激活血小板整合素αⅡbβ3
- Author:
Huaizhu WU
1
;
Jiazeng LI
;
Lin PENG
;
Hanzhi LIU
;
Wenjie WU
;
Yuling ZHOU
;
Qingming HOU
;
Dehong KONG
Author Information
1. 中国医学科学院血液学研究所
- Keywords:
platelets;
integrin αⅡbβ3;
tetraspanin;
monoclonal antibodies
- From:
Chinese Medical Journal
2001;114(1):14-18
- CountryChina
- Language:Chinese
-
Abstract:
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.
