摘要
目的 研究两种 Ｃ Ｄ９ 单克隆抗体（ Ｍｃ Ａｂ） Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 对人血小板膜纤维蛋白原受体功能的调控作用及其可能的作用机制。方法 利用１２５ Ｉ标记人纤维蛋白原（ Ｆｇ） ，观察 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４作用下血小板 Ｆｇ 特异性结合量，反映血小板膜上 Ｆｇ 受体的暴露情况，并观察无 Ｆｇ 存在条件下，由 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 诱导的 Ｆｇ 受体暴露后的变化。结果 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 均能显著诱导血小板与 Ｆｇ 特异性结合，而在无 Ｆｇ 存在时，两种 Ｍｃ Ａｂ 诱导的 Ｆｇ 受体会很快“关闭”，失去结合 Ｆｇ 的能力；抑制蛋白激酶 Ｃ（ Ｐ Ｋ Ｃ） 活性，应用 Ａｓｐｉｒｉｎ 、 Ａｐｙｒａｓｅ 和（ 或） Ｐ Ｇ Ｉ２ 预处理血小板，能不同程度地抑制 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 诱导的血小板膜 Ｆｇ 受体暴露。结论 Ｈ Ｉ１１７ 和 Ｓ Ｊ９ Ａ４ 均能诱发血小板膜 Ｆｇ 受体暴露，两者诱发人血小板 Ｆｇ 受体暴露可能是三条途径综合作用的结果：即二磷酸腺苷释放、血栓烷生成和环磷酸腺苷途径，而 Ｐ Ｋ Ｃ激活可能是三条途径的共同通路。
Objective To investigate the regulatory effect of two anti CD 9 monoclonal antibodies (McAbs), HI117 and SJ9A4, on human platelet fibrinogen receptors, and explore their potential mechanisms. Methods By using 125 I labeled human fibrinogen (Fg), the Fg specifically bound to human platelets induced by HI117 and SJ9A4 was measured,and the changes of anti CD 9 McAbs exposed Fg receptor in the absence of Fg were also observed. Results HI117(10?μg/ml)and SJ9A4 (20?μg/ml) induced markedly the specific binding of Fg to human platelets, suggesting that the two McAbs evoked obvious exposure of Fg receptors .But in the absence of Fg, the McAbs exposed Fg receptors gradually lost their capacity to bind Fg and closed. Further study indicated that HI117 and SJ9A4 induced Fg binding was reduced by pretreatment of platelets with sphingosine, aspirin, apyrase, and/or PGI 2. Conclusion The anti CD 9 McAbs, HI117 and SJ9A4, can reversibly expose platelet Fg receptors, probably via three signaling pathways, i.e. thromboxane, secreted ADP and cAMP,protein kinase C (PKC) activation presumably being the common passage for the signaling.
出处
《中华血液学杂志》
CAS
CSCD
北大核心
1999年第9期456-458,共3页
Chinese Journal of Hematology
基金
国家自然科学基金
关键词
单克隆抗体
CD9
纤维蛋白原受体
血小板膜
Platelet Antibody,monoclonal,CD 9 Platelet glycoprotein GPⅡb Ⅲa complex
