Platelet interaction with vascular smooth muscle in synthesis of prostacyclin.
Platelet interaction with vascular smooth muscle in synthesis of prostacyclin.
复制标题
前列环素合成中血小板与血管平滑肌的相互作用。
DOI：
10.1152/ajpheart.1991.260.5.h1544
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Schafer,AI
中科院分区：
文献类型：
--
作者：
Hechtman,DH;Kroll,MH;GimbroneJr,MA;Schafer,AI
由于血管平滑肌细胞（SMC）可以暴露于血小板在显着的动脉损伤的网站，我们研究了培养的大鼠主动脉SMC是否可以利用血小板衍生的花生四烯酸和前列腺素（PG）内过氧化物（PGG 2/PGH 2）的前列环素（PGI 2）的合成。SMC将外源性PGH 2转化为PGI 2，通过6-酮-PGF 1 α的放射免疫测定（RIA）测量，尽管有环氧合酶抑制或PGH 2受体阻断。SMC产生的PGI 2的数量增加的血小板的存在下，当两种细胞类型与花生四烯酸共孵育。此外，阿司匹林预处理的SMC产生PGI 2响应花生四烯酸，离子载体A23187，或凝血酶在血小板的存在下，但不是在他们的缺席。SMC本身对凝血酶无反应，在与凝血酶刺激的阿司匹林预处理的血小板共孵育期间产生PGI 2。用滤器分离SMC单层和血小板并不能阻止SMC形成血小板依赖性PGI 2。最后，阿司匹林预处理的SMC，在与血小板共悬浮液，抑制血小板聚集与PGI 2的生产。这些数据表明：1）SMC可以从外源性添加的PGH 2和血小板衍生的花生四烯酸酯或内过氧化物合成PGI 2，2）细胞间内过氧化物转移不需要直接细胞-细胞接触，3）SMC可能通过血小板衍生的内过氧化物产生PGI 2来抑制血小板聚集。
Because vascular smooth muscle cells (SMC) can be exposed to platelets at sites of significant arterial injury, we studied whether cultured rat aorta SMC can utilize platelet-derived arachidonate and prostaglandin (PG) endoperoxides (PGG2/PGH2) in the synthesis of prostacyclin (PGI2). SMC converted exogenous PGH2 to PGI2, measured by radioimmunoassay (RIA) of 6-keto-PGF1 alpha, despite cyclooxygenase inhibition or PGH2-receptor blockade. SMC produced increasing amounts of PGI2 in the presence of an increasing number of platelets when the two cell types were coincubated with arachidonate. Furthermore, aspirin-pretreated SMC produced PGI2 in response to arachidonate, ionophore A23187, or thrombin in the presence of platelets but not in their absence. SMC, by themselves unresponsive to thrombin, produced PGI2 during coincubation with thrombin-stimulated aspirin-pretreated platelets. Separation of the SMC monolayer and platelets with a filter did not prevent platelet-dependent PGI2 formation by the SMC. Finally, aspirin-pretreated SMC, in cosuspension with platelets, inhibited platelet aggregation in association with PGI2 production. These data indicate that 1) SMC can synthesize PGI2 from exogenously added PGH2 and from platelet-derived arachidonate or endoperoxides, 2) direct cell-cell contact is not required for intercellular endoperoxide transfer, and 3) SMC can inhibit platelet aggregation possibly through PGI2 production from platelet-derived endoperoxides.