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RED BLOOD CELL SURFACE RECEPTOR EXPRESSION OF BCAM/LU IS REGULATED BY PROTEIN KINASE A ACTIVITY

机译:蛋白质激酶A活性调节BCAM / LU的红色血液细胞表面受体表达

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Irregular sickle red blood cells (RBCs) can contribute to the pathogenesis of vasoocclusion and other complications of sickle cell disease (SCD) via abnormal adherence to the vascular endothelium. It has previously been demonstrated that epinephrine enhances SCD RBC adhesion by activating the BCAM/Lu and ICAM-4 surface receptors . Epinephrine acts on the RBC β2-adrenergic receptor, thereby activating Gas proteins that stimulate adenylyl cyclase (AC). This enzyme catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP), leading to protein kinase A (PKA) activation, an intermediate step in the upregulation of BCAM/Lu and ICAM-4 mediated adhesion. The interaction of BCAM/Lu with the a5 chain of laminin may contribute to vaso-occlusive events in SCD due to overexpression of BCAM on SCD RBCs.
机译:不规则的镰状红细胞(RBC)可能通过异常粘附于血管内皮而导致血管闭塞和镰状细胞病(SCD)的其他并发症的发病机理。先前已证明肾上腺素通过激活BCAM / Lu和ICAM-4表面受体来增强SCD RBC粘附。肾上腺素作用于RBCβ2-肾上腺素受体,从而激活刺激腺苷酸环化酶(AC)的Gas蛋白。该酶催化三磷酸腺苷(ATP)转变为环状单磷酸腺苷(cAMP),导致蛋白激酶A(PKA)活化,这是BCAM / Lu和ICAM-4介导的粘附上调的中间步骤。 BCAM / Lu与层粘连蛋白的a5链的相互作用可能会导致SCD中的血管闭塞事件,这是由于BCAM在SCD RBC上的过表达所致。

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