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EXPRESSION OF FUNCTIONAL GLUCAGON RECEPTORS ON LYMPHOID CELLS

机译：功能性葡聚糖受体在淋巴细胞中的表达

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The objective of the present studies was to determine whether the existence of functional glucagon receptors could be established on lymphoid cells. The glucagon receptor, which positively regulates adenylate cyclase, is a member of the superfamily of seven transmembrane domain G-protein coupled receptors. Previously reported specific binding with [I-125]-glucagon to a variety of lymphoid and myeloid cell preparations suggests that glucagon receptors are expressed within the immune system. In the present study, Northern analysis of polyA RNA isolated from primary mouse and rat derived lymphoid tissues and lymphoid cell lines EL-4.IL-2, Jurkat E6-1, CH12LX, and BCL1-3B3 cells were probed with a P-32-labeled human hepatic glucagon receptor. Mouse spleen and thymus, rat spleen, and the B cell line, CH12LX, all possessed a single 1.5 kb fragment (BCL1-3B3, 1.4 kb) which hybridized to the glucagon receptor cDNA probe, as compared to mouse liver which exhibited a 2.8 kb fragment. EL-4.IL-2 and Jurkat E6-1 cells possessed a 3.7 kb fragment with an additional 2.75 kb band present in Jurkat E6-1 cells. Treatment of mouse splenocytes and T- and B-lymphoma cells with glucagon (0 - 100 nM) produced a dose-dependent enhancement in intracellular cAMP which was maximal at 5 min post treatment followed by a gradual decline. Direct addition of glucagon to spleen cell cultures over a broad concentration range produced no effect on either lymphoproliferation following stimulation with anti-CD3 mAb, or LFS nor on the antibody forming cell (AFC) response to sRBC. Conversely, glucagon effectively reversed the suppression of the sRBC AFC response produced by Delta(9)-tetrahydocannabinol (Delta(9)-THC), and partially reversed the suppression produced by 2',3'-dideoxyadenosine, both of which are potent inhibitors of adenylate cyclase. These studies confirm the expression of functional glucagon receptors on lymphoid cells. [References: 46]
机译：本研究的目的是确定是否可以在淋巴样细胞上建立功能性胰高血糖素受体的存在。积极调节腺苷酸环化酶的胰高血糖素受体是七个跨膜结构域G蛋白偶联受体超家族的成员。先前报道的与[I-125]-胰高血糖素对多种淋巴和髓样细胞制剂的特异性结合表明胰高血糖素受体在免疫系统中表达。在本研究中，对从原代小鼠和大鼠的淋巴样组织和淋巴样细胞系EL-4.IL-2，Jurkat E6-1，CH12LX和BCL1-3B3细胞分离的polyA RNA进行了Northern分析，并用P-32进行了探测。标记的人肝胰高血糖素受体。小鼠脾脏和胸腺，大鼠脾脏和B细胞系CH12LX，都具有一个与胰高血糖素受体cDNA探针杂交的1.5 kb片段（BCL1-3B3，1.4 kb），而小鼠肝脏的2.8 kb分段。 EL-4.IL-2和Jurkat E6-1细胞拥有3.7 kb的片段，在Jurkat E6-1细胞中还存在2.75 kb的条带。用胰高血糖素（0-100 nM）处理小鼠脾细胞和T淋巴瘤和B淋巴瘤细胞会产生剂量依赖性的细胞内cAMP增强，在治疗后5分钟达到最大，随后逐渐下降。将胰高血糖素直接添加到宽浓度范围内的脾细胞培养物中，对用抗CD3 mAb或LFS刺激后的淋巴细胞增殖或对sRBC的抗体形成细胞（AFC）响应均无影响。相反，胰高血糖素有效地逆转了由Delta（9）-四氢大麻酚（Delta（9）-THC）产生的sRBC AFC应答的抑制作用，并部分逆转了由2'，3'-dideoxyadenosine产生的抑制作用，两者都是有效的抑制剂腺苷酸环化酶。这些研究证实了功能性胰高血糖素受体在淋巴样细胞上的表达。 [参考：46]

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