Bühlmann N, Leuthäuser K, Muff R, Fischer J A, Born W
Department of Orthopedic Surgery, University of Zurich, Switzerland.
Endocrinology. 1999 Jun;140(6):2883-90. doi: 10.1210/endo.140.6.6783.
Adrenomedullin (ADM) and alpha- and beta-calcitonin (CT) gene-related peptide (alpha-, betaCGRP) are structurally related vasodilatory peptides with homology to CT and amylin. An originally orphan human CT receptor-like receptor (hCRLR) is a Gs protein-coupled CGRP or ADM receptor when coexpressed with recently identified human single transmembrane domain receptor activity modifying proteins 1 (hRAMP1) or -2 (hRAMP2), respectively. Here, the function of the rat CRLR homologue (rCRLR) has been investigated in rat osteoblast-like UMR-106 cells and in COS-7 cells, in the absence and presence of hRAMP1 and -2 and combinations thereof. Transient expression of rCRLR in UMR-106 cells revealed an ADM receptor, and [125I]rat (r) ADM binding was enhanced with hRAMP2 and inhibited by 50% when hRAMP1 was coexpressed. Detectable [125I]h alphaCGRP binding required the presence of hRAMP1, and the expression of CGRP binding sites was unaffected by coexpressed hRAMP2. Specificity of ADM binding sites in [125I]rADM binding inhibition experiments was reflected by an over 1000-fold higher potency of rADM [half-maximal effective concentration = 0.19 +/- 0.05 nM (mean +/- SEM, n = 4)], compared with r alphaCGRP and r betaGRP, to induce a cAMP-responsive luciferase reporting gene (CRE-luc). In rCRLR and hRAMP1 cotransfected cells, expressing predominantly CGRP binding sites, r betaCGRP, r alphaCGRP, and rADM induced CRE-luc with half-maximal effective concentration of 0.27 +/- 0.17 nM, 0.37 +/- 0.27 nM, and 1.4 +/- 0.9 nM, respectively. In COS-7 cells, the results were comparable, but rCRLR required coexpressed hRAMP2 for ADM receptor function. This is consistent with higher levels of endogenous RAMP2 encoding messenger RNA in UMR-106, compared with COS-7 cells. In conclusion, the recognition of RAMP1 and -2 as mediators of CRLR expression as a CGRP or ADM receptor has been extended, with evidence that endogenous RAMP2 is sufficient to reveal an ADM receptor in UMR-106 cells. Inhibition of RAMP2-evoked ADM receptor expression by RAMP1 and generation of a CGRP receptor is consistent with competitive interactions of the different RAMPs with rCRLR.
肾上腺髓质素(ADM)以及α - 和β - 降钙素(CT)基因相关肽(α - 、β - CGRP)是与CT和胰淀素具有结构相关性的血管舒张肽。最初被认为是孤儿受体的人CT受体样受体(hCRLR),当分别与最近鉴定出的人单跨膜结构域受体活性修饰蛋白1(hRAMP1)或 -2(hRAMP2)共表达时,分别成为与Gs蛋白偶联的CGRP或ADM受体。在此,在大鼠成骨样UMR - 106细胞和COS - 7细胞中,在不存在和存在hRAMP1和 -2及其组合的情况下,对大鼠CRLR同源物(rCRLR)的功能进行了研究。rCRLR在UMR - 106细胞中的瞬时表达显示出一个ADM受体,[125I]大鼠(r)ADM结合在与hRAMP2共表达时增强,而当与hRAMP1共表达时被抑制50%。可检测到的[125I]hαCGRP结合需要hRAMP1的存在,并且CGRP结合位点的表达不受共表达的hRAMP2的影响。在[125I]rADM结合抑制实验中,ADM结合位点的特异性体现在与rαCGRP和rβGRP相比,rADM诱导cAMP反应性荧光素酶报告基因(CRE - luc)的效力高出1000倍以上[半数最大有效浓度 = 0.19±0.05 nM(平均值±标准误,n = 4)]。在共转染rCRLR和hRAMP1的细胞中,主要表达CGRP结合位点,rβCGRP、rαCGRP和rADM诱导CRE - luc的半数最大有效浓度分别为0.27±±0.17 nM、0.37±0.27 nM和1.4±0.9 nM。在COS - 7细胞中,结果类似,但rCRLR需要共表达hRAMP2才能发挥ADM受体功能。这与UMR - 106细胞中内源性RAMP2编码信使RNA的水平高于COS - 7细胞一致。总之,RAMP1和 -2作为CRLR表达为CGRP或ADM受体的介质的认识得到了扩展,有证据表明内源性RAMP2足以在UMR - 106细胞中揭示一个ADM受体。RAMP1对RAMP2诱发的ADM受体表达的抑制以及CGRP受体的产生与不同RAMP与rCRLR的竞争性相互作用一致。