Functional somatostatin receptors on a rat pancreatic acinar cell line.
Functional somatostatin receptors on a rat pancreatic acinar cell line.
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大鼠胰腺腺泡细胞系上的功能性生长抑素受体。
DOI：
10.1152/ajpgi.1988.255.1.g113
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Ribet,A
中科院分区：
文献类型：
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作者：
Viguerie,N;Tahiri-Jouti,N;Esteve,JP;Clerc,P;Logsdon,C;Svoboda,M;Susini,C;Vaysse,N;Ribet,A
对大鼠胰腺腺泡细胞系 AR4-2J 的生长抑素受体进行了生化、结构和功能表征。 125I-[Tyr11]生长抑素与 AR4-2J 细胞的结合是可饱和的，表现出单一类别的高亲和力结合位点 (Kd = 0.55 +/- 0.06 nM)，最大结合能力为 258 +/- 20 fmol/10(6) 细胞。通过将 125I-[Tyr11]生长抑素与其质膜受体共价交联来分析生长抑素受体结构。交联蛋白的凝胶电泳和放射自显影显示含有生长抑素受体的肽（Mr 80,000）。生长抑素以剂量依赖性方式抑制血管活性肠肽 (VIP) 刺激的 3',5'-环单磷酸腺苷 (cAMP) 形成。引起 cAMP 形成半最大抑制 (IC50 = 0.4 nM) 的生长抑素浓度接近生长抑素受体的亲和力。 AR4-2J 细胞的百日咳毒素预处理可防止生长抑素对 VIP 刺激的 cAMP 形成以及生长抑素结合的抑制。我们得出结论，AR4-2J细胞表现出功能性生长抑素受体，保留了胰腺腺泡细胞生长抑素受体的特异性和亲和力，并通过百日咳毒素敏感的鸟嘌呤核苷酸结合蛋白Ni发挥作用，抑制腺苷酸环化酶。
Somatostatin receptors from a rat pancreatic acinar cell line, AR4-2J, were characterized biochemically, structurally, and functionally. Binding of 125I-[Tyr11]somatostatin to AR4-2J cells was saturable, exhibiting a single class of high-affinity binding sites (Kd = 0.55 +/- 0.06 nM) with a maximal binding capacity of 258 +/- 20 fmol/10(6) cells. Somatostatin receptor structure was analyzed by covalently cross-linking 125I-[Tyr11]somatostatin to its plasma membrane receptors. Gel electrophoresis and autoradiography of cross-linked proteins revealed a peptide (Mr 80,000) containing the somatostatin receptor. Somatostatin inhibited vasoactive intestinal peptide (VIP)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) formation in a dose-dependent manner. The concentration of somatostatin that caused half-maximal inhibition of cAMP formation (IC50 = 0.4 nM) was close to the receptor affinity for somatostatin. Pertussis toxin pretreatment of AR4-2J cells prevented somatostatin inhibition of VIP-stimulated cAMP formation as well as somatostatin binding. We conclude that AR4-2J cells exhibit functional somatostatin receptors that retain both specificity and affinity of the pancreatic acinar cell somatostatin receptors and act via the pertussis toxin-sensitive guanine nucleotide-binding protein Ni to inhibit adenylate cyclase.