Akbar M, Okajima F, Tomura H, Majid M A, Yamada Y, Seino S, Kondo Y
Department of Physical Biochemistry, Gunma University, Maebashi, Japan.
FEBS Lett. 1994 Jul 11;348(2):192-6. doi: 10.1016/0014-5793(94)00603-2.
We transfected the COS-7 cells with cDNAs encoding different human somatostatin receptor (hSSTR) subtypes, and found that hSSTR subtypes mediate not only the inhibition of forskolin-induced cAMP accumulation but also the stimulation of phospholipase C (PLC) and Ca2+ mobilization. Activation of PLC by 1 microM somatostatin (SRIF) was in the order of: hSSTR5 > hSSTR2 > hSSTR3 > hSSTR4 >> hSSTR1. Pertussis toxin (PTX) treatment completely or partially reversed the PLC activation. 1 nM SRIF was equally effective for adenylate cyclase (AC) inhibition in a PTX-sensitive manner, in all the cells expressing different hSSTRs, except for hSSTR1. Nevertheless, SRIF stimulated AC even in the presence of forskolin at higher doses of SRIF in PTX-treated hSSTR5-expressing cells. We conclude that the cloned hSSTRs differentially couple to PTX-sensitive and -insensitive G-proteins to modulate PLC, Ca2+ mobilization and AC.
我们用编码不同人类生长抑素受体（hSSTR）亚型的cDNA转染COS-7细胞，发现hSSTR亚型不仅介导对福司可林诱导的cAMP积累的抑制，还介导对磷脂酶C（PLC）的刺激和Ca2+动员。1微摩尔生长抑素（SRIF）对PLC的激活顺序为：hSSTR5 > hSSTR2 > hSSTR3 > hSSTR4 >> hSSTR1。百日咳毒素（PTX）处理完全或部分逆转了PLC的激活。1纳摩尔SRIF以对PTX敏感的方式对腺苷酸环化酶（AC）抑制同样有效，在所有表达不同hSSTR的细胞中，除了hSSTR1。然而，在PTX处理的表达hSSTR5的细胞中，即使存在福司可林，高剂量的SRIF仍能刺激AC。我们得出结论，克隆的hSSTR与对PTX敏感和不敏感的G蛋白有不同的偶联，以调节PLC、Ca2+动员和AC。
