Batty Ian H, Fleming Ian N, Downes C Peter
The Division of Cell Signalling, School of Life Sciences, MSI/WTB Complex, University of Dundee, Dow St, Dundee DD1 5EH, Scotland, UK.
Biochem J. 2004 May 1;379(Pt 3):641-51. doi: 10.1042/BJ20031700.
In 1321N1 astrocytoma cells, stimulation of the IGF-1 (insulin-like growth factor-1) receptor increased the association of PI3K [phosphoinositide (PI) 3-kinase] activity with IRS-1 (insulin re-ceptor substrate 1), and increased the cellular concentration of PtdIns(3,4,5)P3. Carbachol, acting on M3 muscarinic receptors, inhibited insulin-, but not PDGF (platelet-derived growth factor)-, stimulated responses by approximately 50%. The inhibition of IRS-1-associated PI3K activity by carbachol (i) was rapid (<1 min), persistent (> or =60 min) and potent (half-maximal concentration approximately 1 microM); (ii) was reproduced by stimuli for several phospholipase-C-coupled receptors; (iii) was prevented by the inhibition of protein kinase C, but not by chelation of intracellular Ca2+; and (iv) was not blocked or reproduced by inhibitors or stimuli respectively of mitogen-activated protein kinase, PI3K, protein kinase B or the mammalian target of rapamycin. However, the effects of carbachol were prevented by sodium vanadate, a protein tyrosine phosphatase inhibitor, and were accompanied by reduced insulin-stimulated IRS-1 tyrosine phosphorylation and recruitment of the 85 kDa regulatory subunit of PI3K to IRS-1, but not by reduced IGF-1 receptor kinase activity. The inhibitory effect of carbachol was reproduced by okadaic acid, a protein serine/threonine phosphatase inhibitor, but not by PDGF, yet all three agents stimulated the serine phosphorylation of IRS-1 at residues Ser312, Ser616 and Ser636/639, albeit to different extents. Thus muscarinic receptors may inhibit insulin signalling by promoting IRS-1 tyrosine dephosphorylation and/or by uncoupling IRS-1 from the stimulated IGF-1 receptor by stimulating IRS-1 serine phosphorylation. However, the proportion of IRS-1 molecules phosphorylated at a particular site or the phosphorylation of additional IRS-1 serine residues other than those noted above must be important.
在1321N1星形细胞瘤细胞中,胰岛素样生长因子-1(IGF-1)受体的刺激增加了磷脂酰肌醇-3激酶(PI3K)活性与胰岛素受体底物-1(IRS-1)的结合,并增加了磷脂酰肌醇(3,4,5)三磷酸(PtdIns(3,4,5)P3)的细胞浓度。作用于M3毒蕈碱受体的卡巴胆碱抑制胰岛素刺激的反应约50%,但不抑制血小板衍生生长因子(PDGF)刺激的反应。卡巴胆碱对与IRS-1相关的PI3K活性的抑制作用:(i)迅速(<1分钟)、持久(≥60分钟)且强效(半数最大浓度约为1微摩尔);(ii)几种磷脂酶C偶联受体的刺激可重现该作用;(iii)可被蛋白激酶C的抑制所阻止,但细胞内Ca2+螯合不能阻止;(iv)分别不受丝裂原活化蛋白激酶、PI3K、蛋白激酶B或雷帕霉素哺乳动物靶点的抑制剂或刺激的阻断或重现。然而,钒酸钠(一种蛋白酪氨酸磷酸酶抑制剂)可阻止卡巴胆碱的作用,且伴随胰岛素刺激的IRS-1酪氨酸磷酸化减少以及PI3K的85 kDa调节亚基募集至IRS-1减少,但IGF-1受体激酶活性未降低。冈田酸(一种蛋白丝氨酸/苏氨酸磷酸酶抑制剂)可重现卡巴胆碱的抑制作用,但PDGF不能,然而这三种试剂均刺激IRS-1在Ser312、Ser616和Ser636/639残基处的丝氨酸磷酸化,尽管程度不同。因此,毒蕈碱受体可能通过促进IRS-1酪氨酸去磷酸化和/或通过刺激IRS-1丝氨酸磷酸化使IRS-1与受刺激的IGF-1受体解偶联来抑制胰岛素信号传导。然而,在特定位点磷酸化的IRS-1分子比例或上述位点以外的其他IRS-1丝氨酸残基的磷酸化必定很重要。