Activation by 2-arachidonoylglycerol, an endogenous cannabinoid receptor ligand, of p42/44 mitogen-activated protein kinase in HL-60 cells
Activation by 2-arachidonoylglycerol, an endogenous cannabinoid receptor ligand, of p42/44 mitogen-activated protein kinase in HL-60 cells
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DOI：
10.1093/oxfordjournals.jbchem.a002904
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发表时间：
2001-05-01
影响因子：
2.7
通讯作者：
Sugiura, T
中科院分区：
文献类型：
--
作者：
Kobayashi, Y;Arai, S;Sugiura, T
2-花生四烯醇甘油（2-AG）是一种内源性大麻素受体配体，可诱导HL-60细胞p42/44分裂原活化蛋白激酶（MAP激酶）的快速磷酸化。我们证实，2-AG刺激HL-60细胞后，p42/44 MAP激酶酶活性明显增强。在加入2-AG之前，将大麻素CB2受体特异性拮抗剂SR144528添加到细胞中，可以消除2-AG诱导的应答，表明CB2受体参与了应答。G蛋白G(i)或G(o)也被认为参与其中，因为百日咳毒素处理的细胞使2-AG诱导的应答无效。CP55940和anandamide也能诱导p42/44 MAP激酶的激活，但anandamide的激活作用不如2-AG和CP55940明显。这些结果表明，2-AG可能通过激活p42/44 MAP激酶级联在这类细胞中发挥重要的生理作用。
2-Arachidonoylglycerol (2-AG), an endogenous cannabinoid receptor ligand, was shown to induce rapid phosphorylation of p42/44 mitogen-activated protein kinase (MAP kinase) in HL-60 cells. We confirmed that the enzyme activity of p42/44 MAP kinase in HL-60 cells was augmented markedly when the cells were stimulated with 2-AG. The addition of SR144528, a cannabinoid CB2 receptor-specific antagonist, to the cells prior to the addition of 2-AG abolished the response induced by 2-AG, indicating that the CB2 receptor is involved in the response. G protein G(i) or G(o) is also assumed to be involved, because pertussis toxin treatment of the cells nullified the response induced by 2-AG. CP55940 and anandamide also induced the activation of p42/44 MAP kinase, although the activation by anandamide was less pronounced than that by 2-AG or CP55940. These results suggest that 2-AG may play an important physiological role in this type of cell through the activation of the p42/44 MAP kinase cascade.