Liu J, Gao B, Mirshahi F, Sanyal A J, Khanolkar A D, Makriyannis A, Kunos G
Department of Pharmacology & Toxicology, Medical College of Virginia of Virginia Commonwealth University, Richmond, VA 23298, USA.
Biochem J. 2000 Mar 15;346 Pt 3(Pt 3):835-40.
Cannabinoid CB1 receptor mRNA was detected using reverse transcription-polymerase chain reaction (RT-PCR) in endothelial cells from human aorta and hepatic artery and in the ECV304 cell line derived from human umbilical vein endothelial cells. CB1 receptor-binding sites were detected by the high-affinity antagonist radioligand [(125)I]AM-251. In ECV304 cells, both the highly potent synthetic cannabinoid agonist HU-210 and the endogenous ligand anandamide induce activation of mitogen-activated protein (MAP) kinase, and the effect of HU-210 was completely blocked, whereas the effect of anandamide was partially inhibited by SR141716A, a selective CB1 receptor antagonist. Transfection of ECV304 cells with CB1 receptor antisense, but not sense, oligonucleotides caused the same pattern of inhibition as SR141716A. This provides more definitive evidence for the involvement of CB1 receptors in MAP kinase activation and suggests that anandamide may also activate MAP kinase via an additional, CB1 receptor-independent, SR141716A-resistant mechanism. The MAP kinase activation by anandamide in ECV304 cells requires genistein-sensitive tyrosine kinases and protein kinase C (PKC), and anandamide also activates p38 kinase and c-Jun kinase. These findings indicate that CB1 receptors located in human vascular endothelium are functionally coupled to the MAP kinase cascade. Activation of protein kinase cascades by anandamide may be involved in the modulation of endothelial cell growth and proliferation.
利用逆转录 - 聚合酶链反应(RT-PCR)在人主动脉和肝动脉的内皮细胞以及源自人脐静脉内皮细胞的ECV304细胞系中检测到大麻素CB1受体mRNA。通过高亲和力拮抗剂放射性配体[(125)I]AM - 251检测CB1受体结合位点。在ECV304细胞中,高效合成大麻素激动剂HU - 210和内源性配体花生四烯乙醇胺均诱导丝裂原活化蛋白(MAP)激酶活化,HU - 210的作用被完全阻断,而花生四烯乙醇胺的作用被选择性CB1受体拮抗剂SR141716A部分抑制。用CB1受体反义寡核苷酸而非正义寡核苷酸转染ECV304细胞,产生了与SR141716A相同的抑制模式。这为CB1受体参与MAP激酶活化提供了更确凿的证据,并表明花生四烯乙醇胺也可能通过一种额外的、不依赖CB1受体且对SR141716A耐药的机制激活MAP激酶。花生四烯乙醇胺在ECV304细胞中激活MAP激酶需要金雀异黄素敏感的酪氨酸激酶和蛋白激酶C(PKC),并且花生四烯乙醇胺还激活p38激酶和c-Jun激酶。这些发现表明,位于人血管内皮的CB1受体在功能上与MAP激酶级联反应偶联。花生四烯乙醇胺激活蛋白激酶级联反应可能参与内皮细胞生长和增殖的调节。