RESEARCH FOR ALTERATION OF G-PROTEIN GENE IN MYOCARDOPATHY

G蛋白在细胞表面受体和细胞内效应器之间起转导作用。它们由三个亚基组成。β -肾上腺素能受体激酶（betaARK）的脱敏和下调。在心力衰竭中观察到β -肾上腺素能受体（β -肾上腺素能受体）的脱敏和下调。betaARK是参与betaAR脱敏的成分之一。G蛋白- γ亚基通过pleckstrin同源结构域与betaARK结合。因此，我们研究了β - AR刺激对大鼠心脏稳态水平G蛋白β亚基（Gbeta）的影响。采用Langendorff技术灌注相应药物，灌注整个大鼠心脏。使用针对G蛋白β亚基的同种异型特异性抗血清进行免疫印迹检测显示，大鼠心脏含有至少三个G蛋白β亚基，beta1, beta2, beta3。在单独使用ISO或ISO与cGP的情况下，细胞质中Gbeta3的水平显著降低。Gbeta3在EPI存在时也下降。心得安可以阻断kisso诱导的胞质中Gbeta3的减少。相比之下，Gbeta1和Gbeta2的水平在ISO或EPI的存在下没有变化。另一方面，在膜组分中，Gbeta3的水平在ISO或EPI的存在下显著增加。普萘洛尔联合ISO或CGP联合ISO均未改变膜组分中Gbeta3的水平。膜组分中Gbeta1和Gbeta2的水平在ISO或EPI的存在下没有变化。综上所述，β - aar激动剂可能诱导gβ a3从细胞质到膜的异构体特异性易位。

G protein serve as transducers between cell surface receptors and intracellular effectors. They consist of three subunits. The desensitization and down-regulation of beta-adrenergic receptor kinase (betaARK). The desensitization and down-regulation of beta-adrenergic receptors (betaAR) have been observed in the heart failure. betaARK is one of the components involved in desensitization of betaAR.G protein betagamma subunit bind betaARK through the pleckstrin homonogy domein. Therefore, we investigated the effects of beta AR stimulation on steady-state level G protein beta subunit (Gbeta) in the rat heart. The whole rat heart was perfused by Langendorff's techniqe with the indicated agents. Immunoblotting using isoform-specific antisera against G protein beta subunits revealed that the rat heart containings at least three G protein beta subunits, beta1, beta2, beta3. The level of Gbeta3 in the cytosol dramatically decreased in the presence of ISO alone or ISO with cGP.Gbeta3 decreased in the presence of EPI as well. Propranolol could blockISO-induced decrease of Gbeta3 in the cytosol. In contrast, the levels of Gbeta1 and Gbeta2 did not change in the presence of ISO or EPI.On the other hand, in membrane fractions the level of Gbeta3 significantly increased in the presence of ISO or EPI.ISO with propranolol or ISO with CGP did not change the level of Gbeta3 in membrane fraction. The levels of Gbeta1 and Gbeta2 did not change in the presence of ISO or EPI in membrane fractions. Taken together, betaAR agonist might induce isoform-specific translocation of Gbeta3 from the cyctosol to the membrane.