首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >THE ANGIOTENSIN II TYPE 2 (AT(2)) RECEPTOR ANTAGONIZES THE GROWTH EFFECTS OF THE AT(1) RECEPTOR - GAIN-OF-FUNCTION STUDY USING GENE TRANSFER
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THE ANGIOTENSIN II TYPE 2 (AT(2)) RECEPTOR ANTAGONIZES THE GROWTH EFFECTS OF THE AT(1) RECEPTOR - GAIN-OF-FUNCTION STUDY USING GENE TRANSFER

机译:使用基因转移,血管紧张素II 2型(AT(2))受体拮抗AT(1)受体的生长效应-功能增益研究

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The type 1 angiotensin II (AT(1)) receptor is well characterized but the type 2 (AT(2)) receptor remains an enigma. We tested the hypothesis that the AT(2) receptor can modulate the growth of vascular smooth muscle cells by transfecting an AT(2) receptor expression vector into the balloon-injured rat carotid artery and observed that overexpression of the AT(2) receptor attenuated neointimal formation. In cultured smooth muscle cells, AT(2) receptor transfection reduced proliferation and inhibited mitogen-activated protein kinase activity. Furthermore, we demonstrated that the AT(2) receptor mediated the developmentally regulated decrease in aortic DNA synthesis at the latter stages of gestation. These results suggest that the AT(2) receptor exerts an antiproliferative effect, counteracting the growth action of AT(1) receptor. [References: 31]
机译:1型血管紧张素II(AT(1))受体已被很好地表征,但2型(AT(2))受体仍然是一个谜。我们测试了以下假设:AT(2)受体可以通过将AT(2)受体表达载体转染到球囊损伤的大鼠颈动脉中来调节血管平滑肌细胞的生长,并观察到AT(2)受体的过表达减弱了新内膜形成。在培养的平滑肌细胞中,AT(2)受体转染减少增殖并抑制有丝分裂原激活的蛋白激酶活性。此外,我们证明在妊娠后期,AT(2)受体介导了主动脉DNA合成的发育调控减少。这些结果表明,AT(2)受体发挥抗增殖作用,抵消了AT(1)受体的生长作用。 [参考:31]

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