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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mitogenic actions of neuropeptide Y in vascular smooth muscle cells: synergetic interactions with the beta-adrenergic system.
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Mitogenic actions of neuropeptide Y in vascular smooth muscle cells: synergetic interactions with the beta-adrenergic system.

机译：神经肽Y在血管平滑肌细胞中的促丝裂作用：与β-肾上腺素系统的协同相互作用。

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摘要

Neuropeptide Y (NPY), a sympathetic cotransmitter and vasoconstrictor, also stimulates vascular smooth muscle cell (VSMC) growth, but which of its Y1-Y5 receptors are involved remains unclear. In quiescent rat VSMCs, NPY receptor mRNAs were undetectable (reverse transcription-polymerase chain reaction), but Y1, Y2, and Y5 expression were upregulated or induced following NPY treatment. Concomitantly, NPY increased up to twofold [3H]thymidine incorporation and cell number bimodally, with a high-affinity peak at pM and low affinity peak at nM concentrations. The Y1 or Y5 (not Y2) antagonist alone did not change the high-affinity peak but decreased the low affinity peak by 50% and fully blocked NPY's response when combined. In VSMCs lacking NPY receptors and responsiveness, transient Y1 cDNA transfection restored their mitogenic response (blocked by the Y1 antagonist). In VSMCs with low or no NPY responsiveness, pre-exposure to beta-adrenergic receptor agonist (isoproterenol), forskolin, or dibutyryl cAMP augmented NPY's mitogenic effect, while upregulating Y1, Y2, and Y5 receptor expression (isoproterenol only). Thus, NPY is a potent vascular mitogen acting via Y1 and Y5 receptors. However, since their expression is low in nonproliferating cells, amplification of NPY's mitogenic responses requires upregulation of at least the Y1 receptor by NPY itself or beta-adrenergic, cAMP-dependent activation.
机译：神经肽Y（NPY）是一种有交感的共递物和血管收缩剂，也可以刺激血管平滑肌细胞（VSMC）的生长，但是尚不清楚其中涉及哪些Y1-Y5受体。在静止的大鼠VSMC中，无法检测到NPY受体mRNA（逆转录-聚合酶链反应），但是在NPY处理后，Y1，Y2和Y5的表达上调或诱导。伴随地，NPY最多增加了两倍的[3H]胸苷掺入和双峰细胞数量，在pM具有高亲和力峰，在nM浓度具有低亲和力峰。单独使用Y1或Y5（不是Y2）拮抗剂并不会改变高亲和力峰，但将低亲和力峰降低了50％，并在结合时完全阻断了NPY的反应。在缺乏NPY受体和反应能力的VSMC中，瞬时Y1 cDNA转染恢复了它们的促有丝分裂反应（被Y1拮抗剂阻断）。在NPY反应性低或无NPY的VSMC中，预先暴露于β-肾上腺素能受体激动剂（异丙肾上腺素），毛喉素或二丁酰cAMP可以增强NPY的促有丝分裂作用，同时上调Y1，Y2和Y5受体表达（仅异丙肾上腺素）。因此，NPY是通过Y1和Y5受体起作用的有效血管有丝分裂原。但是，由于它们在非增殖细胞中的表达较低，因此NPY有丝分裂反应的扩增需要至少由NPY本身或β-肾上腺素，cAMP依赖性激活来上调Y1受体。

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