血管紧张素II对神经调节的调控：丝裂原活化蛋白激酶激活后的下游信号传导机制
Angiotensin II regulation of neuromodulation: downstream signaling mechanism from activation of mitogen-activated protein kinase.
作者信息
Lu D, Yang H, Raizada M K
机构信息
Department of Physiology, University of Florida, College of Medicine, Gainesville 32610, USA.
出版信息
J Cell Biol. 1996 Dec;135(6 Pt 1):1609-17. doi: 10.1083/jcb.135.6.1609.
Abstract
Angiotensin II (Ang II) stimulates expression of tyrosine hydroxylase and norepinephrine transporter genes in brain neurons; however, the signal-transduction mechanism is not clearly defined. This study was conducted to determine the involvement of the mitogen-activated protein (MAP) kinase signaling pathway in Ang II stimulation of these genes. MAP kinase was localized in the perinuclear region of the neuronal soma. Ang II caused activation of MAP kinase and its subsequent translocation from the cytoplasmic to nuclear compartment, both effects being mediated by AT1 receptor subtype. Ang II also stimulated SRE- and AP1-binding activities and fos gene expression and its translocation in a MAP kinase-dependent process. These observations are the first demonstration of a downstream signaling pathway involving MAP kinase in Ang II-mediated neuromodulation in noradrenergic neurons.
摘要
血管紧张素II（Ang II）可刺激脑神经元中酪氨酸羟化酶和去甲肾上腺素转运体基因的表达；然而，其信号转导机制尚不清楚。本研究旨在确定丝裂原活化蛋白（MAP）激酶信号通路在Ang II对这些基因的刺激作用中的参与情况。MAP激酶定位于神经元胞体的核周区域。Ang II可导致MAP激酶的激活及其随后从细胞质向细胞核区室的转位，这两种效应均由AT1受体亚型介导。Ang II还在一个MAP激酶依赖性过程中刺激SRE和AP1结合活性以及fos基因表达及其转位。这些观察结果首次证明了在去甲肾上腺素能神经元中，Ang II介导的神经调节过程中存在一条涉及MAP激酶的下游信号通路。
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