Post-infarct cardiac sympathetic hyperactivity regulates galanin expression
Post-infarct cardiac sympathetic hyperactivity regulates galanin expression
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DOI：
10.1016/j.neulet.2008.03.012
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发表时间：
2008-05-09
影响因子：
2.5
通讯作者：
Habecker, Beth A.
中科院分区：
文献类型：
--
作者：
Ewert, T. Jarred;Gritman, Kurt R.;Habecker, Beth A.
心肌梗塞（MI）后，神经肽甘丙肽在心脏交感神经支配中升高。甘丙肽抑制迷走神经传导，并可能支持交感神经的再生，从而导致心梗后心律失常和心源性猝死的发生。心肌梗塞后交感神经元甘丙肽产生增加的原因尚不清楚。心脏缺血再灌注后，心脏交感神经元会长期激活，培养物中交感神经元的激活会刺激甘丙肽的表达。因此，我们检验了心肌梗塞后交感神经活动增加刺激心脏交感神经元甘丙肽表达的假设。为了检验这一假设，我们使用了 TGR(ASrAOGEN) 转基因大鼠，该大鼠缺乏脑血管紧张素原，并且不表现出梗塞后交感神经过度活跃。缺血再灌注后1周收集心脏和星状神经节。通过实时 PCR 定量甘丙肽 mRNA，并通过酶联免疫吸附测定法测定肽含量。与未手术和假手术对照相比，两种基因型的心脏交感神经元中 MI 后甘丙肽 mRNA 增加了约 3 倍。然而，心肌梗死后，左心室甘丙肽含量仅在 Sprague-Dawley 大鼠中增加，而在 AOGEN 大鼠中则没有。这些数据表明，梗塞后心脏交感神经过度活跃会刺激甘丙肽的产生，但并不是增加甘丙肽 mRNA 表达所必需的。 (C) 2008 Elsevier Ireland Ltd. 保留所有权利。
The neuropeptide galanin is elevated in the cardiac sympathetic innervation after myocardial infarction (MI). Galanin inhibits vagal transmission and may support the regeneration of sympathetic nerves, thereby contributing to the development of arrhythmia and sudden cardiac death after MI. The reason for increased galanin production in sympathetic neurons after myocardial infarction is not known. Cardiac sympathetic neurons are activated chronically after cardiac ischemia-reperfusion, and activation of sympathetic neurons in culture stimulates galanin expression. Therefore, we tested the hypothesis that increased sympathetic nerve activity stimulates galanin expression in cardiac sympathetic neurons after myocardial infarction. To test this hypothesis we used TGR(ASrAOGEN) transgenic rats, which lack brain angiotensinogen and do not exhibit post-infarct sympathetic hyperactivity. Hearts and stellate ganglia were collected 1 week after ischemia-reperfusion. Galanin mRNA was quantified by real-time PCR and peptide content was assayed by enzyme-linked immunosorbent assay. Galanin mRNA increased approximately 3-fold after MI in cardiac sympathetic neurons of both genotypes compared to unoperated and sham controls. Left ventricular galanin content, however, increased after MI only in Sprague-Dawley rats and not in AOGEN rats. These data suggest that post-infarct cardiac sympathetic hyperactivity stimulates galanin peptide production but is not required for increased galanin mRNA expression. (C) 2008 Elsevier Ireland Ltd. All rights reserved.