Sympathetic nervous remodeling is induced in the intermediolateral nucleus after myocardial infarction ? Role of BDNF-TrkB axis-

Sympathetic nervous remodeling is induced in the intermediolateral nucleus after myocardial infarction ? Role of BDNF-TrkB axis-
复制标题

心肌梗死后中间外侧核诱发交感神经重塑 ?

DOI:
10.1016/j.neulet.2018.08.004
复制
发表时间:
2018
影响因子:
2.5
通讯作者:
Takeishi Yasuchika
Takeishi Yasuchika
中科院分区:
医学4区
文献类型:
--
作者:
Nodera Minoru;Oikawa Masayoshi;Nakazato Kazuhiko;Ishida Takafumi;Takeishi Yasuchika

文献摘要

相似文献

一些研究表明,心肌梗死(MI)可引起星状神经节(SG)的神经重构。目前尚不清楚MI后的神经重塑是否局限于交感神经系统(SNS)内的SG。通过结扎左前降支动脉在大鼠模型中诱导MI。MI后2周通过免疫组织化学评估中间外侧核(IML)和SG的神经重塑。采用定量RT-PCR、免疫组化和Western blotting方法检测MI后1周脑源性神经营养因子(BDNF)、原肌球蛋白相关激酶受体(TrkB)和细胞外信号调节激酶(ERK)的mRNA和蛋白表达。与假手术组相比,MI后IML的神经元大小和轴突密度增加。与假手术组相比,MI后生长相关蛋白-43(一种在经历神经出芽的轴突中上调的蛋白质)的密度增加。MI组IML中BDNF和TrkB的荧光强度明显高于Sham组。此外,脑梗死后Th 2细胞水平的BDNF和TrkB mRNA表达增加。最后,磷酸化ERK免疫反应细胞的百分比在MI组中显著高于假手术组。结论:缺血性脑损伤后神经重构与BDNF-TrkB轴的激活有关。整个SNS的形态学重构可能参与MI后交感神经张力的持续激活。
Several studies have shown that neural remodeling in stellate ganglia (SG) is induced by myocardial infarction (MI). It remains unclear whether neural remodeling after MI is limited in SG within the sympathetic nervous system (SNS). MI was induced in a rat model by ligation of the left anterior descending artery. Neural remodeling in the intermediolateral nucleus (IML) and SG was assessed by immunohistochemistry 2 weeks after MI. The mRNA and protein expressions of brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase receptor (TrkB) and extracellular signal-regulated kinase (ERK) were measured by quantitative RT-PCR, immunohistochemistry and Western blotting 1 week after MI. The neuronal size and axonal density of IML were increased after MI compared to sham. The density of growth-associated protein-43, a protein upregulated in axons undergoing nerve sprouting, was increased after MI compared to sham. The fluorescence intensity of BDNF and TrkB in IML were significantly higher in the MI group than in the sham group. In addition, mRNA expressions of BDNF and TrkB in the spinal cord at the Th2 level was increased after MI. Finally, the percentage of phospho-ERK-immunoreactive cells in IML was significantly higher in the MI group than in the sham group. In conclusion, neural remodeling after MI in IML is associated with the activation of BDNF-TrkB axis. Morphological remodeling throughout the SNS may be involved in sustained activation of sympathetic tone after MI.