NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome.

NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome.
复制标题

DOI:
10.1076/apab.109.4.357.4249
复制
发表时间:
2001-10-01
影响因子:
3
通讯作者:
Aloe, L
Aloe, L
中科院分区:
医学4区
文献类型:
--
作者:
Chaldakov, G N;Fiore, M;Aloe, L

文献摘要

被引文献

相似文献

虽然多种生长因子,细胞因子和免疫细胞被确定在动脉粥样硬化病变,以及一个重要的非神经元功能的神经营养因子参与心血管组织的发展和脂质和葡萄糖代谢,神经营养因子的神经生长因子和脑源性神经营养因子和脂肪因子瘦素在人类冠状动脉粥样硬化和相关疾病,如代谢综合征的作用,仍然不清楚。在这里,我们报告了(i)与尸检病例中获得的对照样本(n = 9)相比,人动脉粥样硬化冠状动脉(n = 12)中NGF的含量和免疫反应性均减少,p75 NGF受体的表达和肥大细胞的数量增加,(ii)与对照组(n = 10)相比,代谢综合征患者(n = 23)的NGF和BDNF血浆水平降低。代谢综合征患者血浆瘦素水平与脂肪组织肥大细胞数量呈正相关,提示瘦素可能是一种新的脂肪免疫介质。总之,这些结果提供了第一个相关证据,表明NGF、BDNF、瘦素和肥大细胞可能参与人类冠状动脉粥样硬化和代谢综合征,这意味着这些心血管疾病的病理生物学中存在神经免疫和脂肪免疫途径。
While multiple growth factor, cytokines, and immune cells are identified in atherosclerotic lesions, as well as an essential nonneuronal function of neurotrophins implicated in cardiovascular tissue development and in lipid and glucose metabolism, the role of the neurotrophins NGF and BDNF and also the adipokine leptin in human coronary atherosclerosis and related disorders, such as metabolic syndrome, remains unclear. Here we report that (i) both the amount and the immunoreactivity of NGF was reduced and the expression of p75NGF receptor and the number of mast cell increased in human atherosclerotic coronary arteries (n = 12) compared with control specimens (n = 9) obtained from autopsy cases, and (ii) NGF and BDNF plasma levels were reduced in patients with metabolic syndrome (n = 23) compared with control subjects (n = 10). Also, in metabolic syndrome patients, a positive correlation between the plasma leptin levels and the number of adipose tissue mast cells was found, suggesting that leptin may be a novel adipoimmune mediator. Altogether, the results provide the first correlative evidence for the potential involvement of NGF, BDNF, leptin, and mast cells in human coronary atherosclerosis and metabolic syndrome, implying neuroimmune and adipoimmune pathways in the pathobiology of these cardiovascular disorders.