Cardiac Telocytes in Regeneration of Myocardium After Myocardial Infarction

Cardiac Telocytes in Regeneration of Myocardium After Myocardial Infarction
复制标题

心肌特洛细胞在心肌梗塞后心肌再生中的作用

DOI:
10.1007/978-981-10-1061-3_15
复制
发表时间:
2016-01-01
期刊:
TELOCYTES: CONNECTING CELLS
影响因子:
--
通讯作者:
Cai Dongqing
Cai Dongqing
中科院分区:
其他
文献类型:
--
作者:
Liao Zhaofu;Cai Dongqing

文献摘要

被引文献

相似文献

最近的研究发现,在心脏的心房中发现了一种新型的间质细胞,称为心脏端细胞(cardiac telocytes,CT)。CT在心肌内既有纵向分布,又有交叉分布,且在心房-心房和心肌基底部CT密度高于心肌中部,心外膜CT密度高于心内膜。此外,我们首次记录了心肌梗死(MI)期间心肌梗死区的CT网络被破坏。这一事实表明,除了心肌细胞的死亡之外,以前未被认识到的CT死亡是导致梗死心肌中观察到的结构损伤和不良愈合和再生的重要机制。此外,我们首次证明了在MI病例中移植CT可缩小梗死面积并改善心肌功能。CT移植的有益作用背后的机制是增加梗死部位和边缘区的血管生成,减少梗死和非梗死区的纤维化,改善左心室的病理重建,以及增加梗死区CT的再生。我们的研究结果表明,CT可以通过以下特征进行特异性鉴定:非常小的细胞体,极度延长并伴有一定程度的扩张,缺血时细胞死亡的倾向,以及分子标记物如c-Kit,CD 34,波形蛋白和PDGFR-β的表达。CT作为心肌中的结构和功能小生境微环境,在维持心肌的完整性和受损心肌的再生中发挥重要作用。
Recent research progress has revealed that a novel type of interstitial cells termed cardiac telocytes (CTs) is found in the interstitium of the heart. We demonstrated that CTs are distributed both longitudinally and within the cross network in the myocardium and that the density of CTs in the atrium-atria and base of the myocardium is higher than that in the middle of the myocardium, while the density of CTs in the epicardium is higher than that in the endocardium. In addition, we documented, for the first time, that the network of CTs in the infarct zone of the myocardium is destroyed during myocardial infarction (MI). This fact shows that, in addition to the death of cardiac myocytes, the previously unrecognized death of CTs is an important mechanism that contributes to the structural damage and poor healing and regeneration observed in the infarcted myocardium. Furthermore, we demonstrated, for the first time, that transplantation of CTs in cases of MI decreases the infarct size and improves myocardial function. The mechanisms behind the beneficial effects of CT transplantation are increased angiogenesis at the infarct site and the border zone, decreased fibrosis in the infarct and non-infarct zones, improved pathological reconstruction of the left ventricle, and increased regeneration of CTs in the infarct zone. Our findings reveal that CTs can be specifically identified by the following characteristics: very small cell bodies, extreme prolongation with some dilation, predisposition to cell death under ischemia, and expression of molecular markers such as c-Kit, CD34, vimentin, and PDGFR-beta. CTs act as a structural and functional niche microenvironment in the myocardium and play an essential role in maintaining the integrity of the myocardium and in the regeneration of damaged myocardium.