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首页> 外文期刊>Journal of Cellular Physiology >Nestin (+) stem cells independently contribute to neural remodelling of the ischemic heart.
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Nestin (+) stem cells independently contribute to neural remodelling of the ischemic heart.

机译：干细胞巢蛋白(+)独立做出贡献神经缺血心脏的改造。

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摘要

Recent studies have revealed the existence of multipotent nestin-immunoreactive cells in the adult mammalian heart. These cells were recruited to infarct site following ischemic injury and differentiated to a vascular lineage leading to de novo blood vessel formation. Here, we show that a sub-population of cardiac resident nestin((+)) cells can further differentiate to a neuronal-like fate in vivo following myocardial infarction. In the ischemically damaged rat heart, neurofilament-M((+)) fibres were detected innervating the peri-infarct/infarct region and the preponderance of these fibres were physically associated with processes emanating from nestin((+)) cells. One week after isogenic heterotopic cardiac transplantation, the beating transplanted rat heart was devoid of neurofilament-M((+)) fibre staining. The superimposition of an ischemic insult to the transplanted heart led to the de novo synthesis of neurofilament-M((+)) fibres by cardiac resident nestin((+)) cells. Nerve growth factor infusion and the exposure of normal rats to intermittent hypoxia significantly increased the density of neurofilament-M((+)) fibres in the heart. However, these newly formed neurofilament-M((+)) fibres were not physically associated with nestin((+)) processes. These data highlight a novel paradigm of reparative fibrosis as a subpopulation of cardiac resident nestin((+)) cells directly contributed to neural remodelling of the peri-infarct/infarct region of the ischemically damaged rat heart via the de novo synthesis of neurofilament-M fibres.
机译：最近的研究显示的存在多功能nestin-immunoreactive细胞成年哺乳动物的心脏。在缺血性损伤和梗塞站点分化血管血统导致新生血管的形成。子总体中心脏的居民巢蛋白(+)细胞可以进一步区分neuronal-like命运体内心肌梗塞。心,neurofilament-M((+))纤维被检测到支配peri-infarct /梗塞区域这些纤维是身体上的优势来自相关流程巢蛋白(+)细胞。异位心脏移植,跳动大鼠心脏移植是没有的neurofilament-M((+))纤维染色。叠加的缺血性侮辱的移植心脏导致从头合成neurofilament-M((+))由心脏纤维居民巢蛋白(+)细胞。输液和曝光正常的老鼠间歇性缺氧显著增加了neurofilament-M密度((+))的纤维的心。neurofilament-M((+))纤维没有身体巢蛋白((+))的过程。突出小说范式的修缮的纤维化作为一个族群的心脏居民巢蛋白((+))直接导致神经细胞peri-infarct /梗塞区域的改造通过de ischemically受损的老鼠心脏新生neurofilament-M的合成纤维。

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