Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease.
Apoptotic neuron-secreted HN12 inhibits cell apoptosis in Hirschsprung's disease.
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凋亡神经元分泌的 HN12 抑制先天性巨结肠症的细胞凋亡
DOI：
10.2147/ijn.s114838
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发表时间：
2016
影响因子：
8
通讯作者：
Tang W
中科院分区：
文献类型：
--
作者：
Du C;Xie H;Zang R;Shen Z;Li H;Chen P;Xu X;Xia Y;Tang W
细胞凋亡的扰动可能导致先天性巨结肠症 (HSCR)，这是一种神经嵴发育的遗传性疾病。据信长非编码RNA (lncRNA) 在HSCR 的进展中发挥作用。这项研究表明，凋亡神经元可以通过分泌含有高水平 HN12 lncRNA 的外泌体来抑制非凋亡细胞的凋亡。非凋亡细胞中升高的外源性 HN12 通过维持线粒体功能（包括 ATP 的产生和细胞色素 C 的释放）有效抑制细胞凋亡。这些结果表明，分泌的 lncRNA 可能作为介导 HSCR 中细胞间通讯的信号分子。此外，循环中的高 HN12 水平可作为预测 HSCR 的生物标志物，为 HSCR 的早期筛查提供一种潜在的、新颖的、无创的诊断方法。
Perturbation in apoptosis can lead to Hirschsprung’s disease (HSCR), which is a genetic disorder of neural crest development. It is believed that long noncoding RNAs (lncRNAs) play a role in the progression of HSCR. This study shows that apoptotic neurons can suppress apoptosis of nonapoptotic cells by secreting exosomes that contain high levels of HN12 lncRNA. Elevated exogenous HN12 in nonapoptotic cells effectively inhibited cell apoptosis by maintaining the function of mitochondria, including the production of ATP and the release of cytochrome C. These results demonstrate that secreted lncRNAs may serve as signaling molecules mediating intercellular communication in HSCR. In addition, high HN12 levels in the circulation worked as a biomarker for predicting HSCR, providing a potential, novel, noninvasive diagnostic approach for early screening of HSCR.