Mitochondrial Uncoupling Protein 2 (UCP2) Regulates Retinal Ganglion Cell Number and Survival.
Mitochondrial Uncoupling Protein 2 (UCP2) Regulates Retinal Ganglion Cell Number and Survival.
复制标题
DOI：
10.1007/s12031-016-0728-5
复制
发表时间：
2016-04
期刊：
影响因子：
--
通讯作者：
Horvath TL
中科院分区：
文献类型：
--
作者：
Barnstable CJ;Reddy R;Li H;Horvath TL
在大脑中，线粒体解偶联蛋白2（UCP2）已成为一种与神经元存活相关的应激信号。在视网膜中，UCP2主要由视网膜神经节细胞表达。在此我们研究了UCP2在小鼠视网膜中的功能相关性。在关键发育时期，UCP2表达增加显著减少了细胞凋亡，从而使成年个体的视网膜神经节细胞数量增多。UCP2水平升高还能防止因眼内注射N -甲基 - D -天冬氨酸（NMDA）或海人酸所诱导的兴奋性毒性细胞死亡。在视网膜细胞的单层培养中，UCP2水平升高增加了细胞存活率，并使细胞不再依赖神经营养因子脑源性神经营养因子（BDNF）和睫状神经营养因子（CNTF）的促存活作用。综上所述，这些数据表明UCP2是发育过程中和成年动物视网膜神经元存活的重要调节因子。
In the brain, mitochondrial uncoupling protein 2 (UCP2) has emerged as a stress signal associated with neuronal survival. In the retina UCP2 is expressed primarily by retinal ganglion cells. Here we investigated the functional relevance of UCP2 in the mouse retina. Increased expression of UCP2 significantly reduced apoptosis during the critical developmental period resulting in elevated numbers of retinal ganglion cells in the adult. Elevated UCP2 levels also protected against excitotoxic cell death induced by intraocular injection of either NMDA or Kainic Acid. In monolayer cultures of retinal cells, elevated UCP2 levels increased cell survival and rendered the cells independent of the survival promoting effects of the neurotrophic factors BDNF and CNTF. Taken together these data implicate UCP2 as an important regulator of retinal neuron survival both during development and in adult animals.