上调人硒蛋白 H 在小鼠海马神经元细胞中的表达可促进线粒体生物发生和功能表现。
Upregulation of human selenoprotein H in murine hippocampal neuronal cells promotes mitochondrial biogenesis and functional performance.
机构信息
Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE) Building 2025, North Carolina Central University, 302 East Lawson Street, Durham, NC 27707, USA.
出版信息
Mitochondrion. 2011 Jan;11(1):76-82. doi: 10.1016/j.mito.2010.07.007. Epub 2010 Jul 23.
Abstract
Overexpression of selenoprotein H (SelH) gene provides neuroprotection in neurons against UVB-induced cell death by blocking the mitochondrial-initiated apoptotic cell death pathway. This study examined the effects of SelH on mitochondrial biogenesis and mitochondrial function. The results demonstrated that overexpression of SelH gene in neuronal HT22 cells significantly increased the levels of mitochondrial biogenesis regulators, nuclear respiratory factor-1 (NRF-1), peroxisome proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α) and mitochondrial transcription factor A (Tfam). Mitochondrial cytochrome c content was elevated, mass was increased and respiration was enhanced. SelH transfection ameliorated ultra violet B (UVB)-induced suppression of mitochondrial biogenesis markers and depolarization of mitochondrial membrane potential. Overexpression of SelH promotes mitochondrial biogenesis and improves mitochondrial functional performance.
摘要
硒蛋白 H（SelH）基因的过表达通过阻断线粒体起始的凋亡细胞死亡途径为神经元提供了对 UVB 诱导的细胞死亡的神经保护作用。本研究探讨了 SelH 对线粒体生物发生和线粒体功能的影响。结果表明，SelH 基因在神经元 HT22 细胞中的过表达显著增加了线粒体生物发生调节剂的水平，核呼吸因子-1（NRF-1）、过氧化物酶体增殖物激活受体-γ共激活因子-1α（PGC-1α）和线粒体转录因子 A（Tfam）。线粒体细胞色素 c 含量升高，质量增加，呼吸增强。SelH 转染改善了超紫外线 B（UVB）诱导的线粒体生物发生标志物的抑制和线粒体膜电位的去极化。SelH 的过表达促进了线粒体生物发生并改善了线粒体功能性能。
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