Increased cytochrome c in rat cerebrospinal fluid after cardiac arrest and its effects on hypoxic neuronal survival.

Increased cytochrome c in rat cerebrospinal fluid after cardiac arrest and its effects on hypoxic neuronal survival.
复制标题

DOI:
10.1016/j.resuscitation.2012.04.009
复制
发表时间:
2012-12
期刊:
影响因子:
6.5
通讯作者:
Hickey RW
Hickey RW
中科院分区:
医学2区
文献类型:
--
作者:
Liu H;Sarnaik SM;Manole MD;Chen Y;Shinde SN;Li W;Rose M;Alexander H;Chen J;Clark RS;Graham SH;Hickey RW

文献摘要

参考文献

被引文献

相似文献

脑脊液蛋白可能是缺氧缺血性脑损伤后神经元死亡和最终预后的有用生物标志物。细胞色素c已被确定在脑脊液中的儿童创伤性脑损伤。细胞色素c是细胞呼吸所必需的,但它也是细胞凋亡内在途径的核心成分。因此,除了作为生物标志物,细胞色素c释放到CSF中可能对相邻神经元的存活有影响。在这项研究中,我们使用蛋白质印迹和ELISA显示,细胞色素c升高,从小儿大鼠心脏骤停复苏后获得的CSF。使用生物素化的人细胞色素c在培养基中,我们表明,细胞色素c穿过细胞膜,并被纳入线粒体的神经元暴露于缺氧。最后,我们发现,除了人细胞色素c暴露于缺氧的原代神经元培养提高生存。据我们所知,这是第一个研究表明,细胞色素c升高,在CSF缺氧缺血性脑损伤。从原代神经元培养的结果表明,细胞外细胞色素c是能够穿过损伤的神经元的细胞膜,纳入线粒体,并促进缺氧后的生存。
Cerebrospinal fluid (CSF) proteins may be useful biomarkers of neuronal death and ultimate prognosis after hypoxic-ischemic brain injury. Cytochrome c has been identified in the CSF of children following traumatic brain injury. Cytochrome c is required for cellular respiration but it is also a central component of the intrinsic pathway of apoptosis. Thus, in addition to serving as a biomarker, cytochrome c release into CSF may have an effect upon survival of adjacent neurons. In this study, we use Western blot and ELISA to show that cytochrome c is elevated in CSF obtained from pediatric rats following resuscitation from cardiac arrest. Using biotinylated human cytochrome c in culture media we show that cytochrome c crosses the cell membrane and is incorporated into mitochondria of neurons exposed to anoxia. Lastly, we show that addition of human cytochrome c to primary neuronal culture exposed to anoxia improves survival. To our knowledge, this is the first study to show cytochrome c is elevated in CSF following hypoxic ischemic brain injury. Results from primary neuronal culture suggest that extracellular cytochrome c is able to cross the cell membrane of injured neurons, incorporate into mitochondria, and promote survival following anoxia.
DOI: 10.1016/j.nbd.2010.09.020
发表时间: 2011-02
影响因子: 6.1
作者:
Liu, Hao;Li, Wenjin;Ahmad, Muzamil;Miller, Tricia M.;Rose, Marie E.;Poloyac, Samuel M.;Uechi, Guy;Balasubramani, Manimalha;Hickey, Robert W.;Graham, Steven H.
通讯作者: Graham, Steven H.
DOI: 10.1161/01.str.31.10.2325
发表时间: 2000-10-01
期刊: STROKE
影响因子: 8.3
作者:
Vila, N;Castillo, J;Chamorro, A
通讯作者: Chamorro, A
DOI: 10.1182/blood.v98.5.1542
发表时间: 2001-09-01
期刊: BLOOD
影响因子: 20.3
作者:
Renz, A;Berdel, WE;Los, M
通讯作者: Los, M
DOI: 10.1046/j.1365-2249.1997.4621483.x
发表时间: 1997-12-01
影响因子: 4.6
作者:
Tarkowski, E;Rosengren, L;Tarkowski, A
通讯作者: Tarkowski, A
DOI: 10.1038/sj.jcbfm.9600088
发表时间: 2005-07-01
影响因子: 6.3
作者:
Satchell, MA;Lai, YC;Clark, RSB
通讯作者: Clark, RSB