Deep hypothermia markedly activates the small ubiquitin-like modifier conjugation pathway; implications for the fate of cells exposed to transient deep hypothermic cardiopulmonary bypass

被引:39
作者
Yang, Wei [1 ]
Ma, Qing [1 ]
Mackensen, G. Burkhard [1 ,2 ]
Paschen, Wulf [1 ,3 ]
机构
[1] Duke Univ, Med Ctr, Dept Anesthesiol, Multidisciplinary Neuroprotect Labs, Durham, NC 27710 USA
[2] Duke Univ, Med Ctr, Dept Anesthesiol, Div Cardiothorac Anesthesiol & Crit Care Med, Durham, NC 27710 USA
[3] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA
关键词
cardiopulmonary bypass; deep hypothermia; gene expression; SUMO conjugation; LEFT-HEART SYNDROME; PROTEIN SUMOYLATION; CIRCULATORY ARREST; ISCHEMIC TOLERANCE; BRAIN TEMPERATURE; INJURY; RAT;
D O I
10.1038/jcbfm.2009.16
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Various cardiovascular operations are performed during conditions of deep hypothermic circulatory arrest. Here we investigated the effects of deep hypothermia on the small ubiquitin-like modifier (SUMO) conjugation pathway using a clinically relevant animal model of deep hypothermic cardiopulmonary bypass (DHCPB). Deep hypothermic cardiopulmonary bypass induced a marked activation of the SUMO conjugation pathway and triggered a nuclear translocation of SUMO2/3-conjugated proteins. Furthermore, DHCBP significantly modified gene expression. Activation of the SUMO conjugation pathway is believed to protect neurons from damage caused by low blood flow. This pathway may, therefore, play a key role in defining the outcome of cells exposed to DHCPB. Journal of Cerebral Blood Flow & Metabolism (2009) 29, 886-890; doi:10.1038/jcbfm.2009.16; published online 25 February 2009
引用
收藏
页码:886 / 890
页数:5
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