Proteomic changes in the brain of the western painted turtle (Chrysemys picta bellii) during exposure to anoxia

被引:12
|
作者
Smith, Richard W. [1 ]
Cash, Phil [2 ]
Hogg, David W. [3 ]
Buck, Leslie T. [3 ]
机构
[1] McMaster Univ, Dept Med Phys & Appl Radiat Sci, Hamilton, ON L8K 2P3, Canada
[2] Univ Aberdeen, Div Appl Med, Aberdeen, Scotland
[3] Univ Toronto, Dept Cellular & Syst Biol, Toronto, ON, Canada
关键词
Animal proteomics; Cognitive function; Glycolytic pathway; Neural degeneration; Neurological repair; Neuronal apoptosis; BLOOD ACID-BASE; PROLONGED SUBMERGENCE; INHIBITS ANGIOGENESIS; METABOLIC DEPRESSION; PROTEIN EXPRESSION; GELSOLIN ACTIVITY; MEDIAL CORTEX; IONIC CHANGES; CRUCIAN CARP; IN-VIVO;
D O I
10.1002/pmic.201300229
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
During anoxia, overall protein synthesis is almost undetectable in the brain of the western painted turtle. The aim of this investigation was to address the question of whether there are alterations to specific proteins by comparing the normoxic and anoxic brain proteomes. Reductions in creatine kinase, hexokinase, glyceraldehyde-3-phosphate dehydrogenase, and pyruvate kinase reflected the reduced production of adenosine triphosphate (ATP) during anoxia while the reduction in transitional endoplasmic reticulum ATPase reflected the conservation of ATP or possibly a decrease in intracellular Ca2+. In terms of neural protection programed cell death 6 interacting protein (PDCD6IP; a protein associated with apoptosis), dihydropyrimidinase-like protein, t-complex protein, and guanine nucleotide protein G((o)) subunit alpha (G(o) alpha; proteins associated with neural degradation and impaired cognitive function) also declined. A decline in actin, gelsolin, and PDCD6IP, together with an increase in tubulin, also provided evidence for the induction of a neurological repair response. Although these proteomic alterations show some similarities with the crucian carp (another anoxia-tolerant species), there are species-specific responses, which supports the theory of no single strategy for anoxia tolerance. These findings also suggest the anoxic turtle brain could be an etiological model for investigating mammalian hypoxic damage and clinical neurological disorders.
引用
收藏
页码:1587 / 1597
页数:11
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