Document Detail

Mechanisms of neuroprotection from hypoxia-ischemia (HI) brain injury by up-regulation of cytoglobin (CYGB) in a neonatal rat model.
MedLine Citation:
PMID:  23585565     Owner:  NLM     Status:  MEDLINE    
This study was designed to investigate the expression profile of CYGB, its potential neuroprotective function, and underlying molecular mechanisms using a model of neonatal hypoxia-ischemia (HI) brain injury. Cygb mRNA and protein expression were evaluated within the first 36 h after the HI model was induced using RT-PCR and Western blotting. Cygb mRNA expression was increased at 18 h in a time-dependent manner, and its level of protein expression increased progressively in 24 h. To verify the neuroprotective effect of CYGB, a gene transfection technique was employed. Cygb cDNA and shRNA delivery adenovirus systems were established (Cygb-cDNA-ADV and Cygb-shRNA-ADV, respectively) and injected into the brains of 3-day-old rats 4 days before they were induced with HI treatment. Rats from different groups were euthanized 24 h post-HI, and brain samples were harvested. 2,3,5-Triphenyltetrazolium chloride, TUNEL, and Nissl staining indicated that an up-regulation of CYGB resulted in reduced acute brain injury. The superoxide dismutase level was found to be dependent on expression of CYGB. The Morris water maze test in 28-day-old rats demonstrated that CYGB expression was associated with improvement of long term cognitive impairment. Studies also demonstrated that CYGB can up-regulate mRNA and protein levels of VEGF and increase both the density and diameter of the microvessels but inhibits activation of caspase-2 and -3. Thus, this is the first in vivo study focusing on the neuroprotective role of CYGB. The reduction of neonatal HI injury by CYGB may be due in part to antioxidant and antiapoptotic mechanisms and by promoting angiogenesis.
Shu-Feng Tian; Han-Hua Yang; Dan-Ping Xiao; Yue-Jun Huang; Gu-Yu He; Hai-Ran Ma; Fang Xia; Xue-Chuan Shi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-04-12
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  288     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-06-04     Completed Date:  2013-08-06     Revised Date:  2014-06-03    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  15988-6003     Citation Subset:  IM    
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MeSH Terms
Acute Disease
Animals, Newborn
Antioxidants / metabolism
Apoptosis / genetics
Brain Injuries / genetics,  metabolism*,  pathology,  physiopathology,  therapy
Brain Ischemia / genetics,  metabolism*,  pathology,  physiopathology,  therapy
Caspase 3 / genetics,  metabolism
Cerebrovascular Circulation / genetics
Cysteine Endopeptidases / genetics,  metabolism
Globins / biosynthesis*,  genetics
Maze Learning
Neovascularization, Physiologic / genetics
Nerve Tissue Proteins / genetics,  metabolism*
RNA, Messenger / biosynthesis,  genetics
Rats, Sprague-Dawley
Time Factors
Transduction, Genetic
Vascular Endothelial Growth Factor A / biosynthesis,  genetics
Reg. No./Substance:
0/Antioxidants; 0/Nerve Tissue Proteins; 0/RNA, Messenger; 0/Vascular Endothelial Growth Factor A; 0/cytoglobin; 0/vascular endothelial growth factor A, rat; 9004-22-2/Globins; EC 3.4.22.-/Casp2 protein, rat; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Cysteine Endopeptidases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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