Document Detail


Molecular mechanism of c-jun antisense gene transfection in alleviating injury of cardiomyocytes treated with burn serum and hypoxia.
MedLine Citation:
PMID:  15573245     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To explore the molecular mechanism of c-jun antisense gene transfection in alleviating injury of cardiomyocytes treated with burn serum and hypoxia, burn serum was collected from Wistar rats inflicted with 30% third-degree burn of the total body surface area. The cardiomyocytes of neonatal Wistar rats were cultured and then treated with burn serum and hypoxia (a gas mixture containing 1% O2). The constructed c-jun antisense gene recombinant was transfected into the cardiomyocytes of neonatal Wistar rats. TdT-mediated d-utp nick end labeling (TUNEL) was adopted to examine cardiomyocyte apoptosis. Morphological changes of cardiomyocytes were observed under an optic-microscope and an electron-microscope. Expression of troponin T and beta-tubulin protein, c-jun protein, protein kinase Ca (PKCa), and c-jun N-terminal kinase (JNK) were assayed with Western blot in the transfected and non-transfected groups. The morphology of cardiomyocytes in the non-transfected group changed explicitly, but the change was not so obvious in the transfected cardiomyocytes. The expression of beta-tubulin and troponin increased significantly in the transfected group as compared with the non-transfected group. In the non-transfected group, numbers of apoptotic cardiomyocytes were significantly higher than in the transfected group. The c-jun protein, PKCa, and JNK were significantly expressed in the non-transfected group, and they reached a maximum at the 24th hour after cardiomyocytes were treated with burn serum and hypoxia. In the transfected group, however, expressions of c-jun protein, PKCa, and JNK decreased significantly compared with the non-transfected group. The c-jun antisense gene recombinant transfection alleviates injury to cardiomyocytes treated with burn serum and hypoxia, probably through low expression of PKCa and JNK.
Authors:
Yuesheng Huang; Angeng Hu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-09-29
Journal Detail:
Title:  World journal of surgery     Volume:  28     ISSN:  0364-2313     ISO Abbreviation:  World J Surg     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-12-01     Completed Date:  2005-02-08     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7704052     Medline TA:  World J Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  951-7     Citation Subset:  IM    
Affiliation:
Institute of Burn Research, Southwestern Hospital, Third Military Medical University, 400038, Chongqing, People's Republic of China. yshuang@public.cta.cq.cn
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Apoptosis / physiology
Blotting, Western
Cells, Cultured
Genes, jun / genetics*
In Situ Nick-End Labeling
JNK Mitogen-Activated Protein Kinases / metabolism
Myocytes, Cardiac / metabolism*
Proto-Oncogene Proteins c-jun / metabolism
Rats
Rats, Wistar
Signal Transduction / physiology
Transfection*
Troponin T / metabolism
Tubulin / metabolism
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-jun; 0/Troponin T; 0/Tubulin; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases

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


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