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The effects of apoptosis vulnerability markers on the myocardium in depression after myocardial infarction

Wang, Yiming, Liu, Xingde, Zhang, Dongfeng, Chen, Jianhui, Liu, Shuzheng and Berk, Michael 2013, The effects of apoptosis vulnerability markers on the myocardium in depression after myocardial infarction, BMC medicine, vol. 11, Article 32, pp. 1-9.

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Title The effects of apoptosis vulnerability markers on the myocardium in depression after myocardial infarction
Author(s) Wang, Yiming
Liu, Xingde
Zhang, Dongfeng
Chen, Jianhui
Liu, Shuzheng
Berk, Michael
Journal name BMC medicine
Volume number 11
Season Article 32
Start page 1
End page 9
Total pages 9
Publisher BioMed Central
Place of publication London, England
Publication date 2013
ISSN 1741-7015
Keyword(s) major depressive disorder
myocardial infarction
apoptosis
myocardium
stress
cardiac
comorbidity
Summary Background : There is an increased incidence of major depressive disorder (MDD) in individuals after myocardial infarction (MI), but the pathophysiological processes mediating this association are unclear. Our previous study demonstrated an increase in pro-apoptotic pathways in the myocardium and hippocampus in MDD, which was reversed by venlafaxine. This study aimed to attempt to confirm the effects of apoptosis vulnerability markers on the myocardium in a model of depression after myocardial infarction.

Methods :
Rats were divided into four groups: sham (N = 8), depression (N = 8, chronic mild unpredictable stress and separation were used in the depression group), MI (N = 13) and post-MI depression (N = 7). The rats in all four groups underwent the same open field and sucrose preference behavioral tests. Evan Blue staining was used to determine the area at risk of myocardial infarction in the left ventricle, and 2,3,5-triphenyl tetrazolium chloride (1.5% TTC) dye was used to detect the size of the myocardial infarction. The expression of bax and bcl-2 protein in the myocardium was investigated by immunohistochemistry, and the mRNA expression of bax, bcl-2 and caspase-3 in the myocardium was investigated by real time RT-PCR. Apoptosis was estimated in the myocardium by measuring the Bax:Bcl-2 ratio.

Results :
In the depression and post-MI depression rats, there were significantly decreased movements and total sucrose consumption, modeling behavioral deficits and an anhedonic-like state. In terms of myocardial infarction size, no difference was seen between the MI and post-MI depression groups. There was an up-regulated Bax:Bcl-2 ratio in the depression, MI and post-MI depression groups. Furthermore, in the latter group, there was a greater up-regulated Bax:Bcl-2 ratio. However, caspase-3 did not differ among the four groups.

Conclusions :
These results of this animal model suggest that active pro-apoptotic pathways may be involved in the nexus between myocardial infarction and depression. This mechanism may be germane to understanding this relationship in humans.
Language eng
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2013, BioMed Central
Persistent URL http://hdl.handle.net/10536/DRO/DU:30052831

Document type: Journal Article
Collections: School of Medicine
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.