Role of bcl-2 transcriptional regulation induced by calmodulin I pressure overload rat hypertrophic hearts.
- Author:
Qi ZHOU
1
;
Ying-Bin XIAO
;
Jian LIU
;
Pei-Yong WANG
;
Lin CHEN
;
Qian-Jin ZHONG
;
Xue-Feng WANG
Author Information
1. Department of Cardiovascular Surgery, Xinqiao Hospital, Chongqing 400037, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta, Abdominal;
pathology;
Calmodulin;
physiology;
Cardiomegaly;
metabolism;
physiopathology;
Constriction;
Cyclic AMP Response Element-Binding Protein;
genetics;
metabolism;
Male;
Phosphorylation;
Proto-Oncogene Proteins c-bcl-2;
genetics;
metabolism;
RNA, Messenger;
genetics;
metabolism;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2005;57(6):731-736
- CountryChina
- Language:Chinese
-
Abstract:
This study was designed to evaluate the role of bcl-2 transcriptional regulation induced by calmodulin I (CaM I) in pressure overload rat hypertrophic hearts. The model of hypertensive Sprague-Dawley rat was established by abdominal aortic constriction. The hearts were collected four weeks after abdominal aortic constriction. Velocity and isopyknic gradient centrifugation was employed to fractionate rat myocardial nuclei. Western blot analysis revealed a marked increase in phosphorylated cAMP response-element binding protein (pCREB) of cardiac hypertrophy group compared with that in control group (P<0.05), while the protein level of cAMP response-element binding protein (CREB) was constant (P>0.05). Immunohistochemistry results showed a significant increase of CaM I protein in cardiac hypertrophy group relative to the control group (P<0.05). Nuclear run off transcription assay displayed a significant increase in bcl-2 mRNA treated with trifluoperazne compared with non-drug treatment (P<0.05). The results obtained suggest that the transcription of bcl-2 is possibly regulated by CaM I hypertrophic rat hearts, and CREB phosphorylation seems to be a minor factor in bcl-2 transcriptional regulation.
