Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure

BMC Medical Genomics

Beata Burzynska¹  Monika Gora¹  Agata Maciejak¹  Michal Maczewski²  Urszula Mackiewicz²  Dorota Tulacz¹ 

[1]Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawinskiego 5a, 02-106 Warsaw, Poland

[2]Department of Clinical Physiology, Medical Centre of Postgraduate Education, Marymoncka 99/103, 02-813 Warsaw, Poland

关键词: Tetraspanin 12;    Ceruloplasmin;    Microarrays;    Gene expression profiling;    Extracellular matrix;    Myocardial infarction;    Heart failure;    Left ventricular remodelling;   

Others  :  1091369
DOI  :  10.1186/1755-8794-6-49

 received in 2013-07-26, accepted in 2013-11-01,  发布年份 2013

【 摘 要 】

Background

Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. The aim of this study was to investigate gene expression in the LV and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs).

Methods

MI was induced in rats by ligation of the proximal left coronary artery. Rats with small, moderate, and large MI size were included into the experiment two months after the operation. The development of heart failure was estimated by echocardiography and catheterization. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals.

Results

Only rats with a large MI developed extensive LV remodeling and heart failure. 840 transcripts were altered in LV of failing hearts, and especially numerous were those associated with the extracellular matrix. In contrast, no significant gene expression changes were seen in LVs of rats with moderate or small MI that had compensated LV injury. We showed that ceruloplasmin was similarly overexpressed in the heart and blood in response to HF, whereas downregulation of tetraspanin 12 was significant only in the PBMCs.

Conclusion

A large size of infarcted area is critical for progression of LV remodeling and HF development, associated with altered gene expression in the heart. Ceruloplasmin and tetraspanin 12 are potential convenient markers in readily obtainable PBMCs.

【 授权许可】

   
2013 Tulacz et al.; licensee BioMed Central Ltd.

【 图 表 】

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