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Abstract
BackgroundMyocardial 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).MethodsMI 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.ResultsOnly 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.ConclusionA 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.
Highlights
Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF)
Microarrays results from heart tissues The microarray data after normalization were subjected to principal component analysis (PCA) analysis to visualize gene expression differences between control and treated animals
From the total 840 transcripts altered in the L-MI group, 814 (553 - upregulated, 261 downregulated) were supported with gene annotations provided by RefSeq, GeneBank or Ensembl
Summary
Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). Left ventricular (LV) remodelling is crucial in the development of heart failure (HF) and is associated with increased mortality after myocardial infarction (MI). It is characterized by complex structural alterations connected with infarct expansion, scar formation, wall thinning, progressive chamber dilation and hypertrophy [1]. LV remodelling involves numerous cellular changes, but is essentially connected with dynamic alterations in the Peripheral blood mononuclear cells (PMBCs), being obtainable, could be used as a proxy to study changes associated with heart diseases. PBMCs contribute to the inflammatory response in the infarcted myocardium and are considered a source of factors crucial in matrix remodelling, such as matrix metalloproteinase 9 [15]
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