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

Tulacz D, Mackiewicz U, Maczewski M, Maciejak A, Gora M, Burzynska B - BMC Med Genomics (2013)

Bottom Line: Rats with small, moderate, and large MI size were included into the experiment two months after the operation.In contrast, no significant gene expression changes were seen in LVs of rats with moderate or small MI that had compensated LV injury.Ceruloplasmin and tetraspanin 12 are potential convenient markers in readily obtainable PBMCs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawinskiego 5a, 02-106 Warsaw, Poland. mgora@ibb.waw.pl.

ABSTRACT

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.

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Principal component analysis of left ventricular gene expression profiles. PCA plot shows the first three principal components of microarray data in respect to their correlation. Sham - sham-operated; S-MI - small-size infarction; M-MI - moderate-size infarction; L-MI - large-size infarction.
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Figure 1: Principal component analysis of left ventricular gene expression profiles. PCA plot shows the first three principal components of microarray data in respect to their correlation. Sham - sham-operated; S-MI - small-size infarction; M-MI - moderate-size infarction; L-MI - large-size infarction.

Mentions: The microarray data after normalization were subjected to PCA analysis to visualize gene expression differences between control and treated animals. The PCA plot (FigureĀ 1) demonstrates a distinct separation between sham-operated rats and rats with L-MI in contrast to animals with S-MI and M-MI, which clustered together with the sham group.


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

Tulacz D, Mackiewicz U, Maczewski M, Maciejak A, Gora M, Burzynska B - BMC Med Genomics (2013)

Principal component analysis of left ventricular gene expression profiles. PCA plot shows the first three principal components of microarray data in respect to their correlation. Sham - sham-operated; S-MI - small-size infarction; M-MI - moderate-size infarction; L-MI - large-size infarction.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4226214&req=5

Figure 1: Principal component analysis of left ventricular gene expression profiles. PCA plot shows the first three principal components of microarray data in respect to their correlation. Sham - sham-operated; S-MI - small-size infarction; M-MI - moderate-size infarction; L-MI - large-size infarction.
Mentions: The microarray data after normalization were subjected to PCA analysis to visualize gene expression differences between control and treated animals. The PCA plot (FigureĀ 1) demonstrates a distinct separation between sham-operated rats and rats with L-MI in contrast to animals with S-MI and M-MI, which clustered together with the sham group.

Bottom Line: Rats with small, moderate, and large MI size were included into the experiment two months after the operation.In contrast, no significant gene expression changes were seen in LVs of rats with moderate or small MI that had compensated LV injury.Ceruloplasmin and tetraspanin 12 are potential convenient markers in readily obtainable PBMCs.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Biochemistry and Biophysics Polish Academy of Sciences, Pawinskiego 5a, 02-106 Warsaw, Poland. mgora@ibb.waw.pl.

ABSTRACT

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.

Show MeSH
Related in: MedlinePlus