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Published on: August 16, 2019
Myocardial gene expression of matched hibernating and control tissue from patients with ischemic left ventricular
Dietlind Zohlnhöfer1, Thomas G Nührenberg, Felix Haas
1Medizinische Klinik und Deutsches Herzzentrum, Technischen Universität München, Munich, Germany. d_zohlnhoefer@yahoo.com
Insights
Researchers identified distinct gene expression patterns in hibernating myocardium (HM) in humans. Key findings include altered expression of genes involved in apoptosis and intercellular communication, notably reduced desmoplakin, offering new insights into HM pathophysiology.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genomics
Background:
- Hibernating myocardium (HM) in humans is poorly understood at the molecular level.
- Ischemic left ventricular dysfunction often involves HM, a state of myocardial dysfunction and remodeling.
- Identifying molecular signatures of HM is crucial for understanding its pathophysiology.
Purpose of the Study:
- To identify gene expression patterns characteristic of human hibernating myocardium.
- To compare gene expression in HM versus normally perfused myocardium in patients with ischemic left ventricular dysfunction.
Main Methods:
- cDNA array analysis of myocardial biopsies from 5 patients with HM and matched controls.
- Validation using gene-specific polymerase chain reaction and immunohistochemical staining for desmoplakin.
Main Results:
- Out of 4171 transcripts, 86 were differentially expressed in HM compared to normal myocardium.
- 65 genes showed decreased expression, and 21 showed increased expression in HM.
- Significant changes observed in genes related to transcription, protein modification, apoptosis, and intercellular communication, including reduced desmoplakin expression at both gene and protein levels.
Conclusions:
- Gene expression analysis reveals novel insights into the molecular changes in human hibernating myocardium.
- Downregulation of desmoplakin suggests impaired intercellular communication may contribute to contractile dysfunction in HM.
- These findings provide a molecular basis for understanding HM and potential therapeutic targets.
Abstract:
Limited data are available in humans regarding the molecular biology of hibernating myocardium (HM). The aim of this study was to identify gene expression patterns distinctive for human HM. We compared in patients with ischemic left ventricular dysfunction the gene expression profile of myocardial biopsies from HM (n = 5), as identified by positron emission tomography, with expression profiles of matched biopsies from normally perfused myocardium by using cDNA array analysis. Gene-specific polymerase chain reaction of selected genes and immunohistochemical staining of desmoplakin were used to validate our technical approach. Of 4171 transcripts examined, we identified 86 to be differentially expressed. Compared to normally perfused myocardium, 21 genes showed an increased expression and 65 genes a decreased expression in HM. Functional clustering revealed changes in the expression of genes associated with transcription, protein modification and phosphorylation, regulation of apoptosis, and intercellular communication. Besides the reported upregulation of beta-adrenergic receptor kinase-1 in heart failure, we observed new gene expression patterns, such as the upregulation of fas-activated serine/threonine kinase (FAST) or reduced expression of desmoplakin. Downregulation of desmoplakin in cardiomyocytes from HM was also seen on the protein level. Gene expression analysis provided novel insights into the pathophysiological changes of HM. Impaired intercellular communication as suggested by decreased expression of desmoplakin may be an important feature of contractile dysfunction in HM.
