The heart is characterized by a remarkable degree of heterogeneity. Since different cardiac pathologies affect different cardiac regions, it is important to understand molecular mechanisms by which these parts respond to pathological stimuli. In addition to already described left ventricular (LV)/right ventricular (RV) and transmural differences, possible baso-apical heterogeneity has to be taken into consideration. The aim of our study has been, therefore, to compare proteomes in the apical and basal parts of the rat RV and LV. Two-dimensional electrophoresis was used for the proteomic analysis. The major result of this study has revealed for the first time significant baso-apical differences in concentration of several proteins, both in the LV and RV. As far as the LV is concerned, five proteins had higher concentration in the apical compared to basal part of the ventricle. Three of them are mitochondrial and belong to the "metabolism and energy pathways" (myofibrillar creatine kinase M-type, L-lactate dehydrogenase, dihydrolipoamide dehydrogenase). Myosin light chain 3 is a contractile protein and HSP60 belongs to heat shock proteins. In the RV, higher concentration in the apical part was observed in two mitochondrial proteins (creatine kinase S-type and proton pumping NADH:ubiquinone oxidoreductase). The described changes were more pronounced in the LV, which is subjected to higher workload. However, in both chambers was the concentration of proteins markedly higher in the apical than that in basal part, which corresponds to the higher energetic demand and contractile activity of these segments of both ventricles.

• Keywords
• Heart, Myocardial heterogeneity, Proteomics, Two-dimensional electrophoresis, Ventricle, Ventricular myocardium,
• MeSH
• Electrophoresis, Gel, Two-Dimensional MeSH
• Chaperonin 60 metabolism   MeSH
• Chromatography, Liquid MeSH
• Dihydrolipoamide Dehydrogenase metabolism   MeSH
• Energy Metabolism MeSH
• Creatine Kinase, MM Form metabolism   MeSH
• L-Lactate Dehydrogenase metabolism   MeSH
• Myosin Light Chains metabolism   MeSH
• Mitochondrial Proteins metabolism   MeSH
• Rats, Wistar MeSH
• Proteomics * MeSH
• Electron Transport Complex I metabolism   MeSH
• Heart Ventricles enzymology   metabolism   MeSH
• Muscle Proteins isolation & purification   metabolism   MeSH
• Tandem Mass Spectrometry MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Chaperonin 60 MeSH
• Dihydrolipoamide Dehydrogenase MeSH
• Hspd1 protein, rat MeSH Browser
• Creatine Kinase, MM Form MeSH
• L-Lactate Dehydrogenase MeSH
• Myosin Light Chains MeSH
• Mitochondrial Proteins MeSH
• Electron Transport Complex I MeSH
• Muscle Proteins MeSH

Regulation of organ growth is critical during embryogenesis. At the cellular level, mechanisms controlling the size of individual embryonic organs include cell proliferation, differentiation, migration, and attrition through cell death. All these mechanisms play a role in cardiac morphogenesis, but experimental studies have shown that the major determinant of cardiac size during prenatal development is myocyte proliferation. As this proliferative capacity becomes severely restricted after birth, the number of cell divisions that occur during embryogenesis limits the growth potential of the postnatal heart. We summarize here current knowledge concerning regional control of myocyte proliferation as related to cardiac morphogenesis and dysmorphogenesis. There are significant spatial and temporal differences in rates of cell division, peaking during the preseptation period and then gradually decreasing toward birth. Analysis of regional rates of proliferation helps to explain the mechanics of ventricular septation, chamber morphogenesis, and the development of the cardiac conduction system. Proliferation rates are influenced by hemodynamic loading, and transduced by autocrine and paracrine signaling by means of growth factors. Understanding the biological response of the developing heart to such factors and physical forces will further our progress in engineering artificial myocardial tissues for heart repair and designing optimal treatment strategies for congenital heart disease.

• MeSH
• Models, Biological MeSH
• Cell Differentiation genetics   MeSH
• Myocytes, Cardiac metabolism   physiology   MeSH
• Humans MeSH
• Morphogenesis genetics   physiology   MeSH
• Myocardium metabolism   MeSH
• Cell Proliferation * MeSH
• Heart embryology   growth & development   MeSH
• Gene Expression Regulation, Developmental MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Research Support, N.I.H., Extramural MeSH