Expression of N-cadherin proteins in myocardial hypertrophy in rats

Mu, Lingmin; Jing, Changqin; Guo, Zhikun

doi:10.3892/etm.2013.1431

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…CDH2 comes from a superfamily of adhesion molecules that mediate Ca 2+ -dependent cell-to-cell adhesion in tissues [48]. In a model of myocardial hypertrophy, CDH2 was postulated as one of the mechanisms that enables the heart to maintain its physical structure and mechanical function by enhancing cell-to-cell contact and membrane connections [49]. Mitochondrial HSPA9 is a chaperone protein in the biogenesis and refolding of mitochondrial iron-sulfur proteins; it may also have a role in cell proliferation and cellular aging [46].…”

Section: Oxidative Stress (Hf Vs Con Diet): Supplemental Tablementioning

confidence: 99%

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression

et al. 2020

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The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks (n = 10/group). At sacrifice, left ventricles were either frozen or preserved in formalin. Serum was stored for glucose and insulin measurements. Protein spectra was obtained using an Orbitrap analyzer, processed with Sequest and fold changes assessed with Scaffold Q +. Treatment effects for body weights, glucose and insulin were assessed using one-way ANOVA, and the differential protein expression was assessed by a Mann–Whitney U test. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes identified pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and also quantified; differences were identified using Chi-square analyses and Mann-Whitney U tests. HF diet fed rats were significantly (p < 0.05) heavier than CON, and 23 proteins involved in mitochondrial function and lipid metabolism were differentially expressed between HF and CON. Between HF-FOS and HF, 117 proteins involved in contractility, lipid and carbohydrate metabolism were differentially expressed. HF cardiomyocytes were significantly (p < 0.05) more hypertrophic than CON. We conclude that high-fat feeding and FOS are associated with subcellular deviations in cardiac metabolism and contractility, which may influence myocardial function and alter the risk of cardiovascular disease.

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Section: Oxidative Stress (Hf Vs Con Diet): Supplemental Tablementioning

confidence: 99%

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression

et al. 2020

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“…The expression of adhesion molecules including CD11a, CD11b and CD11c was increased in rats with myocardial hypertrophy. 115 Walsh reported that the inhibition of stress-induced activin A/Smad2 signalling triggered the expression of follistatin-like in hypertrophied cardiac myocytes. 116 Follistatin-like 3 is a stress-induced regulator of cardiac hypertrophy and may regulate myocyte size via Smad signalling.…”

Section: Other Moleculesmentioning

confidence: 99%

Molecular biomarkers in cardiac hypertrophy

Zhu

Liu

et al. 2019

J Cellular Molecular Medi

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Cardiac hypertrophy is characterized by an increase in myocyte size in the absence of cell division. This condition is thought to be an adaptive response to cardiac wall stress resulting from the enhanced cardiac afterload. The pathogenesis of heart dysfunction, which is one of the primary causes of morbidity and mortality in elderly people, is often associated with myocardial remodelling caused by cardiac hypertrophy. In order to well understand the potential mechanisms, we described the molecules involved in the development and progression of myocardial hypertrophy. Increasing evidence has indicated that micro‐RNAs are involved in the pathogenesis of cardiac hypertrophy. In addition, molecular biomarkers including vascular endothelial growth factor B, NAD‐dependent deacetylase sirtuin‐3, growth/differentiation factor 15 and glycoprotein 130, also play important roles in the development of myocardial hypertrophy. Knowing the regulatory mechanisms of these biomarkers in the heart may help identify new molecular targets for the treatment of cardiac hypertrophy.

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Expression of N-cadherin proteins in myocardial hypertrophy in rats

Cited by 2 publications

References 24 publications

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression

Effects of High-Fat Diet Induced Obesity and Fructooligosaccharide Supplementation on Cardiac Protein Expression

Molecular biomarkers in cardiac hypertrophy

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