Proliferative Activity of Cadriomyocytes in Chronic Hypercholesterolemia

Лушникова, Е. Л.; Nepomnyashchikh, L. M.; Клинникова, М. Г.; Молодых, О. П.; Yuzhik, E. I.; Nepomnyashchikh, R. D.; Pichigin, V. I.

doi:10.1007/s10517-014-2399-y

Cited by 2 publications

(2 citation statements)

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“…The alterations may act at transcriptional and post-transcriptional levels, and be effectively modulated by natural or synthetic active compounds. In this study, decreased cell proliferation and accelerated senescence in the heart of ApoE –/– mice were noted, which were consistent with the previous research [21]. The coexistence of decreased total number of cardiomyocytes and decreased proliferation marker expression implied that the micro-environmental change induced by hypercholesterolemia weakened the intact proliferative activity of cardiomyocytes.…”

Section: Discussionsupporting

confidence: 92%

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Astragaloside IV Prevents Cardiac Remodeling in the Apolipoprotein E-Deficient Mice by Regulating Cardiac Homeostasis and Oxidative Stress

Ding²,

et al. 2017

Cell Physiol Biochem

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Background: Hypercholesterolemia is a risk factor for the development of cardiac hypertrophy. Astragaloside IV (AST-IV) possesses cardiovascular protective properties. We hypothesize that AST-IV prevents cardiac remodeling with hypercholesterolemia via modulating tissue homeostasis and alleviating oxidative stress. Methods: The ApoE^-/- mice were treated with AST-IV at 1 or 10 mg/kg for 8 weeks. The blood lipids tests, echocardiography, and TUNEL were performed. The mRNA expression profile was detected by real-time PCR. The myocytes size and number, and the expressions of proliferation (ki67), senescence (p16^INK4a), oxidant (NADPH oxidase 4, NOX4) and antioxidant (superoxide dismutase, SOD) were observed by immunofluorescence staining. Results: Neither 1 mg/kg nor 10 mg/kg AST-IV treatment could decrease blood lipids in ApoE^-/- mice. However, the decreased left ventricular ejection fraction (LVEF) and fractional shortening (FS) in ApoE^–/– mice were significantly improved after AST-IV treatment. The cardiac collagen volume fraction declined nearly in half after AST-IV treatment. The enlarged myocyte size was suppressed, and myocyte number was recovered, and the alterations of genes expressions linked to cell cycle, proliferation, senescence, p53-apoptosis pathway and oxidant-antioxidants in the hearts of ApoE^-/- mice were reversed after AST-IV treatment. The decreased ki67 and increased p16^INK4a in the hearts of ApoE^-/- mice were recovered after AST-IV treatment. The percentages of apoptotic myocytes and NOX4-positive cells in AST-IV treated mice were decreased, which were consistent with the gene expressions. Conclusion: AST-IV treatment could prevent cardiac remodeling and recover the impaired ventricular function induced by hypercholesterolemia. The beneficial effect of AST-IV might partly be through regulating cardiac homeostasis and anti-oxidative stress.

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Section: Discussionsupporting

confidence: 92%

“…Cell regeneration, the proliferative activity of cardiomyocytes, is the basis of the heart providing its structural integrity and functional activity [18-21]. Almost all types of heart disease are based on the cardiomyocytes deficiency, which is caused by lower cell regeneration and/or higher cell death (e.g.…”

Section: Introductionmentioning

confidence: 99%