The present study was undertaken in order to advance our earlier studies directed to define genetic risk of atherosclerotic vascular lesion development on a base on the analysis of sets of mutational load relevant to the mitochondrial genome mutations. A comparative evaluation of the two study participants' populations (that included coronary heart disease (CHD) patients who underwent myocardial infarction and apparently healthy donors with no clinical manifestations of coronary heart disease) on heteroplasmy levels of nine mutations of the mitochondrial genome (A1555G, C3256T, T3336C, С5178А, G12315A, G13513A, G14459A, G14846А and G15059A) that were shown previously to be associated with risk factors for atherosclerosis was performed. Close associations with the risk of cardiovascular disease were confirmed for mutation C3256T (gene MT-TL1), G12315A (gene MT-TL2), G13513A (gene MT-ND5) and G15059A (gene MT-CYB) by RT-PCR.
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Analysis of mitochondrial DNA heteroplasmic mutations A1555G, C3256T, T3336C, С5178А, G12315A, G13513A, G14459A, G14846А and G15059A in CHD patients with the history of myocardial infarction.
Exp Mol Pathol
February 2016
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russian Federation; Institute for Atherosclerosis Research, Skolkovo Innovative Centre, Moscow Region, Russian Federation; Department of Biophysics, Biological Faculty, Moscow State University, Moscow, Russian Federation.
The present study was undertaken in order to advance our earlier studies directed to define genetic risk of atherosclerotic vascular lesion development on a base on the analysis of sets of mutational load relevant to the mitochondrial genome mutations. A comparative evaluation of the two study participants' populations (that included coronary heart disease (CHD) patients who underwent myocardial infarction and apparently healthy donors with no clinical manifestations of coronary heart disease) on heteroplasmy levels of nine mutations of the mitochondrial genome (A1555G, C3256T, T3336C, С5178А, G12315A, G13513A, G14459A, G14846А and G15059A) that were shown previously to be associated with risk factors for atherosclerosis was performed. Close associations with the risk of cardiovascular disease were confirmed for mutation C3256T (gene MT-TL1), G12315A (gene MT-TL2), G13513A (gene MT-ND5) and G15059A (gene MT-CYB) by RT-PCR.
View Article and Find Full Text PDF[Association of mitochondrial genome mutations with lipofibrous plaques in human aortic intima].
Patol Fiziol Eksp Ter
August 2015
Atherosclerosis is a basis of development for many cardiovascular diseases, which are leading causes of death among people in the 21-st century. One of possible causes of atherosclerosis may be somatic mutations of human mitochondrial genome. In order to identify mutations associated with atherosclerosis, we analyzed 42 mitochondrial mutations found in various pathologies.
View Article and Find Full Text PDFMosaicism of mitochondrial genetic variation in atherosclerotic lesions of the human aorta.
Biomed Res Int
December 2015
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, Moscow 125315, Russia ; Institute for Atherosclerosis Research, Skolkovo Innovation Centre, Moscow 121552, Russia.
Objective: The aim of the present study was an analysis of heteroplasmy level in mitochondrial mutations 652delG, A1555G, C3256T, T3336C, 652insG, C5178A, G12315A, G13513A, G14459A, G14846A, and G15059A in normal and affected by atherosclerosis segments of morphologically mapped aortic walls.
Methods: We investigated the 265 normal and atherosclerotic tissue sections of 5 human aortas. Intima of every aorta was divided according to morphological characteristics into segments with different types of atherosclerotic lesions: fibrous plaque, lipofibrous plaque, primary atherosclerotic lesion (fatty streak and fatty infiltration), and normal intima from human aorta.
Changes of mitochondria in atherosclerosis: possible determinant in the pathogenesis of the disease.
Atherosclerosis
April 2013
Russian Cardiology Research and Production Complex, 121552 Moscow, Russia.
Electron-microscopic analysis of atherosclerotic lesions demonstrated a high variability in the ultrastructural appearance of mitochondria in human aortic atherosclerotic lesions compared with the appearance of mitochondria in the normal parts of the aortic intima. This prompted us to suggest that the structural variations in the appearance of mitochondria might reflect the existence of somatic mutations in the human mitochondrial genome which could be a determinant of atherosclerosis. To test this hypothesis, we have compared the levels of heteroplasmy for several mitochondrial mutations previously proposed to be associated with different types of atherosclerotic lesions.
View Article and Find Full Text PDFMitochondrial mutations are associated with atherosclerotic lesions in the human aorta.
Clin Dev Immunol
January 2013
Russian Cardiology Research and Production Complex, 121552 Moscow, Russia.
Somatic mutations of the human mitochondrial genome can be a possible determinant of atherosclerosis. To test this possibility, forty mitochondrial mutations were analyzed in the present study in order to see which of these mutations might be associated with atherosclerosis. Ten mitochondrial mutations belonging to mitochondrial genes MT-RNR1 (rRNA 12S); MT-TL1 (tRNA-Leu, recognizes UUR); MT-TL2 (tRNA-Leu, recognizes CUN); MT-ND1, MT-ND2, MT-ND5, and MT-ND6 (subunits 1, 2, 5, and 6, respectively, of NADH dehydrogenase); and MT-CYB (cytochrome b) were potentially associated with atherosclerosis.
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