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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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[CHARACTERISTIC OF APOPTOSIS OF CORONARY ARTERY CELLS WITH ATHEROSCLEROTIC LESIONS].

T E Vladimirskaya, I A Shved

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    PubMed
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    Early atherosclerosis involves significant cell death (apoptosis) in coronary arteries. This apoptosis decreases as atherosclerosis progresses, with smooth muscle cell apoptosis linked to lesion thickness.

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    Area of Science:

    • Cardiovascular Biology
    • Cellular Pathology
    • Atherosclerosis Research

    Background:

    • Atherosclerosis is a chronic inflammatory disease characterized by plaque buildup in arteries.
    • Understanding early cellular events, like apoptosis, is crucial for developing interventions.
    • Endothelial cells (EC), macrophages (MF), and smooth muscle cells (SMC) are key players in atherogenesis.

    Purpose of the Study:

    • To investigate apoptosis in EC, MF, and SMC during early atherosclerosis.
    • To elucidate the mechanisms driving apoptosis in these cells.
    • To assess the impact of apoptosis on atherosclerosis progression.

    Main Methods:

    • Histopathological analysis of human coronary arteries (n=63) from deceased patients.
    • TUNEL assay to quantify the apoptotic index (AI).
    • Immunohistochemistry to detect active caspase-3 (AC-3) and apoptosis-inducing factor (AIF), and to phenotype cells.

    Main Results:

    • Apoptotic index (AI) was significantly higher in atherosclerotic coronary arteries compared to unaffected vessels.
    • AI of SMC and EC decreased with disease progression.
    • A moderate inverse correlation was found between SMC AI and neointimal thickness (r=-0.44, p<0.0001).
    • AC-positive SMC and EC were significantly higher in lipoidosis than liposclerosis stages.
    • AIF expression was noted in EC nuclei within hyperplastic intima.

    Conclusions:

    • Early atherosclerotic lesions exhibit high rates of EC, MF, and SMC apoptosis.
    • Apoptosis intensity in SMC and EC declines as atherosclerosis advances.
    • Intimal hyperplasia progression correlates with reduced SMC apoptosis and increased MF apoptosis.
    • SMC and MF apoptosis are caspase-dependent.
    • EC apoptosis can be caspase-dependent or independent (involving AIF).