PMID: 9417747Aug 1, 1997Paper

Decreased apoptosis as a pathogenic factor in intimal hyperplasia of human arteriosclerosis lesions

Zeitschrift für Kardiologie
G BauriedelB Lüderitz

Abstract

Restenosis remains a persistent problem following intravascular reconstruction. Smooth muscle cell proliferation, extracellular matrix production and remodeling are accepted mechanisms of restenotic lesion formation. Decreased programmed cell death (apoptosis) may also contribute to restenosis by prolonging the life span of intimal cells, with their subsequent accumulation and development of hyperplastic lesions. The objectives of the present study were as follows: i) to identify cell death, ii) to distinguish and quantify apoptosis from necrosis, and iii) to compare restenotic with primary lesions. To this end, human atherectomy specimens from 25 primary and 14 restenotic coronary and peripheral lesions were studied by TUNEL test (TdT-mediated dUTP Nick End Labeling; detection of cell death by the presence of fragmented DNA), transmission electron microscopy and morphometric analysis. Intimal hyperplasia was more consistent with restenosis than with primary lesion origin, and was mainly attributed to increased smooth muscle cell density (649 vs. 219 cells/mm2; p < 0.001). The main finding of the present study is that hypercellular restenotic tissue contains fewer TUNEL+ cells than hypocellular plaques (14% vs. 27%; p < 0.05). ...Continue Reading

Related Concepts

Related Feeds

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis