Title of article :
ADAM-10 could mediate cleavage of N-cadherin promoting apoptosis in human atherosclerotic lesions leading to vulnerable plaque: A morphological and immunohistochemical study
Author/Authors :
Musumeci، نويسنده , , Giuseppe and Coleman، نويسنده , , Raymond and Imbesi، نويسنده , , Rosa and Magro، نويسنده , , Gaetano and Parenti، نويسنده , , Rosalba and Szychlinska، نويسنده , , Marta Anna and Scuderi، نويسنده , , Rosario and Cinà، نويسنده , , Claudio Salvatore and Castorina، نويسنده , , Sergio and Castrogiovanni، نويسنده , , Paola، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
11
From page :
1148
To page :
1158
Abstract :
Atherosclerosis remains a major cause of mortality. Whereas the histopathological progression of atherosclerotic lesions is well documented, much less is known about the development of unstable or vulnerable plaque, which can rupture leading to thrombus, luminal occlusion and infarct. Apoptosis in the fibrous cap, which is rich in vascular smooth muscle cells (VSMCs) and macrophages, and its subsequent weakening or erosion seems to be an important regulator of plaque stability. The aim of our study was to improve our knowledge on the biological mechanisms that cause plaque instability in order to develop new therapies to maintain atherosclerotic plaque stability and avoid its rupture. In our study, we collected surgical specimens from atherosclerotic plaques in the right or left internal carotid artery of 62 patients with evident clinical symptoms. Histopathology and histochemistry were performed on wax-embedded sections. Immunohistochemical localization of caspase-3, N-cadherin and ADAM-10 was undertaken in order to highlight links between apoptosis, as expressed by caspase-3 immunostaining, and possible roles of N-cadherin, a cell-cell junction protein in VSMCs and macrophages that provides a pro-survival signal reducing apoptosis, and ADAM-10, a “disintegrin and metalloproteases” that is able to cleave N-cadherin in glioblastomas. Our results showed that when apoptosis, expressed by caspase-3 immunostaining, increased in the fibrous cap, rich in VSMCs and macrophages, the expression of N-cadherin decreased. The decreased N-cadherin expression, in turn, was linked to increased ADAM-10 expression. This study shows that apoptotic events are probably involved in the vulnerability of atherosclerotic plaque.
Keywords :
caspase-3 , n-cadherin , Atherosclerotic plaque , Vascular smooth muscle cells. , ADAM-10
Journal title :
Acta Histochemica
Serial Year :
2014
Journal title :
Acta Histochemica
Record number :
1760408
Link To Document :
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