کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5937519 | 1573408 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Apoptosis Signal-Regulating Kinase 1 Deficiency Attenuates Vascular Injury-Induced Neointimal Hyperplasia by Suppressing Apoptosis in Smooth Muscle Cells
ترجمه فارسی عنوان
کمبود کیناز 1 تنظیم کننده سیگنال آپوپتوز باعث کاهش هیپرپلازی نئوئیستمی ناشی از آسیب عروقی توسط سرکوب آپوپتوز در سلول های عضلانی صاف
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موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
چکیده انگلیسی
Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that plays a crucial role in stress-induced apoptosis. Recently, we have reported that suppressed macrophage apoptosis in ASK1 and apolipoprotein E double-knockout mice accelerates atheromatous plaques in the hyperlipidemia-induced atherosclerotic model. However, the pathogenic role of smooth muscle cell (SMC) apoptosis in atherosclerosis still remains unclear. We investigated neointimal remodeling in ligated carotid arteries of ASK1-deficient mice (ASK1â/â) for 3 weeks. ASK1â/â mice had significantly more suppressed intimal formation, inversely manifesting as potential anti-atherogenic aspects of ASK1 deficiency, characterized by fewer SMCs and less collagen synthesis; and fewer apoptotic SMCs, infiltrating T lymphocytes, and microvessels, associated with decreased apoptosis of luminal endothelial cells, compared with those of wild-type mice. Injured arteries of ASK1â/â mice also showed significantly down-regulated expression of pro-apoptotic markers, adhesion molecules, and pro-inflammatory signaling factors. Moreover, tumor necrosis factor-α-induced apoptosis was markedly suppressed in cultured aortic SMCs from ASK1â/â mice. These findings suggest that ASK1 accelerates mechanical injury-induced vascular remodeling with activated SMC migration via increased neovascularization and/or enhanced SMC and endothelial cell apoptosis. ASK1 expression, especially in the SMCs, might be crucial, and reciprocally responsible for various pro-atherogenic functions, and SMC apoptosis seems to be detrimental in this model.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The American Journal of Pathology - Volume 182, Issue 2, February 2013, Pages 597-609
Journal: The American Journal of Pathology - Volume 182, Issue 2, February 2013, Pages 597-609
نویسندگان
Takashi Tasaki, Sohsuke Yamada, Xin Guo, Akihide Tanimoto, Ke-Yong Wang, Atsunori Nabeshima, Shohei Kitada, Hirotsugu Noguchi, Satoshi Kimura, Shohei Shimajiri, Kimitoshi Kohno, Hidenori Ichijo, Yasuyuki Sasaguri,