کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259789 | 1534645 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The flavo-oxidase QSOX1 supports vascular smooth muscle cell migration and proliferation: Evidence for a role in neointima growth
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کلمات کلیدی
HRPPCNAALRPDGFECMbFGFIgGDAB3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide - 3- (4،5-dimethyl-2-thiazolyl) -2،5-difenyl-2H-tetrazolium bromide3,3′-diaminobenzidine - 3،3'-diaminobenzidineERK1/2 - ERK1 / 2MTT - MTTProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیimmunoglobulin G - ایمونوگلوبولین GAugmenter of liver regeneration - تقویت کننده بازسازی کبدplatelet-derived growth factor - فاکتور رشد حاصل از پلاکتbasic fibroblast growth factor - فاکتور رشد فیبروبلاست پایهExtracellular matrix - ماتریکس خارج سلولیHorseradish peroxidase - پراکسیداز هوررادیشextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Quiescin sulfhydryl oxidase 1 (QSOX1) is a flavoenzyme largely present in the extracellular milieu whose physiological functions and substrates are not known. QSOX1 has been implicated in the regulation of tumor cell survival, proliferation and migration, in addition to extracellular matrix (ECM) remodeling. However, data regarding other pathophysiological conditions are still lacking. Arterial injury by balloon catheter is an established model of post-angioplasty restenosis. This technique induces neointima formation due to migration and proliferation of vascular smooth muscle cells (VSMC), followed by ECM synthesis and remodeling. Here, we show that QSOX1 knockdown inhibited VSMC migration and proliferation in vitro. In contrast, QSOX1 overexpression stimulated these processes. While migration could be induced by the incubation of cells with the active recombinant QSOX1, proliferation was induced by addition of the active and also of an inactive mutant QSOX1 protein. The proliferation induced by both recombinants was independent of intracellular hydrogen peroxide and dependent of the MEK/ERK pathway. To recapitulate in vivo VSMC pathophysiology, balloon-induced arterial injury was performed. The expression of QSOX1 in the neointimal layer of balloon-injured rat carotids was high and peaked at 14Â days post-injury. In vivo QSOX1 knockdown led to a significant decrease in PCNA expression at day 14 post-injury and a decreased intima/media area ratio at day 21 post-injury, compared with scrambled siRNA transfection. In summary, our findings demonstrate that QSOX1 induces VSMC migration and proliferation in vitro and contributes to neointima thickening in balloon-injured rat carotids.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 7, July 2015, Pages 1334-1346
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 7, July 2015, Pages 1334-1346
نویسندگان
Beatriz E. Borges, Márcia H. Appel, Axel R. Cofré, Maiara L. Prado, Chelin A. Steclan, Frédéric Esnard, Silvio M. Zanata, Francisco R.M. Laurindo, Lia S. Nakao,