کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8308915 | 1538500 | 2018 | 42 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The IL-6/STAT3 pathway regulates adhesion molecules and cytoskeleton of endothelial cells in thromboangiitis obliterans
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کلمات کلیدی
DAPIP-eNOSp-FAKJanus Kinase 2JAK2eNOSMMP-9FAKGAPDHICAM-1IL-6FITC4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولl-NAME - L-NAMEl-NG-Nitroarginine methyl ester - L-NG-Nitroarginine متیل استرinterleukin-6 - اینترلوکین ۶analysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتmatrix metallopeptidase 9 - ماتریکس متالوپپتیداز 9intercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1focal adhesion kinase - کیناز چسبندگی کانونیglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: The IL-6/STAT3 pathway regulates adhesion molecules and cytoskeleton of endothelial cells in thromboangiitis obliterans The IL-6/STAT3 pathway regulates adhesion molecules and cytoskeleton of endothelial cells in thromboangiitis obliterans](/preview/png/8308915.png)
چکیده انگلیسی
Thromboangiitis obliterans (TAO) (also known as Buerger's disease) is an inflammatory vascular disease that predominantly affects small- and medium-sized blood vessels of extremities. Endothelial cells play critical roles in the initiation and progression of this disease, but the underlying mechanisms remain unclear. In the present study, we demonstrate that patients with TAO had significantly higher levels of interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in their plasmas, and the involved arterial tissues expressed higher levels of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), ICAM-1 and VCAM-1. In exploring the molecular mechanisms with human aortic endothelial cells (HAECs), we found that recombinant IL-6 activated the STAT3 pathway, leading to the upregulation and overproduction of ICAM-1 and VCAM-1. RhoA (Ras homolog family member A), eNOS (endothelial nitric oxide synthase) and MMP-9 (matrix metalloproteinase-9) participated in this cellular signaling, and their interaction regulated the expression of ICAM-1 and VCAM-1. The activated STAT3 pathway by IL-6 also modulated the cytoskeleton of HAECs by regulating phosphorylation of focal adhesion kinase (FAK) and acetylation of α-tubulin through interplaying with RhoA. In summary, the present results indicate that activation of the IL-6/STAT3 pathway contributes to the pathogenesis of TAO by regulating cellular adhesion molecules and cytoskeleton of vascular endothelial cells, suggesting that targeting this pathway may provide a potential approach for the management of TAO.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 44, April 2018, Pages 118-126
Journal: Cellular Signalling - Volume 44, April 2018, Pages 118-126
نویسندگان
Zheng Wei, Wenjing Jiang, Hengzhen Wang, Hali Li, Bo Tang, Bing Liu, Hongchi Jiang, Xueying Sun,