کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2775547 1152332 2010 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
CXCR4 positive bone mesenchymal stem cells migrate to human endothelial cell stimulated by ox-LDL via SDF-1α/CXCR4 signaling axis
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی بالینی
پیش نمایش صفحه اول مقاله
CXCR4 positive bone mesenchymal stem cells migrate to human endothelial cell stimulated by ox-LDL via SDF-1α/CXCR4 signaling axis
چکیده انگلیسی

BackgroundBone mesenchymal stem cells (BMSCs) are attractive candidates for cell based therapies to cardiovascular disease such as infarction and atherosclerosis; however, the mechanisms responsible for stem cell chemotaxis and homing remain unknown. Chemokine stromal cell-derived factor 1 (SDF-1α) is involved in the process of atherogenesis. This study was aimed at investigating whether the SDF-1α of human umbilical vein endothelial cells (HUVECs) plays a role in migration of BM-derived CXCR4+(receptor for SDF-1α) stem cells.MethodsHUVECs were cultured from human umbilical cords and was treated with ox-LDL. The mRNA and protein expression of SDF-1α was detected in HUVECs. CXCR4+BMSCs from bone marrow were isolated and were tested by migration and adhesion assays.ResultsIt was found that ox-LDL induced HUVECs to increase the mRNA and protein expression of SDF-1α. Ox-LDL increased the migratory and adhesion response of CXCR4+BMSCs. When the neutralizing SDF-1α antibody abrogated the secreted SDF-1α, the migration and adhesion response of CXCR4+BMSCs markedly decreased.ConclusionsOur data indicated that the endothelial cells (ECs) stimulated by ox-LDL could increase the BMSCs migratory response via SDF-1α/CXCR4 signaling axis. These findings provide a new paradigm for biological effects of ox-LDL and have implications for novel stem cell therapeutic strategies for atherosclerosis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental and Molecular Pathology - Volume 88, Issue 2, April 2010, Pages 250–255
نویسندگان
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