| SDF-1α/CXCR4 axis is involved in glucose-potentiated proliferation and chemotaxis in rat vascular smooth muscle cells. | |
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MedLine Citation:
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PMID: 20586815 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Excessive proliferation of vascular smooth muscle cells (VSMCs), which migrate from the tunica media to the subendothelial region, is one of the primary lesions involved in atherogenesis in diabetes. Here, we investigated whether high glucose potentiated the proliferation and chemotaxis of VSMCs by activating SDF-1α/CXCR4/PI-3K/Akt signalling. The expression of SDF-1α, CXCR4 and PCNA was up-regulated in tunica media of thoracic aortas by streptozotocin-induced hyperglycaemic Sprague-Dawley rats. Exposure of primary VSMCs to high glucose (25 mM) led to the up-regulated expression of SDF-1α and CXCR4, activated PI-3K/Akt signalling, and consequently promoted the proliferation and chemotaxis of VSMCs. Interestingly, the administration of SDF-1 siRNA or neutralizing antibody against SDF-1α abolished high glucose-induced up-regulation of CXCR4. Moreover, pretreatment with SDF-1α neutralizing antibody, CXCR4 specific inhibitor (AMD3100) or PI-3K inhibitor (LY294002) attenuated the high glucose-potentiated proliferation and chemotaxis in VSMCs. These results suggested that high glucose activated the SDF-1α/CXCR4/PI-3K/Akt signalling pathway in VSMCs in an autocrine manner, which enhanced the proliferation and chemotaxis of VSMCs. |
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Authors:
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Wei Jie; Xiaoyan Wang; Yuhong Zhang; Junli Guo; Dong Kuang; Pengcheng Zhu; Guoping Wang; Qilin Ao |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of experimental pathology Volume: 91 ISSN: 1365-2613 ISO Abbreviation: Int J Exp Pathol Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-11-16 Completed Date: 2010-12-17 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 9014042 Medline TA: Int J Exp Pathol Country: England |
Other Details:
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Languages: eng Pagination: 436-44 Citation Subset: IM |
Copyright Information:
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© 2010 The Authors. Journal compilation © 2010 Blackwell Publishing Ltd. |
Affiliation:
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Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aorta / pathology Cell Division / drug effects, physiology Cells, Cultured Chemokine CXCL12 / genetics, metabolism* Chemotaxis / drug effects, physiology* Diabetes Mellitus, Experimental / pathology*, physiopathology Diabetes Mellitus, Type 1 / pathology, physiopathology Diabetic Angiopathies / pathology*, physiopathology Gene Expression / drug effects, physiology Glucose / pharmacology Hyperglycemia / pathology, physiopathology Muscle, Smooth, Vascular / pathology*, physiology Phosphatidylinositol 3-Kinases / metabolism Proto-Oncogene Proteins c-akt / metabolism Rats Rats, Sprague-Dawley Receptors, CXCR4 / genetics, metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Chemokine CXCL12; 0/Cxcr4 protein, rat; 0/Receptors, CXCR4; 50-99-7/Glucose; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
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