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毕研文教授指导博士生岳韦明、何晓鹏发表SCI论著各1篇

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   我科毕研文教授指导的博士研究生岳韦明、何晓鹏在国外著名杂志Stem Cells and Development(影响因子 3.9) 和Transplant Proc.各发表论著1篇,并被SCI收录,链接分别为:http://www.liebertonline.com/doi/abs/10.1089/scd.2007.0243 和http://www.ncbi.nlm.nih.gov/sites.nentrez
 
  Stem Cells and Development
  Mesenchymal Stem Cells Differentiate into an Endothelial Phenotype, Reduce Neointimal Formation, and Enhance Endothelial Function in a Rat Vein Grafting Model
Wei-Ming Yue, Wei Liu, Yan-Wen Bi, Xiao-Peng He, Wen-Yu Sun, Xin-Yan Pang, Xing-Hua Gu, Xue-Ping Wang. Stem Cells and Development.
  Autologous vein grafts are still commonly used for arterial reconstructive procedures. Their success is limited by the development of neointimal hyperplasia. Clinical and experimental evidence suggest that the bone marrow–derived mesenchymal stem cells (MSC) participate in the neovascularization. The current study used a direct approach to test the hypothesis that, after vein grafting in a rat model, MSCs have potential effects on re-endothelialization and neointimal formation. MSCs were isolated by bone marrow cell adherence. An autologously interpositioning of the left external jugular vein (LEJV) to the left common carotid artery-induced vein grafting model of rat was utilized. Vascular lesion formation after transplantation of MSCs labeled with 4",6-diamidino-2-phenylindole (DAPI) was investigated. Two weeks after implantation, immunofluorescence studies revealed that engrafted cells acquired an endothelial phenotype, and some expressed endothelial nitric oxide synthase (eNOS). Furthermore, proliferation of cells and neointimal formation decreased significantly after MSC implantation. Real-time reverse transcription-PCR and Western blot analysis showed a rise of eNOS expression in the MSC group compared with the vein grafting group. Therefore, engrafted MSCs appeared to differentiate into endothelial cells, diminish the neointimal formation, and contribute to the improvement of endothelial function, which indicates that MSCs may exert an important function as repair mechanism in vascular injury after vein grafting.

  Transplant Proc. 2008 Jun;40(5):1722-6. Links
  The proteasome inhibitor bortezomib inhibits intimal hyperplasia of autologous vein grafting in rat model.
He XP, Li XX, Bi YW, Yue WM, Sun WY, Pang XY, Gu XH.
Department of Cardiovascular Surgery, Qi Lu Hospital of Shandong University, Jinan, Shandong Province, China.
  OBJECTIVE: Increasing evidence indicates that inflammation plays an important role in intimal hyperplasia (IH) induced by autologous vein grafts. The proteasome inhibitor bortezomib shows anti-inflammatory effects, so we used an autologous vein transplantation model to test whether bortezomib inhibits neointimal formation in transplant-induced vasculopathy. MATERIALS AND METHODS: We subjected 88 rats to autologous external jugular vein grafting surgery randomly assigned to be treated with bortezomib or vehicle. After 24 or 72 hours, rats were humanely killed and vein grafts processed for real-time RT-PCR (24 and 72 hours), ELISA (24 hours), or neutrophil chemotaxis assay (24 hours). Subsequently, rats were humanely killed at 1 and 2 weeks after grafting with samples processed for morphometric analysis. RESULTS: Bortezomib significantly inhibited IH at 2 weeks compared with untreated controls (P < .05). Expression of mRNA for vascular cell adhesion molecule-1, intercellular adhesion molecule-1, cytokine-induced neutrophil chemoattractant 2beta, monocyte chemoattractant-1, interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha markedly increased in injured vessels during the first day after surgery declining over the following 3 days. Bortezomib significantly attenuated gene expression and protein levels of most inflammatory mediators (P < .05), simultaneously inhibiting neutrophil chemotactic activity of vessel homogenates. CONCLUSIONS: Bortezomib inhibited neointimal formation at least partially by attenuating the inflammatory response in transplant-induced vasculopathy. It may become a novel vasoprotective agent in the clinical field.
PMID: 18589180 [PubMed - indexed for MEDLINE]http://www.liebertonline.com/doi/abs/10.1089/scd.2007.0243http://www.ncbi.nlm.nih.gov/sites.nentrez

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