Dan Yang

Publications (2)4.81 Total impact

• Source

  Available from: ccmu.edu.cn

  Article: Epigallocatechin gallate inhibits angiotensin II-induced endothelial barrier dysfunction via inhibition of the p38 MAPK/HSP27 pathway.

  Dan Yang, Jing Liu, Cui Tian, Yong Zeng, Yue-hong Zheng, Quan Fang, Hui-hua Li
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  ABSTRACT: To investigate the effect of epigallocatechin gallate (EGCG) on angiotensin II (Ang II)-induced stress fiber formation and hyperpermeability in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were treated with Ang II in the absence or presence of EGCG or mitogen-activated protein kinases (MAPKs) inhibitors. The resulting stress fibers were stained with rhodamine-phalloidin and examined using confocal microscopy. The permeability of the endothelium was tested with fluorescein-isothiocyanate labeled bovine serum albumin (FITC-BSA), and the phosphorylation levels of several proteins were determined using Western blot analysis. Ang II (1-100 nmol/L) treatment markedly provoked stress fiber formation and hyperpermeability in HUVECs in a time- and dose-dependent manner. These effects were abolished by pretreatment with the p38 MAPK inhibitor SB203580 10 μmol/L, indicating that the Ang II-induced endothelial barrier dysfunction was via activation of the p38 MAPK/HSP27 pathway. Furthermore, treatment with EGCG (5-25) μmol/L inhibited Ang II-induced activation of the p38 MAPK/HSP27 pathway, thereby reducing endothelial stress fiber formation and hyperpermeability. Our data demonstrate that EGCG inhibits Ang II-induced endothelial stress fiber formation and hyperpermeability via inactivation of p38 MAPK/HSP27 pathway, and suggest that EGCG may protect against endothelial barrier dysfunction and injury.
  Acta Pharmacologica Sinica 10/2010; 31(10):1401-6. · 1.95 Impact Factor
• Source

  Available from: ccmu.edu.cn

  Article: Transcriptomic analysis of mild hypothermia-dependent alterations during endothelial reperfusion injury.

  Dan Yang, Yong Zeng, Cui Tian, Jing Liu, Shu-Bin Guo, Yue-Hong Zheng, Hui-Hua Li
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  ABSTRACT: Background: Mild hypothermia (32-34 degrees C) improves resistance to ischemia-reperfusion (I/R) injury. However, the mechanisms by which it affects human cellular function are not fully elucidated. To further test for hypothermic modulation of global biological processes, we used DNA microarray technique to detect the overall gene expression profile. Methods: Human umbilical endothelial cells (HUVECs) were incubated under control condition (37 degrees C) or mild hypothermia (33 degrees C) for 2 hours after stimulated ischemia. Detection of differentially expressed genes was performed with Affymetrix U133 plus 2.0 arrays and PARTEK software. We used DAVID and KEGG Pathways database to identify global trends in gene expression data. Results: Our analysis has identified numerous interesting genes and processes that are differentially presented in hypothermic group when compared with normothermic control. The cell cycle was the most prominent process; several genes involved in cell apoptosis and proliferation displayed significantly differential expression; lower transcriptional level was observed for genes involved in chemokine and cell adhesion processes; genes associated with activity of transmembrane transporter and lipase were also under-expressed. Conclusion: Our data indicated that mild hypothermia altered endothelial expression pattern under the condition of I/R, preferably through varying the expression of genes associated with cell cycle, apoptosis, proliferation, and inflammatory response.
  Cellular Physiology and Biochemistry 01/2010; 25(6):605-14. · 2.86 Impact Factor