Shuyun Wang

Publications (2)5.72 Total impact

• Article: THE P38[alpha] AND P38[delta] MAP KINASES MAY BE GENE THERAPY TARGETS IN THE FUTURE TREATMENT OF SEVERE BURNS

  Shuyun Wang, Qiaobing Huang, Xiaohua Guo, Ulf T. Brunk, Jiahuai Han, Keseng Zhao, Ming Zhao
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  ABSTRACT: Microvascular barrier damage, induced by thermal injury, imposes life-threatening problems owing to the pathophysiological consequences of plasma loss and impaired perfusion that finally may lead to multiple organ failure. The aim of the present study was to define the signaling role of selected mitogen-activated protein kinases (MAPKs) in general vessel hyperpermeability caused by burns and to look for a potential gene therapy. Rearrangement of cytoskeletons and cell tight junctions were evaluated by phalloidin labeling of actin and immunocytochemical demonstration of the ZO-1 protein, whereas blood vessel permeability was evaluated by a fluorescence ratio technique. The p38 MAPK inhibitor SB203580 largely blocked burn serum-induced stress-fiber formation and tight-junction damage. Using the adenoviral approach to transfect dominant negative forms of p38 MAPKs, we found that p38α and p38δ had similar effects. The in vivo part of the study showed that transfection of these two constructs significantly lowered general venular hyperpermeability and enhanced the survival of burned animals. Because the p38 MAPK pathway seems to play a crucial role in burn-induced vascular hyperpermeability, general transfection with p38 MAP dominant negative constructs might become a new therapeutic method to block burn-induced plasma leakage. ABBREVIATIONS-EC-endothelial cell; ERK-extracellular signal-related kinase; FCS-fetal calf serum; HUVECs-human umbilical vein endothelial cells; JNK-c-Jun N-terminal kinase; MAPKs-mitogen-activated protein kinases; MKK3b-mitogen-activated protein kinase kinase 3b; MKK6b-mitogen-activated protein kinase kinase 6b; MLC-myosin light chain; MYPT1-myosin-specific phosphatase 1; PKC-protein kinase C
  Shock 07/2010; 34(2):176-182. · 2.85 Impact Factor
• Article: The P38alpha and P38delta MAP kinases may be gene therapy targets in the future treatment of severe burns.

  Shuyun Wang, Qiaobing Huang, Xiaohua Guo, Ulf T Brunk, Jiahuai Han, Keseng Zhao, Ming Zhao
  [show abstract] [hide abstract]
  ABSTRACT: Microvascular barrier damage, induced by thermal injury, imposes life-threatening problems owing to the pathophysiological consequences of plasma loss and impaired perfusion that finally may lead to multiple organ failure. The aim of the present study was to define the signaling role of selected mitogen-activated protein kinases (MAPKs) in general vessel hyperpermeability caused by burns and to look for a potential gene therapy. Rearrangement of cytoskeletons and cell tight junctions were evaluated by phalloidin labeling of actin and immunocytochemical demonstration of the ZO-1 protein, whereas blood vessel permeability was evaluated by a fluorescence ratio technique. The p38 MAPK inhibitor SB203580 largely blocked burn serum-induced stress-fiber formation and tight-junction damage. Using the adenoviral approach to transfect dominant negative forms of p38 MAPKs, we found that p38alpha and p38delta had similar effects. The in vivo part of the study showed that transfection of these two constructs significantly lowered general venular hyperpermeability and enhanced the survival of burned animals. Because the p38 MAPK pathway seems to play a crucial role in burn-induced vascular hyperpermeability, general transfection with p38 MAP dominant negative constructs might become a new therapeutic method to block burn-induced plasma leakage.
  Shock (Augusta, Ga.) 12/2009; 34(2):176-82. · 2.87 Impact Factor