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| 1 | Dephosphorylation of cardiomyocyte Cx43 is associated with myocardial ischemia and reperfusion injury显示文摘Objective:Myocardial ischemia/reperfusion(I/R) injury is the leading cause of death in the world. However,the details of the mechanism of its pathophysiology are still unknown. The present study was designed to investigate the role of connexin 43(Cx43) in acute models of myocardial I/R injury. Methods:Male C57BL/6 mice were subjected to myocardial ischemia(45 min) followed by reperfusion(4 hrs) in vivo. The whole operation was monitored using a two-lead ECG. Hearts were harvested and the level of protein was assessed by western blot analysis. Haematoxylin and Eosin(HE) staining was used to detect the extent of neutrophil infiltration. The expression level of IL-6 was detected by ELISA. Results:A murine myocardial I/R injury model was constructed successfully. Phosphorylated Cx43 decreased 83. 45% while non-phosphorylated Cx43 increased 1.62-fold in the myocardium after I/R injury. Neutrophil infiltration and the expression of the inflammatory cytokine IL-6 increased in the myocardium following I/R. Conclusion:During myocardial I/R injury,cardiomyocyte Cx43 is dephosphorylated,and this may be associated with an inflammatory response. | Zhijuan Cao Xuan Xu Linli Que Qi Chen Yuehua Li | 2009 | Journal of Nanjing Medical University2009，23，3： | 6 |
| 2 | TIR/BB-loop mimetic AS-1 protects vascular endothelial cells from injury induced by hypoxia/reoxygenation显示文摘Morphological and functional abnormalities of vascular endothelial cells(VECs) are risk factors of ischemiareperfusion in skin flaps.Signaling pathway mediated by interleukin-1 receptor(IL-1 R) is essential to hypoxia/reoxygenation(H/R) injury of VECs.While the TIR/BB-loop mimetic(AS-1) disrupts the interaction between IL-1 R and myeloid differentiation primary-response protein 88(MyD88),its role in the VECs dysfunction under H/R is unclear.In this study,we first showed that there was an infiltration of inflammatory cells and the apoptosis of VECs by using a skin flap section from patients who received flap transplantation.We then showed that the H/R treatment induced apoptosis and loss of cell migration of endothelial cell line H926 were attenuated by AS-1.Furthermore,our data suggested that AS-1 inhibits the interaction between IL-1 R and MyD88,and subsequent phosphorylation of IκB and p38 pathway,as well as the nuclear localization of NF-κB subunit p65/p50.Thus,this study indicated that the protective role of AS-1 in H/R induced cellular injury may be due to the AS-1 mediated down-regulation of IL-1 R signaling pathway. | Zhijia Zhang Yuxing Hou Jiantao Li Chao Tang Linli Que Qian Tan Yuehua Li | 2020 | The Journal of Biomedical Research2020，34，5： | 2 |
| 3 | Varicella-zoster virus ORF7 interacts with ORF53 and plays a role in its trans-Golgi network localization显示文摘Varicella-zoster virus(VZV) is a neurotropic alphaherpesvirus that causes chickenpox and shingles. ORF7 is an important virulence determinant of VZV in both human skin and nerve tissues,however, its specific function and involved molecular mechanism in VZV pathogenesis remain largely elusive. Previous yeast two-hybrid studies on intraviral protein-protein interaction network in herpesviruses have revealed that VZV ORF7 may interact with ORF53, which is a virtually unstudied but essential viral protein. The aim of this study is to identify and characterize VZV ORF53, and to investigate its relationship with ORF7. For this purpose, we prepared monoclonal antibodies against ORF53 and, for the first time, characterized it as a ~40 k Da viral protein predominantly localizing to the trans-Golgi network of the infected host cell. Next, we further confirmed the interaction between ORF7 and ORF53 by co-immunoprecipitation and co-localization studies in both plasmid-transfected and VZV-infected cells. Moreover, interestingly, we found that ORF53 lost its trans-Golgi network localization and became dispersed in the cytoplasm of host cells infected with an ORF7-deleted recombinant VZV, and thus ORF7 seems to play a role in normal subcellular localization of ORF53. Collectively, these results suggested that ORF7 and ORF53 may function as a complex during infection, which may be implicated in VZV pathogenesis. | Wei Wang Wenkun Fu Dequan Pan Linli Cai Jianghui Ye Jian Liu Che Liu Yuqiong Que Ningshao Xia Hua Zhu Tong Cheng | 2017 | Virologica Sinica2017，32，5： | 1 |
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