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Articles by Xiaoping Chen
Total Records ( 3 ) for Xiaoping Chen
  Zhengxiang He , Li Qin , Lili Chen , Nanzheng Peng , Jianlan You and Xiaoping Chen
  The synergy of the activities between chloroquine and various human immunodeficiency virus protease inhibitors was investigated in chloroquine-resistant and -sensitive malaria parasites. In both in vitro and in vivo assay systems, ritonavir was found to be the most potent in potentiating the antimalarial action of chloroquine.
  Deyu Li , Xiaoping Chen and Haibo Yu
  Resveratrol (trans-3, 4’, 5-trihydroxystilbene) is a natural phytoalexin found in grapes and other plants that has anti-cancer and anti-inflammatory effects. The aim of this study was to find that resveratrol suppresses matrix metalloproteinase-2(MMP-2) expression in hepatoma in vivo. Tumor volume and invasion ability of liver transplanted tumor in nude mice were observed. MMP-2 mRNA and protein of the tumor were investigated by RT-PCR and Western-blot. NF-kappa B activity was measured by EMSA. Growth of the transplanted tumor was obviously by resveratrol at 50 mg kg-1 (p<0.05) and 100 mg kg-1 (p<0.05). Liver metastasis of the tumor was inhibited by 100 mg kg-1 resveratrol (p<0.05). MMP-2 protein was down regulated due to decreased MMP-2 mRNA expression. NF-kappa B activity was also extensively inhibited by resveratrol at 50 and 100 mg kg-1. The results suggest that resveratrol may inhibit growth and invasion ability by down regulate MMP-2 expression of hepatoma in nude mice. This effect was regulated by NF-kappa B pathway.
  Mohamed El Gazzar , Barbara K. Yoza , Xiaoping Chen , Jean Hu , Gregory A. Hawkins and Charles E. McCall
  TNFα gene expression is silenced in the endotoxin tolerant phenotype that develops in blood leukocytes after the initial activation phase of severe systemic inflammation or sepsis. The silencing phase can be mimicked in vitro by LPS stimulation. We reported that the TNFα transcription is disrupted in endotoxin tolerant THP-1 human promonocyte due to changes in transcription factor binding and enrichment with histone H3 dimethylated on lysine 9 (H3K9). Here we show that the TNFα promoter is hypermethylated during endotoxin tolerance and that H3K9 methylation and DNA methylation interact to silence TNFα expression. Chromatin immunoprecipitation and RNA interference analysis demonstrated that, in tolerant cells, TNFα promoter is bound by the H3K9 histone methyltransferase G9a which dimethylates H3K9 and creates a platform for HP1 binding, leading to the recruitment of the DNA methyltransferase Dnmt3a/b and an increase in promoter CpG methylation. Knockdown of HP1 resulted in a decreased Dnmt3a/b binding, sustained G9a binding, and a modest increase in TNFα transcription, but had no effect on H3K9 dimethylation. In contrast, G9a knockdown-disrupted promoter silencing and restored TNFα transcription in tolerant cells. This correlated with a near loss of H3K9 dimethylation, a significant decrease in HP1 and Dnmt3a/b binding and promoter CpG methylation. Our results demonstrate a central role for G9a in this process and suggest that histone methylation and DNA methylation cooperatively interact via HP1 to silence TNFα expression during endotoxin tolerance and may have implication for proinflammatory gene silencing associated with severe systemic inflammation.
 
 
 
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