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Articles by Wen Zhou
Total Records ( 4 ) for Wen Zhou
  Wen Zhou , Wen Chen and Dong Xiao Wang
  The objective of this research is to explore the impacts of El Niño-Southern Oscillation (ENSO) on a possible connection between winter monsoon and summer monsoon over South China. In boreal winter, the strong or weak northerly anomalies due to the East Asian winter monsoon (EAWM), sweep across the continent to the costal regions, which might be favorable for the occurrence of an ENSO event. In boreal summer, South China tends to experience less (more) rainfall and more (less) temperature extremes which might be in the mature phase of a warm (cold) ENSO event. It is also found that more frequent cold surges might be followed by less temperature extremes in the coming year. The possible connection might be that the western Pacific subtropical high after a strong (weak) EAWM year would move northward (southward) through the modification of a ENSO event; this northward (southward) western Pacific subtropical high might result in earlier (later) south China summer monsoon onset and lead to a strong (weak) summer monsoon in the coming year.
  Li-Peng Wu , Xi Wang , Lian Li , Ying Zhao , Shaoli Lu , Yu Yu , Wen Zhou , Xiangyu Liu , Jing Yang , Zhixin Zheng , Hui Zhang , Jingnan Feng , Yang Yang , Haiying Wang and Wei-Guo Zhu
  Histone deacetylase inhibitor (HDACi) has been shown to demethylate the mammalian genome, which further strengthens the concept that DNA methylation and histone modifications interact in regulation of gene expression. Here, we report that an HDAC inhibitor, depsipeptide, exhibited significant demethylating activity on the promoters of several genes, including p16, SALL3, and GATA4 in human lung cancer cell lines H719 and H23, colon cancer cell line HT-29, and pancreatic cancer cell line PANC1. Although expression of DNA methyltransferase 1 (DNMT1) was not affected by depsipeptide, a decrease in binding of DNMT1 to the promoter of these genes played a dominant role in depsipeptide-induced demethylation and reactivation. Depsipeptide also suppressed expression of histone methyltransferases G9A and SUV39H1, which in turn resulted in a decrease of di- and trimethylated H3K9 around these genes` promoter. Furthermore, both loading of heterochromatin-associated protein 1 (HP1α and HP1β) to methylated H3K9 and binding of DNMT1 to these genes` promoter were significantly reduced in depsipeptide-treated cells. Similar DNA demethylation was induced by another HDAC inhibitor, apicidin, but not by trichostatin A. Our data describe a novel mechanism of HDACi-mediated DNA demethylation via suppression of histone methyltransferases and reduced recruitment of HP1 and DNMT1 to the genes` promoter.
  Yan Sun , Fei Meng , ZhaoHui Chen , QingWei Zhang , Wei Qiao , Wen Zhou and Xue Qin
  Background: Semen Zizyphi Sponosae (SZS), a traditional Chinese medicine for the treatment of insomnia and anxiety symptoms. The present study aimed to discuss whether total alkaloids from SZS have anti-depression effect and investigate the antidepressant potential of total alkaloids isolated from Semen Zizyphi Sponosae (TAS) and its possible monoaminergic mechanism in mice. Methods: Mouse models of depression including the forced swimming test (FST), the Tail Suspension Test (TST) and Chronic Unpredicted Mild Stress (CUMS) were used to evaluate the effects of TAS. The possible mechanisms were examined by using fluorospectrophotometry to measure monoamine neurotransmitters in mice hippocampus and frontal cortex. The contents of monoamine neurotransmitters including 5-hydroxytryptamine (5-HT), Norepinephrine (NE) and Dopamine (DA). Results: The results showed that intragastric administration of the TAS (5, 10, 20 mg kg-1) or Venlafaxine 9.4 mg kg-1 significantly reduced the duration of immobility in TST and FST. However, the effect was not dose-dependent. TAS 10 and 20 mg kg-1 significantly increases the 5-HT levels in both of the two brain regions. Conclusion: These findings demonstrated that TAS produced an antidepressant-like effect and the mechanism of action involves the serotonergic, noradrenergic and monoamine oxidase enzyme systems although underlying mechanism still remains to be further elucidated.
  Haiying Wang , Ying Zhao , Lian Li , Michael A. McNutt , Lipeng Wu , Shaoli Lu , Yu Yu , Wen Zhou , Jingnan Feng , Guolin Chai , Yang Yang and Wei-Guo Zhu
  Most agents that damage DNA act through posttranslational modifications of p53 and activate its downstream targets. However, whether cellular responses to nucleoside analogue-induced DNA damage also operate through p53 posttranslational modification has not been reported. In this study, the relationship between p53 activation and its posttranslational modifications was investigated in the human cancer cell lines A549 and HCT116 in response to 5-aza-2`-deoxycytidine (5-aza-CdR) or cytarabine treatment. 5-Aza-CdR induces p53 posttranslational modifications through activation of an ATM- and Rad3-related (ATR) signaling pathway, and 5-aza-CdR-induced association of replication protein A with chromatin is required for the binding of ATR to chromatin. Upon treatment with 5-aza-CdR, ATR activation is clearly associated with p53 phosphorylation at Ser15, but not at Thr18, Ser20, or Ser37. This specific p53 phosphorylation at Ser15 in turn results in acetylation of p53 at Lys320 and Lys373/Lys382 through transcriptional cofactors p300/CBP-associated factor and p300, respectively. These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21Waf1/Cip1 expression because the binding activity of acetylated p53 at Lys320/Lys373/Lys382 to the p21Waf1/Cip1 promoter, as well as p21Waf1/Cip1 expression itself are significantly increased after 5-aza-CdR treatment. It is of interest that p53 phosphorylation at Ser15 and acetylations at Lys320/Lys373/Lys382 mutually interact in the 5-aza-CdR induced p21Waf1/Cip1 expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells. These data taken together show for the first time that 5-aza-CdR activates the ATR signaling pathway, which elicits a specific p53 phosphorylation-acetylation cascade to induce p21Waf1/Cip1 expression.

 
 
 
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