Xuhu Mao

Publications (2)7.64 Total impact

• Article: Enhanced Membrane-tethered Mucin 3 (MUC3) Expression by a Tetrameric Branched Peptide with Conserved TFLK Motif Inhibits Bacteria Adherence.

  Qiong Pan, Yin Tian, Xiaohuan Li, Jun Ye, Yun Liu, Lili Song, Yongtao Yang, Rong Zhu, Yonghong He, Lei Chen, Wensheng Chen, Xuhu Mao, Zhihong Peng, Rongquan Wang
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  ABSTRACT: We investigated whether a synthetic tetrameric branched peptide based on the conserved TFLK-motif from M-SAA3 is more efficient than the monomeric peptide at up-regulating MUC3 expression and examined the possible mechanism(s) and biological significance of this process. We used standard solid-phase methods to synthesize a tetrameric branched peptide (sequence GWLTFLKAAG) containing a trilysine core, termed the TFLK-containing 10-mer BP. The aberrant expression of transcription factors (TF) was analyzed using a transcription factor protein/DNA array. MUC3 and relevant TFs were detected using real-time PCR and (or) Western blots. The luciferase assay, EMSA and ChIP assays were used to analyze the activity of the human MUC3 promoter. The bacterial adherence assay was used to evaluate the in vitro inhibition of enteropathogenic Escherichia coli (EPEC) or enterohemorrhagic Escherichia coli serotype O157:H7 (EHEC O157:H7) adherence to HT-29-Gal cells after treatment with the TFLK-containing 10-mer BP. In HT-29-Gal cells, the TFLK-containing 10-mer BP induced higher levels of MUC3 expression than the M-SAA3 derived N-terminal 10-mer monomeric peptide, and MUC3 expression was activated through transcriptional mechanisms, including the induction of multiple transcription factors and further binding with their cis-elements between nucleotides -242 and -62 within MUC3 promoter. Interestingly, the TFLK-containing 10-mer BP dramatically inhibited EPEC and EHEC O157:H7 adherence to the HT-29-Gal cells compared with the controls. This finding suggests a potential therapeutic use for this peptide to prevent gastrointestinal infection.
  Journal of Biological Chemistry 01/2013; · 4.77 Impact Factor
• Article: H. pylori induces the expression of Hath1 in gastric epithelial cells via interleukin-8/STAT3 phosphorylation while suppressing Hes1.

  Xin Zhang, Yongtao Yang, Rong Zhu, Jianying Bai, Yin Tian, Xiaohuan Li, Zhihong Peng, Yonghong He, Lei Chen, Dianchun Fang, Wensheng Chen, Quanming Zou, Xuhu Mao, Rongquan Wang
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  ABSTRACT: Chronic gastritis associated with Helicobacter pylori is a leading cause of gastric intestinal metaplasia (IM), which arises from abnormal cell differentiation of the epithelium in the gastric mucosa. However, the mechanisms involved in H. pylori-mediated IM remain elusive. The aim of our study was to explore the effects and the underlying mechanisms of H. pylori on the abnormal expression of Hath1 and Sox2 and to reveal its relationship to the development of gastric IM. We found that Hath1 and Sox2 were overexpressed in gastric IM tissue. Hath1 expression was up-regulated, whereas Sox2 expression, which was independent of the CagA virulence factor, was down-regulated in gastric epithelial cells and coincided with increased IL-6 and IL-8 levels in the culture media. Stimulation with H. pylori-related cytokine IL-8, but not IL-6 or IL-1β, was induced by Hath1 expression in the gastric epithelial cells. Although IL-8 and IL-6 levels correlated with STAT3 (signal transducer and activator of transcription) phosphorylation before and after H. pylori eradication in the gastric mucosa, only the blocking of IL-8-induced STAT3 activation using AG490 or STAT3-targeting RNA interference altered Hath1 expression. Additionally, we found that H. pylori down-regulated Hes1, which is a direct downstream target gene of Notch signaling and a repressor of Hath1 expression. These findings suggest that H. pylori induced inflammation up-regulate Hath1 expression via interleukin-8/STAT3 (IL-8) phosphorylation while suppressing Hes1, which provides a novel molecular connection between a H. pylori infection and intestinal metaplasia. J. Cell. Biochem. 113: 3740-3751, 2012. © 2012 Wiley Periodicals, Inc.
  Journal of Cellular Biochemistry 07/2012; 113(12):3740-51. · 2.87 Impact Factor