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Articles by H Tang
Total Records ( 6 ) for H Tang
  H Tang , F Chen , Q Tan , S Tan , L Liu and F. Zhang
 

Polycomb repressive complex 2 (PRC2), which mediates trimethylation of lysine 27 on histone H3 (K27me3), plays an important role in many types of stem cell differentiation. Here, we try to reveal how PRC2, PRC2-mediated repressive histone marker H3K27me3, and active histone marker histone H4 acetylation (acH4) regulate the CD11b transcription during all-trans retinoic acid (ATRA)-induced HL-60 leukemia cell differentiation. By using quantitative real-time polymerase chain reaction (qPCR) and western blot analysis, we found that the mRNA and protein expression levels of two members of PRC2 were decreased during ATRA-induced HL-60 differentiation, respectively. When treated with ATRA for 72 h, the EZH2 and SUZ12 mRNA levels were decreased to 35% and 38% of the control group, respectively. At the same time, the granulocytic mature surface marker CD11b expression was increased significantly at mRNA level detected by qPCR and protein level detected by flow cytometry. By using chromatin immunoprecipitation assay, we compared the local changes in SUZ12 binding and PRC2-mediated H3K27me3 at the promoter of CD11b during ATRA-induced HL-60 differentiation. Both the levels of SUZ12 binding and PRC2-mediated H3K27me3 at the promoter of CD11b were decreased for 4.1 and 3.8 folds, respectively. And we also found the increase in the acH4 level up to 4 folds after 72 h of ATRA treatment. These results suggested that the histone modification including PRC2-mediated repressive histone marker H3K27me3 and active histone marker acH4 may involve in CD11b transcription during HL-60 leukemia cells reprogramming to terminal differentiation.

  A Loesch , H Tang , M. A Cotter and N. E. Cameron
 

Erythropoiesis-stimulating agents (ESAs) are used to treat anemia associated with renal failure. It is now known that these agents also show a broad range of cell- and tissue-protective effects. In the current study, we explored whether an ESA, epoetin delta, affects vascular pathology linked to diabetes mellitus (DM). In a rat model of streptozotocin-induced DM, we investigated, by pre-embedding electron-immunocytochemistry, whether epoetin delta affects DM-induced structural changes in cerebrovascular endothelium of the rat basilar artery and influences the subcellular distribution of endothelial nitric oxide synthase (eNOS). Epoetin delta treatment influenced DM-induced changes to the distribution of eNOS in, and the structure of, the endothelial cell. This may indicate potential beneficial effects of epoetin delta on cerebrovascular endothelium and suggests eNOS as a possible target molecule of epoetin delta in DM.

  L Zhang , T Deng , X Li , H Liu , H Zhou , J Ma , M Wu , M Zhou , S Shen , Z Niu , W Zhang , L Shi , B Xiang , J Lu , L Wang , D Li , H Tang and G. Li
 

microRNAs (miRNAs) are small non-coding RNAs and have been implicated in the pathology of various diseases, including cancer. Here we report that the miRNA profiles have been changed after knockdown of one of the most important oncogene c-MYC or re-expression of a candidate tumor suppressor gene SPLUNC1 in nasopharyngeal carcinoma (NPC) cells. Both c-MYC knockdown and SPLUNC1 re-expression can down-regulate microRNA-141 (miR-141). miR-141 is up-regulated in NPC specimens in comparison with normal nasopharyngeal epithelium. Inhibition of miR-141 could affect cell cycle, apoptosis, cell growth, migration and invasion in NPC cells. We found that BRD3, UBAP1 and PTEN are potential targets of miR-141, which had been confirmed following luciferase reporter assays and western blotting. BRD3 and UBAP1 are both involved in NPC carcinogenesis as confirmed through our previous studies and PTEN is a crucial tumor suppressor in many tumor types. BRD3 is involved in the regulation of the Rb/E2F pathway. Inhibition of miR-141 could affect some important molecules in the Rb/E2F, JNK2 and AKT pathways. It is well known that carcinogenesis of NPC is involved in the networks of genetic and epigenetic alteration events. We propose that miR-141- and tumor-related genes c-MYC, SPLUNC1, BRD3, UBAP1 and PTEN may constitute a gene–miRNA network to contribute to NPC development.

  H Tang , X Dong , R. S Day , M. M Hassan and D. Li
 

To test the hypothesis that polymorphic variants of antioxidant genes modify the risk of pancreatic cancer, we examined seven single-nucleotide polymorphisms (SNPs) of genes coding for superoxide dismutase (SOD) 2, glutathione S-transferase alpha 4 (GSTA4), catalase and glutathione peroxidase in 575 patients with pancreatic adenocarcinoma and 648 healthy controls in a case–control study. Information on risk factors was collected by personal interview and dietary information was collected by a self-administered food frequency questionnaire. Genotypes were determined using the Taqman method. Adjusted odds ratio (AOR) and 95% confidence interval (CI) were estimated by unconditional logistic regression. No significant main effect of genotype was observed. A borderline significant interaction between diabetes and SOD2 Ex2+24T>C CT/TT genotype was observed (Pinteraction = 0.051); the AORs (95% CI) were 0.98 (0.73–1.32) for non-diabetics carrying the CT/TT genotype, 1.73 (0.94–3.18) for diabetics carrying the CC genotype and 3.49 (2.22–5.49) for diabetics carrying the CT/TT genotype compared with non-diabetics carrying the CC genotype. Moreover, the SOD2 –1221G>A AA genotype carriers had a significantly increased risk for pancreatic cancer among those with a low dietary vitamin E intake but decreased risk among those with a high vitamin E intake (Pinteraction = 0.002). There was a non-significant interaction between diabetes and GSTA4 Ex5–64G>A genotypes (Pinteraction = 0.078). No significant interaction between genotype with cigarette smoking or vitamin C intake was observed. These data suggest that genetic variations in antioxidant defenses modify the risk of pancreatic cancer in diabetics or individuals with a low dietary vitamin E intake.

  S Wright , D Klausner , B Baird , M. E Williams , T Steinman , H Tang , R Ragasa and A. S. Goldfarb Rumyantzev
 

Background and objectives: The optimal time of dialysis initiation is unclear. The goal of this analysis was to compare survival outcomes in patients with early and late start dialysis as measured by kidney function at dialysis initiation.

Design, setting, participants, & measurements: We performed a retrospective analysis of patients entering the U.S. Renal Data System database from January 1, 1995 to September 30, 2006. Patients were classified into groups by estimated GFR (eGFR) at dialysis initiation.

Results: In this total incident population (n = 896,546), 99,231 patients had an early dialysis start (eGFR >15 ml/min per 1.73 m2) and 113,510 had a late start (eGFR ≤5 ml/min per 1.73 m2). The following variables were significantly (P < 0.001) associated with an early start: white race, male gender, greater comorbidity index, presence of diabetes, and peritoneal dialysis. Compared with the reference group with an eGFR of >5 to 10 ml/min per 1.73 m2 at dialysis start, a Cox model adjusted for potential confounding variables showed an incremental increase in mortality associated with earlier dialysis start. The group with the earliest start had increased risk of mortality, wheras late start was associated with reduced risk of mortality. Subgroup analyses showed similar results. The limitations of the study are retrospective study design, potential unaccounted confounding, and potential selection and lead-time biases.

Conclusions: Late initiation of dialysis is associated with a reduced risk of mortality, arguing against aggressive early dialysis initiation based primarily on eGFR alone.

  X Wang , H Tang , J. E Bowers and A. H. Paterson
 

Whole-genome duplication produces massive duplicated blocks in plant genomes. Sharing appreciable sequence similarity, duplicated blocks may have been affected by illegitimate recombination. However, large-scale evaluation of illegitimate recombination in plant genomes has not been possible previously. Here, based on comparative and phylogenetic analysis of the sequenced genomes of rice and sorghum, we report evidence of extensive and long-lasting recombination between duplicated blocks. We estimated that at least 5.5% and 4.1% of rice and sorghum duplicated genes have been affected by nonreciprocal recombination (gene conversion) over nearly their full length after rice–sorghum divergence, while even more (8.7% and 8.1%, respectively) have been converted over portions of their length. We found that conversion occurs in higher frequency toward the terminal regions of chromosomes, and expression patterns of converted genes are more positively correlated than nonconverted ones. Though converted paralogs are more similar to one another than nonconverted ones, elevated nucleotide differences between rice–sorghum orthologs indicates that they have evolved at a faster rate, implying that recombination acts as an accelerating, rather than a conservative, element. The converted genes show no change in selection pressure. We also found no evidence that conversion contributed to guanine-cytosine (GC) content elevation.

 
 
 
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