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Articles by L. Zeng
Total Records ( 3 ) for L. Zeng
  Q Wang , J Li , J Gu , B Huang , Y Zhao , D Zheng , Y Ding and L. Zeng
 

The green tea constituent, (–)-epigallocatechin-3-gallate (EGCG), has chemopreventive and anticancer effects. This is partially because of the selective ability of EGCG to induce apoptosis and death in cancer cells without affecting normal cells. In the present study, the activity of EGCG against the myeloma cell line, KM3, was examined. Our results demonstrated, for the first time, that the treatment of the KM3 cell line with EGCG inhibits cell proliferation and induces apoptosis, and there is a synergistic effect when EGCG and bortezomib are combined. Further experiments showed that this effect involves the NF-B pathway. EGCG inhibits the expression of the P65 mRNA and P65/pP65 protein, meanwhile it downregulates pIB expression and upregulates IB expression. EGCG also activates caspase-3, -8, cleaved caspase-9, and poly-ADP-ribose polymerase (PARP) and subsequent apoptosis. These findings provided experimental evidence for efficacy of EGCG alone or in combination with bortezomib in multiple myeloma therapy.

  A Margariti , A Zampetaki , Q Xiao , B Zhou , E Karamariti , D Martin , X Yin , M Mayr , H Li , Z Zhang , E De Falco , Y Hu , G Cockerill , Q Xu and L. Zeng
 

Rationale: Histone deacetylase (HDAC)7 is expressed in the early stages of embryonic development and may play a role in endothelial function.

Objective: This study aimed to investigate the role of HDAC7 in endothelial cell (EC) proliferation and growth and the underlying mechanism.

Methods and Results: Overexpression of HDAC7 by adenoviral gene transfer suppressed human umbilical vein endothelial cell (HUVEC) proliferation by preventing nuclear translocation of β-catenin and downregulation of T-cell factor-1/Id2 (inhibitor of DNA binding 2) and cyclin D1, leading to G1 phase elongation. Further assays with the TOPFLASH reporter and quantitative RT-PCR for other β-catenin target genes such as Axin2 confirmed that overexpression of HDAC7 decreased β-catenin activity. Knockdown of HDAC7 by lentiviral short hairpin RNA transfer induced β-catenin nuclear translocation but downregulated cyclin D1, cyclin E1 and E2F2, causing HUVEC hypertrophy. Immunoprecipitation assay and mass spectrometry analysis revealed that HDAC7 directly binds to β-catenin and forms a complex with 14-3-3 , , and proteins. Vascular endothelial growth factor treatment induced HDAC7 degradation via PLC-IP3K (phospholipase C–inositol-1,4,5-trisphosphate kinase) signal pathway and partially rescued HDAC7-mediated suppression of proliferation. Moreover, vascular endothelial growth factor stimulation suppressed the binding of HDAC7 with β-catenin, disrupting the complex and releasing β-catenin to translocate into the nucleus.

Conclusions: These findings demonstrate that HDAC7 interacts with β-catenin keeping ECs in a low proliferation stage and provides a novel insight into the mechanism of HDAC7-mediated signal pathways leading to endothelial growth.

  X Du , Z Chen , W Li , Y Tan , J Lu , X Zhu , T Zhao , G Dong and L. Zeng
 

The objectives of this study are to establish microsatellite loci for the Mongolian gerbil based on mouse microsatellite DNA sequences and to investigate genetic variation in the laboratory gerbil (Capital Medical University, CMU) and 2 wild gerbil populations (from Yin Chuan city [YIN] and the Hohehot Municipality [HOH]). In total, 536 mouse microsatellite markers were chosen to identify polymorphic dinucleotide repeat loci in the gerbil by cross-amplification. Of these markers, 313 (58.39%) have been discretely amplified from the CMU laboratory gerbil and been sequenced. Of the 313 sequenced markers, 130 were confirmed as simple sequence repeat (SSR) loci in the gerbil. In total, 6 of those newly identified loci plus 6 identified in previous reports were used to estimate the genetic polymorphism for 30 laboratory gerbils and 54 wild gerbils (27 each of the HOH and YIN groups). A total of 29 alleles were observed in the 3 populations, and 11 of 12 loci (91.67%) are polymorphic markers. Nei's standard genetic distances of 0.0592 (CMU vs. HOH) and 0.1033 (CMU vs. YIN) were observed. The averages of observed versus expected heterozygosity are 0.5231/0.4008, 0.5051/0.3882, and 0.4825/0.3665 for the YIN, HOH, and CMU populations, respectively. These results show that cross-amplification using mouse microsatellite primers is an efficient way to identify gerbil SSR loci. By using these 12 selected markers, we have demonstrated that genetic variation level within the CMU population is higher than that has been reported previously and are comparable with the levels found in 2 wild populations.

 
 
 
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