Guo-Qing Chen

Wuhan Institute of Physical Education, Wu-han-shih, Hubei, China

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Publications (7)10.51 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The present study aimed to investigate the effects of exercise intensity on mitochondrial DNA (mtDNA) alterations of copy numbers and mutations in the gastrocnemii of mice. A total of 50 male mice were randomly divided into 5 groups; control group (K) and groups A-D, which underwent 10,30,60 and 90 min of swimming per day, respectively. Samples were obtained after 20 weeks of exercise. Total DNA was collected to analyze mutations in the mtDNA displacement loop (D-loop) regions. mtDNA content was quantified by real‑time PCR. Point mutations, monobase insertions and deletions were observed in the mtDNA D-loop regions in the skeletal muscles of the mice. A deletion of 16,232 bp was found in certain groups. The mutation base of the control group was higher than that of the exercise groups. The exercise groups demonstrated significantly altered copy numbers; the 30 min exercise group had the highest copy number. These results suggest that moderate exercise intensity reduces mutations in the mtDNA D-loop regions, and enhances the copy number of mtDNA in the gastrocnemus muscles of mice.
    Molecular Medicine Reports 05/2012; 6(2):426-8. · 1.17 Impact Factor
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    ABSTRACT: Previous studies have shown decreased expression of repulsive guidance molecule member A (RGMa) in colorectal cancer. However, the relationship between the expression levels and promoter DNA methylation status of RGMa and the clinical characteristics of colorectal cancer has not been previously reported. Here, we investigated the expression of RGMa by immunohistochemistry, real-time PCR and western blotting and analyzed the methylation status of the RGMa promoter using Sequenom's MassARRAY platform in colorectal cancer tissues and adjacent normal colorectal tissues. The results showed that RGMa expression was decreased in cancer tissues compared with adjacent normal tissues (p<0.01). Furthermore, a tendency for decreased expression in tumor tissues was observed from Dukes' stage A to stage D (p<0.01). In addition, significantly higher levels of hypermethylation in promoter regions of RGMa were observed in colorectal cancer tissues, compared with those in adjacent normal colorectal tissues (p<0.01). Moreover, the methylation levels of RGMa in tumor tissues were significantly increased in Dukes' stage C and D compared with Dukes' stage A and B (p<0.01). Our results indicate that RGMa expression and promoter methylation status are closely related to colorectal cancer genesis and progression. Determination of the expression level and methylation frequency of RGMa in colorectal cancer tissues may have benefit for early diagnosis and for evaluating patient prognosis.
    Oncology Reports 05/2012; 27(5):1653-9. · 2.30 Impact Factor
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    ABSTRACT: Skeletal muscle insulin resistance induced by a high-fat diet has been implicated in the development of type 2 diabetes. However, the precise molecular mechanisms involved are only partially understood. Recently, studies have shown that microRNAs play an important role in insulin resistance in various tissues. In this study, microRNA expression profiles of skeletal muscle of mice fed a high-fat or normal diet were analyzed using microarrays and the results were confirmed by real-time reverse-transcription polymerase chain reaction. Gene Ontology (GO) and pathway mapping tools were employed to analyze systemically the biological processes and signaling pathways affected by the differential expression of microRNAs. In this study, we show that 30 microRNAs are differentially expressed between 2 groups of mice. Compared to the mice fed a normal diet, there were 8 microRNAs up-regulated and 22 microRNAs down-regulated in the high-fat diet-fed mice. Furthermore, we confirm that the MAPK signaling pathway highlighted in this study is involved in skeletal muscle insulin resistance. These results indicate that skeletal muscle insulin resistance induced by a high-fat diet is associated with a group of microRNAs. GO and pathway mapping are a valid and effective approach for analyzing the function of microRNAs and the results could be a guideline for further investigation.
    Molecular Medicine Reports 03/2012; 5(5):1362-8. · 1.17 Impact Factor
  • Guo-Qing Chen, Song Wang, Sheng-Yu Hu
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    ABSTRACT: Osteoporotic fractures commonly occur in the elderly. Current studies regarding cell proliferation and apoptosis during osteoporotic fracture healing are limited. In this study, we established an osteoporotic fracture healing model. Bone loss and callus formation were monitored with DXA, cell proliferation was examined using immunohistochemistry with BrdU monoclonal antibody and apoptotic cells were detected using the TUNEL method. Both cell proliferation and apoptosis occurred during the entire period of the study. BrdU immunostaining showed a decreasing tendency in the process of fracture healing. On days 20 and 30 post-fracture, the percentage of BrdU-positive cells in ovariectomized rats was significantly higher compared to sham-operated rats. TUNEL-positive chondrocytes reached a peak on day 20 post-fracture. There was no significant difference between the two groups. Our results indicate that osteoporosis markedly delays the fracture healing process, mostly due to increased chondrocyte proliferation without a change in chondrocyte apoptosis.
    Molecular Medicine Reports 09/2011; 5(1):202-6. · 1.17 Impact Factor
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    ABSTRACT: MuRF1 E3 ubiquitin ligase has been identified as a mediator of skeletal muscle wasting in various skeletal muscle atrophy models, and its expression is upregulated by oxidative stress. Exercise training could decrease oxidative stress and restore the atrophied skeletal muscle. Here, our aim was to investigate whether exercise training has any effect on MuRF1 expression in rats with diabetes. Rats with streptozotocin-induced diabetes were subjected to exercise training, after which oxidative stress was determined, and MuRF1 expression was analyzed by immunohistochemistry, real-time RT-PCR and Western blot analysis. In addition, we analyzed C2C12 myotubes in an in vitro model to examine the effects of oxidative stress on the protein levels of MuRF1 and myosin heavy chain (MHC). While oxidative stress and MuRF1 expression were increased in rats with diabetes, exercise training diminished the skeletal muscle wasting in diabetic rats by decreasing oxidative stress and inhibiting MuRF1 expression at both the mRNA and protein levels. In addition, oxidative stress-induced MuRF1 upregulation promoted proteasome dependent degradation of the myosin heavy chain (MHC) in C2C12 myotubes. Our study provides the first evidence that the beneficial anti-atrophy effects of exercise training on diabetes might be mediated by inhibiting oxidative stress-induced MuRF1 upregulation and preventing MuRF1-mediated degradation of MHC.
    Life sciences 07/2011; 89(1-2):44-9. · 2.56 Impact Factor
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    ABSTRACT: To determine whether muscle-specific RING finger protein 1 (MuRF1) expression induced by oxidative stress lead to muscle wasting in diabetes rats. The diabetes rat model was established by high-carbohydrate, high-fat diet and injection of streptozotocin. The expression of MuRF1 in gastrocnemius was detected by immunohistochemistry and real time PCR. The level of lipid peroxidation, SOD and fiber size of gastrocnemius was also detected. Further more, C2C12 myotubes were cultured with different concentration of H2O2 (0, 0.01, 0.05, 0.10 and 0.20 mmol/L), the level of MuRF1 protein was detected by western blot. Compared with the control group, the diabetes rats showed higher level of thiobarbituric acid reactive substances (TBARS) and MuRF1 mRNA and lower fiber size in gastrocnemius (P < 0.01). The oxidative stress induced by H2O2 (0.05, 0.10 and 0.20 mmol/L) upregulated the expression of MuRF1 (P < 0.01) in C2C12 myotube cells. Our results indicated that diabetes modulated the expression of MuRF1 leading to muscle wasting, and the mechanism might be involved with oxidative stress.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 05/2011; 42(3):349-52.
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    ABSTRACT: Multidrug resistance remains a major clinical obstacle to successful treatment of breast cancer and leads to poor prognosis for the patients. Recently studies have shown that microRNAs play an important role in breast cancer cell resistance to chemotherapeutic agents. In this study, microRNA expression profiles of MCF-7/AdrVp and MCF-7 were analyzed using microarray and the results were confirmed by real-time RT-polymerase chain reaction. Gene Ontology (GO) and pathways mapping tools were employed to analyse systemically the biological processes and signaling pathways affected by differential expression microRNAs. Here, we showed that 181 human microRNAs were differentially expressed between two cell lines. Compared to MCF-7 cells, there were 16 microRNAs down-regulated and 165 microRNAs up-regulated in MCF-7/AdrVp. Western blot confirmed the correlation between specific microRNA expression and corresponding changes in protein levels of their targets, specifically those that have a documented role in cancer drug resistance. Furthermore, we validated that signaling pathway highlighted in the study was involved in drug resistance. These results indicated that breast cancer cell resistant to chemotherapy was associated with a group of microRNAs. GO and pathway mapping are valid and effective approach to analyse the function of microRNAs and the results could be a guideline for further investigation.
    Medical Oncology 06/2009; 27(2):406-15. · 2.14 Impact Factor

Publication Stats

34 Citations
10.51 Total Impact Points

Institutions

  • 2011–2012
    • Wuhan Institute of Physical Education
      Wu-han-shih, Hubei, China
  • 2009
    • Sichuan University
      • Department of Human Anatomy
      Chengdu, Sichuan Sheng, China