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Journal Cover Biomedical Research and Therapy
   [6 followers]  Follow    
  This is an Open Access Journal Open Access journal
     ISSN (Print) 2198-4093 - ISSN (Online) 2198-4093
     Published by Vietnam National University Homepage  [1 journal]
  • Hypoxia condition promoted the adipose derived stem cell proliferation via
           VEGF production

    • Authors: Phuc Van Pham, Ngoc Bich Vu, Nhung Hai Truong, Loan Thi-Tung Dang, Nhan Lu-Chinh Phan, Ngoc Kim Phan
      Abstract: Adipose-derived stem cells (ADSCs) are a promising mesenchymal stem cells source with therapeutic applications. Some recent studies showed that ADSCs could be expanded in vitro without phenotype changes. This study aimed to evaluate the effect of hypoxia condition on ADSC proliferation in vitro and to determine the role of VEGF in ADSC proliferation. ADSCs were selectively cultured from stromal vascular fraction that obtained from adipose tissue in the DMEM/F12 medium supplemented with 10% FBS, 1% antibiotic-antimycotic. ADSCs were cultured in two conditions included hypoxia (5% O2) and normal oxygen (21% O2). Effects of oxygen concentration on cell proliferation were recorded by cell cycle and doubling time. Expression of VEGF was evaluated by real-time RT-PCR and ELISA assays. And the role of VEGF on ADSC proliferation was studied by neutralizing VEGF with anti-VEGF monoclonal antibody. The results showed that ADSC proliferation rate was increased 2.5 times in hypoxia compared to normal oxygen. And hypoxia condition, ADSCs also triggered VEGF synthesis at both mRNA and translational level. However, neutralizing VEGF with anti-VEGF monoclonal antibody significantly reduced the proliferation rate. These results suggested that hypoxia stimulated ADSC proliferation related to VEGF production. This finding will contribute not only in stem cell technology but also in obese treatment.
      PubDate: 2014-12-13
      Issue No: Vol. 1, No. 5 (2014)
       
  • Mouse model for myocardial injury caused by ischemia

    • Authors: Truc Le-Buu Pham, Dung Thi-Phuong Nguyen, Oanh Thi-Kieu Nguyen, Tam Thanh Nguyen
      Abstract: Mouse model is one of the most useful tools to understand disease’s mechanism as well as evaluate treatment’s efficiency of the disease by novel therapies. To create a mouse model for myocardial injury for cell therapeutic studies, an occluding suture of the left coronary artery in mice was made with sewing thread Prolene 7-0. That left anterior descending artery (LAD) closing caused infarction leading to ischemia and death of cells after that. The animals were then monitored survival ratio, body weight, blood pressure and analyzed Histopathology using Hematoxylin and Eosin (H&E) stain, Trichrome stain, and Immunohistochemistry (IHC) stain to evaluate the injuries of myocardium. The results showed that six weeks after narrowing the left coronary artery, the survival percentage of the experimental group was 77% (survival 17/22), body weight and blood pressure of the experimental group (n=17) tended to decrease comparing to the control group (n=10) or heart function of the experimental group was weakening.  Supporting for that results, Histopathology assessments were also showed that the damages and the death of myocardium in the experiment group. H&E stain gave the presentation that heart septum of the experimental group was thinner than the control group. Collagen formation was also observed in the experimental group by Trichrome stain results. In addition, IHC stain also indicated that the Annexin-V (death cell marker) was expressed much stronger than those of the control group. In conclusion, the mouse model for myocardial injury caused by ischemia has been created successfully by LAD ligation.
      PubDate: 2014-12-12
      Issue No: Vol. 1, No. 5 (2014)
       
  • Constitutive Photomorphogensis Protein1 (COP1) mediated p53 pathway and
           its oncogenic role

    • Authors: Sk Amir Hossain, Md. Golam Rabbani, Khandker Khaldun Islam, Sarder Nasir Uddin
      Abstract: We have reviewed the COP1 mediated tumor suppressor protein p53 pathway and its oncogenic role. COP1 is a negative regulator of p53 and acts as a pivotal controller of p53-Akt death-live switch (Protein kinase B). In presence of p53, COP1 is overexpressed in breast, ovarian, gastric cancers, even without MDM2 (Mouse double minute-2) amplification. Following DNA damage, COP1 is phosphorylated instantly by ATM (Ataxia telangiectasia mutated) and degraded by 14-3-3σ following nuclear export and enhancing ubiquitination. In ATM lacking cell, other kinases, i.e. ATR (ataxia telangiectasia and Rad3-related protein), Jun kinases and DNA-PK (DNA-dependent protein kinase) cause COP1 & CSN3 (COP9 signalosome complex subunit-3) phosphorylation and initiate COP1’s down regulation. Although, it has been previously found that co-knockout of MDM2 and COP1 enhance p53’s half life by eight fold, the reason is still unknown. Additionally, while interacting with p53, COP1 upregulate MDM2’s E3 ubiquitin ligase, Akt, CSN6 (COP9 signalosome 6) activity and inhibit 14-3-3σ’s negative regulation on MDM2 and COP1 itself. Conclusively, there persists an amplification loop among COP1, MDM2, Akt and 14-3-3σ to regulate p53’s stability and activity. However, the role of another tumor suppressor PTEN (phosphatase and tensin homologue) is yet to be discovered. This study provides insight on the molecular genetic pathways related to cancer and might be helpful for therapeutic inventions. 
      PubDate: 2014-12-03
      Issue No: Vol. 1, No. 5 (2014)
       
  • Immune-o-toxins as the magic bullet for therapeutic purposes

    • Authors: Suchita Srivastava, Suaib Luqman
      Abstract: Immunotoxins are chimeric molecules embodied with a protein toxin and a ligand which is either a growth factor or an antibody. The ligand part of the immunotoxin recognizes and binds to an antigen of the target cell, allowing the internalization of the toxin,moiety and permitting its drift to the cytoplasm where it can destroy the cell. Target specificity of the chimeric protein is determined via the binding attributes of the chosen antibody. Predominantly, immunotoxins are purposefully constructed to slay cancer cells as part of novel treatment approach. In addition they are also used for various autoimmune, viral and other infectious diseases. With the advent of biotechnology, recombinant immunotoxins have been created and are clinically tested to target malignant cells. Our article summarizes foremost progress in the development of immunotoxin based therapeutics and presents a comprehensive portrayal of the immunotoxin generation.

      PubDate: 2014-12-03
      Issue No: Vol. 1, No. 5 (2014)
       
  • Direct reprogramming of somatic cells: an update

    • Authors: Phuc Van Pham
      Abstract:             Direct reprogramming is a technique that converting an adult cell into another differentiated cells – such from fibroblasts into cardiomyocytes – without passage through an undifferentiated pluripotent stage. This is a novel technology that opening a new chance for both biological research and regenerative medicine. Some preliminary studies about direct reprogramming started in the 1980s when differentiated adult cells could be converted into another differentiated cells by over-expressing some transcription factor genes. These studies showed that differentiated cells or mature cells also have the plasticity. To date, direct reprogramming becomes a powerful tool in the biological research and regenerative medicine, especially personalized medicine. Here, this review aimed to summarize all direct reprogramming studies of somatic cells by master control genes into others as well as potential applications of these techniques in research and treatment of some human diseases.
      PubDate: 2014-06-28
      Issue No: Vol. 1, No. 3 (2014)
       
 
 
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