Bone marrow mononuclear cells and acute myocardial infarction.

Department of Cardiology, London Chest Hospital, Bonner Road, London E2 9JX, UK.
Stem Cell Research & Therapy (Impact Factor: 3.65). 01/2012; 3(1):2. DOI: 10.1186/scrt93
Source: PubMed

ABSTRACT Stem cell transplantation is emerging as a potential therapy to treat heart diseases. Promising results from early animal studies led to an explosion of small, non-controlled clinical trials that created even further excitement by showing that stem cell transplantation improved left ventricular systolic function and enhanced remodelling. However, the specific mechanisms by which these cells improve heart function remain largely unknown. A large variety of cell types have been considered to possess the regenerative ability needed to repair the damaged heart. One of the most studied cell types is the bone marrow-derived mononuclear cells and these form the focus of this review. This review article aims to provide an overview of their use in the setting of acute myocardial infarction, the challenges it faces and the future of stem cell therapy in heart disease.

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    ABSTRACT: It has been reported bone marrow mesenchymal stem cells (BMMSCs) facilitate liver regeneration after toxic injuries. However, the effect of BMMSCs on liver regeneration after massive hepatectomy is barely studied. Here we explored if infusion of BMMSCs promotes liver regeneration in a rat massive hepatectomy model. Hypoxia preconditioning was achieved by culturing BMMSCs under hypoxia environment. 85% hepatectomy was performed and hypoxia or normoxia preconditioned BMMSCs were infused into the portal vein. A group of rats received vascular endothelial growth factor (VEGF) neutralizing antibody peri-operatively, underwent 85% hepatectomy and subsequently infusion of hypoxia preconditioned BMMSCs to verify the role of VEGF in BMMSC's effects on liver regeneration. Liver samples were collected and liver regeneration was evaluated post-operatively. Hypoxia preconditioning enhanced the expression of VEGF in BMMSCs in vitro. Infusion of BMMSCs promoted proliferation of hepatocyte as reflected by elevated cyclinD1 expression and proliferating cell nuclear antigen (PCNA)-positive hepatocytes. However, BMMSC infusion didn't improve serum albumin level, liver weight/body weight ratio (LBWR), and survival after operation. Infusion of hypoxia preconditioned BMMSCs significantly elevated cyclinD1, PCNA-positive hepatocytes, LBWR, and survival compared with normoxia preconditioned BMMSCs, accompanied by increased serum albumin level. And the level of VEGF in liver homogenate was much higher in hypoxia preconditioned BMMSC treated animals than other groups. In addition, the peri-operative injection of VEGF neutralizing antibody significantly blocked the therapeutic effects of hypoxia preconditioned BMMSCs on liver injury and regeneration in this model. Hypoxia preconditioned BMMSCs enhanced liver regeneration after massive hepatectomy in rats, possibly by up-regulating the level of VEGF.
    Stem Cell Research & Therapy 07/2013; 4(4):83. · 3.65 Impact Factor
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    ABSTRACT: Abstract Objectives. Mesenchymal stem cells are sensitive to hypoxia under myocardial micro-environment of ischemia and reperfusion. Ischemic postconditioning, which is cardioprotective against ischemia-reperfusion injury, enhances in vivo survival and therapeutic effects of transplanted stem cells. In this study, we investigated the effects of coronary effluent from postconditioned rat hearts on proliferation and survival of mesenchymal stem cells in vitro under hypoxia. Design. Isolated perfused rat hearts were divided into 3 groups (n=6): the Sham group: receiving a 90 min perfusion; the Control group: receiving a 30 min global ischemia followed by a 60 min reperfusion; the ischemic postconditioning group: before sustained reperfusion, 3 cycles of 30 sec reperfusion and 30 sec ischemia were performed. Inflammation-related factors in coronary effluent were assessed by ELISA. Mesenchymal stem cells from bone marrow of Sprague-Dawley rats were cultured with coronary effluent under hypoxia (95% nitrogen, 5% carbon dioxide, and <1% oxygen) for 6 or 18 hours. Cell proliferation was determined by methyl thiazolyl tetrazolium. Survival rate was measured by Annexin V/PI. Results: Compared with ischemia-reperfusion treatment alone, postconditioning treatment increased the level of interleukin-10 and decreased the level of tumor necrosis factor-α, interleukin-1β in coronary effluent (P<0.01). Stem cells cultured with postconditioned effluent, compared with those with ischemia-reperfusion effluent, had a higher proliferation (optical density value), more surviving cells and less necrosis (P<0.01). Conclusions. Coronary effluent from postconditioned hearts may promote the proliferation and survival of mesenchymal stem cells under hypoxia, and the suppression of inflammation may be involved in this process.
    Scandinavian cardiovascular journal: SCJ 01/2014; · 1.07 Impact Factor
  • European Heart Journal 10/2013; · 14.72 Impact Factor


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