Wednesday, September 1, 2010

9/2 TE-RegenMed-StemCell feed

     
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YIA6 Effects of GLP-1 eluting stem cell therapy on collagen remodelling, infarct size and apoptosis in a porcine model of myocardial infarction.
September 1, 2010 at 8:49 AM
 
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YIA6 Effects of GLP-1 eluting stem cell therapy on collagen remodelling, infarct size and apoptosis in a porcine model of myocardial infarction.

Heart. 2010 Sep;96(17):e10-1

Authors: Wright EJ, Farrell KA, Wallrapp C, Geigle P, Lewis AL, Stratford PW, Malik N, Holt CM

Glucagon-like peptide-1 (GLP-1) is a gut incretin hormone with cardioprotective effects. Human stem cells secreting a GLP-1 fusion protein and encapsulated in an alginate matrix (GLP-1 CellBeads) have been developed as a novel therapeutic agent. This study investigated the effects of GLP-1 CellBeads on post-myocardial infarction (MI) healing in a porcine model. GLP-1 CellBeads were delivered to the left anterior descending coronary artery to create micro-infarcts, with cell-free beads as controls. Hearts were explanted at 1 and 4 weeks post-MI. Gross infarct size was measured as a percentage of left ventricular area. Tissue was analysed for inflammation (number of MAC 387 positive cells/mm(2)), apoptosis (% TUNEL positive cells) and collagen (% picrosirius red staining). Compared with controls (n=4), the GLP-1-treated group (n=6) exhibited less infarct at one (6.21%+/-0.64 vs 9.78%+/-1.80% 2LV, p=NS) and 4 weeks post-MI (4.7%+/-2.1 vs 21.8%+/-4.8% LV, p=0.02). Within the infarct there was increased inflammation in GLP-1-treated groups at both time points (1 week: 97.22%+/-19.62 vs 36.67%+/-7.78, p=0.01; 4 weeks: 24.2%+/-4.57 vs 12.3%+/-3.16, p=0.03). At 1 week, apoptosis rates in the infarct area were similar in both groups (1.46 %+/-0.57 vs 1.47 %+/-0.17, p=NS), with less apoptosis in the GLP-1-treated group at 4 weeks (0.51%+/-0.18 vs 1.84%+/-0.62, p=NS). Collagen content at 1 week was lower (5.14%+/-1.19 vs 9.95%+/-1.42, p=0.05) and at 4 weeks higher in the treated group (20.89%+/-8.25 vs 6.87%+/-2.92, p=NS). GLP-1 CellBeads have an effect on post-MI infarct size, inflammation and ventricular remodelling. These findings require further validation before clinical translation.

PMID: 20801784 [PubMed - in process]

   
   
Translation of stem cell therapy for neurological diseases.
September 1, 2010 at 8:49 AM
 
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Translation of stem cell therapy for neurological diseases.

Transl Res. 2010 Sep;156(3):155-160

Authors: Schwarz SC, Schwarz J

"Regenerative medicine" hopefully will provide novel therapies for diseases that remain without effective therapy. This development is also true for most neurodegenerative disorders including Alzheimer's disease, Huntington's disease, or Parkinson's disease. Transplantation of new neurons to the brain has been performed in Parkinson's disease and in Huntington's disease. The restoration of dopaminergic neurons in patients with Parkinson's disease via implantation of embryonic midbrain tissue was taken from animal experiments to clinical applications, showing a limited efficacy. Clinical trials in patients with Huntington's disease using fetal striatal tissue currently are underway. Today, it seems possible to generate functional dopaminergic or striatal neurons form a variety of stem cells including embryonic or neural stem cells as well as induced pluripotent stem cells. First clinical trials using neural stem cell or embryonic-stem-cell-derived tissue are approved or already underway. Such cells allow for extensive in vitro and in vivo testing as well as "good manufacturing production," reducing the risks in clinical application.

PMID: 20801412 [PubMed - as supplied by publisher]

   
   
New therapies for the failing heart: trans-genes versus trans-cells.
September 1, 2010 at 8:49 AM
 
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New therapies for the failing heart: trans-genes versus trans-cells.

Transl Res. 2010 Sep;156(3):130-135

Authors: Lionetti V, Recchia FA

During the past 30 years, hundreds of pharmacological agents have been developed for the treatment of heart failure; yet few of them ultimately have been tested in patients. Such a disconcerting debacle has spurred the search for non pharmacological therapies, including those based on cardiac delivery of transgenes and stem cells. Cardiac gene therapy preceded stem cell therapy by approximately 10 years; however, both of them already have known an initial phase of enormous enthusiasm followed by moderate-to-strong skepticism, not necessarily justified. The aim of the present review is to discuss succinctly some key aspects of these 2 biological therapies and to argue that, after a phase of disillusionment, gene therapy for the failing heart likely will have the chance to regain the stage. In fact, discoveries in stem cell biology might revitalize gene therapy and, vice versa, gene therapy might potentiate synergistically the regenerative capacity of stem cells.

PMID: 20801409 [PubMed - as supplied by publisher]

   
     
 
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