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Cell survival and redistribution after transplantation into damaged myocardium.

Zhang H, Chen H, Wang W, Wei Y, Hu S - J. Cell. Mol. Med. (2010)

Bottom Line: However, poor cell survival and extensive redistribution throughout the body can drastically affect the outcome and safety of cell therapy.Although various approaches have been attempted to support the survival and engraftment of implanted cells, we need to apply a new comprehensive strategy by melding the in vitro and in vivo approaches to recondition the cells and infarcted myocardium.Here we summarize our understanding of cell survival and migration after transplantation into the damaged heart.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiac Surgery, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing, China.

ABSTRACT
A hybrid approach to support cell survival and decrease cell escape Cell transplantation has become an attractive option for cardiac regenerative therapy. However, poor cell survival and extensive redistribution throughout the body can drastically affect the outcome and safety of cell therapy. Although various approaches have been attempted to support the survival and engraftment of implanted cells, we need to apply a new comprehensive strategy by melding the in vitro and in vivo approaches to recondition the cells and infarcted myocardium. Here we summarize our understanding of cell survival and migration after transplantation into the damaged heart.

Show MeSH
Quantification of implanted male MSCs in female rats by real-time polymerase chain reaction. The data are expressed as the average percentage, relative to the initial number of injected cells.
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fig02: Quantification of implanted male MSCs in female rats by real-time polymerase chain reaction. The data are expressed as the average percentage, relative to the initial number of injected cells.

Mentions: In another preliminary study, we injected male MSCs into a sex-mismatched rat chronic MI model (Fig. 2). One hour after CTx, 56% of injected cells were untraceable and 8% of cells were harboured by filter organs. Interestingly, we found 3% and 4% of cells in venous and arterial blood, respectively. These findings indicate that cell migration is initiated in an ultra-early stage after transplantation and that blood flow is the main ‘highway’ for cell escape. Thus venous blood could collect escaped cells from the right and left side of the heart and transport them into the lung. Similarly, cells washed from the left side of the heart could be pumped into the systemic circulation via the left ventricular space and then captured by reticulo-endothelial systems, mainly located in liver and spleen. Two weeks later, no evidence for cell viability in peripheral blood was found. We presume that the survived cells had been integrated into the micro-environment at a late stage after CTx. Therefore, the myocardial contractile force would not squeeze more retained cells into the blood at a late stage. However, the total amount of escaped cells accounted for 37% of total traceable cells at 2 weeks after transplantation.


Cell survival and redistribution after transplantation into damaged myocardium.

Zhang H, Chen H, Wang W, Wei Y, Hu S - J. Cell. Mol. Med. (2010)

Quantification of implanted male MSCs in female rats by real-time polymerase chain reaction. The data are expressed as the average percentage, relative to the initial number of injected cells.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822744&req=5

fig02: Quantification of implanted male MSCs in female rats by real-time polymerase chain reaction. The data are expressed as the average percentage, relative to the initial number of injected cells.
Mentions: In another preliminary study, we injected male MSCs into a sex-mismatched rat chronic MI model (Fig. 2). One hour after CTx, 56% of injected cells were untraceable and 8% of cells were harboured by filter organs. Interestingly, we found 3% and 4% of cells in venous and arterial blood, respectively. These findings indicate that cell migration is initiated in an ultra-early stage after transplantation and that blood flow is the main ‘highway’ for cell escape. Thus venous blood could collect escaped cells from the right and left side of the heart and transport them into the lung. Similarly, cells washed from the left side of the heart could be pumped into the systemic circulation via the left ventricular space and then captured by reticulo-endothelial systems, mainly located in liver and spleen. Two weeks later, no evidence for cell viability in peripheral blood was found. We presume that the survived cells had been integrated into the micro-environment at a late stage after CTx. Therefore, the myocardial contractile force would not squeeze more retained cells into the blood at a late stage. However, the total amount of escaped cells accounted for 37% of total traceable cells at 2 weeks after transplantation.

Bottom Line: However, poor cell survival and extensive redistribution throughout the body can drastically affect the outcome and safety of cell therapy.Although various approaches have been attempted to support the survival and engraftment of implanted cells, we need to apply a new comprehensive strategy by melding the in vitro and in vivo approaches to recondition the cells and infarcted myocardium.Here we summarize our understanding of cell survival and migration after transplantation into the damaged heart.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiac Surgery, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Beijing, China.

ABSTRACT
A hybrid approach to support cell survival and decrease cell escape Cell transplantation has become an attractive option for cardiac regenerative therapy. However, poor cell survival and extensive redistribution throughout the body can drastically affect the outcome and safety of cell therapy. Although various approaches have been attempted to support the survival and engraftment of implanted cells, we need to apply a new comprehensive strategy by melding the in vitro and in vivo approaches to recondition the cells and infarcted myocardium. Here we summarize our understanding of cell survival and migration after transplantation into the damaged heart.

Show MeSH