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Archives of cardiovascular diseases
Volume 102, n° S1
page 39 (mars 2009)
Doi : 10.1016/S1875-2136(09)72220-X
Themes et posters

D010 Mesenchymal stem cells protect cardiomyocytes from reperfusion injury through a paracrine activation of the PI3 kinase pathway
 

D. Angoulvant 1, F. Ivanes 1, R. Ferrera 1, P.G. Matthews 1, S. Nataf 2, N. Cheriaa 1, M. Ovize 1
1 Inserm U886, Université Claude Bernard Lyon 1, Lyon, France 
2 Inserm U842, Université Claude Bernard Lyon 1, Lyon, France 

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Objectives

Previous data suggest that implantation of mesenchymal stem cells (MSCs) improves heart function after myocardial infarction. We investigated whether protection afforded by MSCs might involve a paracrine activation of the PI3 kinase pathway in reperfused cardiomyocytes.

Method

MSCs and neonatal rat cardiomyocytes (NRCs) were isolated and cultured separately. NRCs (2.106) were subjected to 5 hours of ischemia followed by 16 hours of reperfusion. At the time of reperfusion, NRCs (n=8-14/group) received either fresh medium (control group), or the following treatments: MSCs (2.105 MSCs in fresh medium), conditioned SN (MSCs supernatant alone (i.e. without MSCs) obtained after 8 hours of serum deprived culture), [conditioned SN + LY294002] (15 microM of LY294002 a specifi c inhibitor of PI3K), [conditioned SN + Wortmannin] (100 nM of wortmannin, a non specifi c inhibitor of PI3K), or CsA (200 nM in fresh medium) a potent inhibitor of the mitochondrial permeability transition pore. Cell death was assessed by LDH release in NRCs supernatant at the end of reperfusion.

Results

As expected, LDH activity was dramatically reduced by CsA, averaging 4 % of control values. LDH activity was signifi cantly reduced by MSCs alone and by conditioned SN, averaging 29 % and 12 % of control value, respectively. Both LY294002 and wortmannin signifi cantly attenuated conditioned SN induced protection.

Conclusion

our data suggest that MSCs can protect NRCs from reperfusion injury through a paracrine activation of the PI3K pathway.

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