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. 2015 May 8;4(5):e001614. doi: 10.1161/JAHA.114.001614

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© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Long-term, limited engraftment of implanted stem cells. Chronic (3 months) stress, imposed by TAC upon Kir6.2-deficient hearts, mobilized endogenous Sca-1⁺ stem cells from the perivascular niche prestress [TAC(−); A] to the myocardial parenchyma [TAC-iPS(−); B and C]. In stem cell-treated ventricles under equivalent TAC-induced stress [TAC-iPS(+)], Sca-1⁺ cells were recruited into the perivascular stem cell niche and colocalized with transplanted stem cells tracked by β-galactosidase expression (D through F). CI indicates confidence interval; DAPI, 4′,6′-diamidino-2-phenylindole; iPS, induced pluripotent stem; TAC, transverse aortic constriction; α-actinin, sarcomeric α-actinin; β-gal, β-galactosidase.