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First published online May 14, 2007
doi: 10.1242/10.1242/jcs.006122

Journal of Cell Science 120, 1791-1800 (2007)
Published by The Company of Biologists 2007
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Research Article

Clonally amplified cardiac stem cells are regulated by Sca-1 signaling for efficient cardiovascular regeneration

Kento Tateishi1,2, Eishi Ashihara1, Naofumi Takehara1, Tetsuya Nomura1,2, Shoken Honsho2, Takuo Nakagami2,3, Shigehiro Morikawa4, Tomosaburo Takahashi1,2, Tomomi Ueyama1, Hiroaki Matsubara1,2,* and Hidemasa Oh1,*

1 Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, Kyoto 606-8507, Japan
2 Department of Cardiovascular Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
3 Departments of Pathology and Cell Regulation, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
4 Molecular Neuroscience Research Center, Shiga University of Medical Science, Shiga 520-2192, Japan

* Authors for correspondence (e-mail: matsubah{at}koto.kpu-m.ac.jp; hidemasa{at}kuhp.kyoto-u.ac.jp)

Accepted 25 March 2007

Recent studies have shown that cardiac stem cells (CSCs) from the adult mammalian heart can give rise to functional cardiomyocytes; however, the definite surface markers to identify a definitive single entity of CSCs and the molecular mechanisms regulating their growth are so far unknown. Here, we demonstrate a single-cell deposition analysis to isolate individually selected CSCs from adult murine hearts and investigate the signals required for their proliferation and survival. Clonally proliferated CSCs express stem cell antigen-1 (Sca-1) with embryonic stem (ES) cell-like and mesenchymal cell-like characteristics and are associated with telomerase reverse transcriptase (TERT). Using a transgene that expresses a GFP reporter under the control of the TERT promoter, we demonstrated that TERTGFP-positive fractions from the heart were enriched for cells expressing Sca-1. Knockdown of Sca-1 transcripts in CSCs led to retarded ex vivo expansion and apoptosis through Akt inactivation. We also show that ongoing CSC proliferation and survival after direct cell-grafting into ischemic myocardium require Sca-1 to upregulate the secreted paracrine effectors that augment neoangiogenesis and limit cardiac apoptosis. Thus, Sca-1 might be an essential component to promote CSC proliferation and survival to directly facilitate early engraftment, and might indirectly exert the effects on late cardiovascular differentiation after CSC transplantation.

Key words: Cardiac stem cells, Proliferation, Regeneration, Stem cell antigen-1, Survival, Telomerase




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