TY - JOUR
T1 - Tbx6 induces cardiomyocyte proliferation in postnatal and adult mouse hearts
AU - Haginiwa, Sho
AU - Sadahiro, Taketaro
AU - Kojima, Hidenori
AU - Isomi, Mari
AU - Tamura, Fumiya
AU - Kurotsu, Shota
AU - Tani, Hidenori
AU - Muraoka, Naoto
AU - Miyake, Noriko
AU - Miyake, Koichi
AU - Fukuda, Keiichi
AU - Ieda, Masaki
N1 - Funding Information:
This work was supported by research grants from the Research Center Network for Realization of Regenerative Medicine , and the Practical Research Project for Rare/Intractable Diseases funded by the Japan Agency for Medical Research and Development , the Japan Society for the Promotion of Science (JSPS) [grant number 17H04179 ], and Takeda Science Foundation (to M.I.); and research grants from JSPS to S.H [grant number 18K15861 ] and T.S. [grant numbers 16K19426, 18K08114 ]. The authors declare no conflict of interest.
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/6/11
Y1 - 2019/6/11
N2 - Cardiovascular disease is a leading cause of death worldwide. Mammalian cardiomyocytes (CMs) proliferate during embryonic development, whereas they largely lose their regenerative capacity after birth. Defined factors expressed in cardiac progenitors or embryonic CMs may activate the cell cycle and induce CM proliferation in postnatal and adult hearts. Here, we report that the overexpression of Tbx6, enriched in the cardiac mesoderm (progenitor cells), induces CM proliferation in postnatal and adult mouse hearts. By screening 24 factors enriched in cardiac progenitors or embryonic CMs, we found that only Tbx6 could induce CM proliferation in primary cultured postnatal rat CMs. Intriguingly, it did not induce the proliferation of cardiac fibroblasts. We next generated a recombinant adeno-associated virus serotype 9 vector encoding Tbx6 (AAV9-Tbx6) for transduction into mouse CMs in vivo. The subcutaneous injection of AAV9-Tbx6 into neonatal mice induced CM proliferation in postnatal and adult mouse hearts. Mechanistically, Tbx6 overexpression upregulated multiple cell cycle activators including Aurkb, Mki67, Ccna1, and Ccnb2 and suppressed the tumor suppressor Rb1. Thus, Tbx6 promotes CM proliferation in postnatal and adult mouse hearts by modifying the expression of cell cycle regulators.
AB - Cardiovascular disease is a leading cause of death worldwide. Mammalian cardiomyocytes (CMs) proliferate during embryonic development, whereas they largely lose their regenerative capacity after birth. Defined factors expressed in cardiac progenitors or embryonic CMs may activate the cell cycle and induce CM proliferation in postnatal and adult hearts. Here, we report that the overexpression of Tbx6, enriched in the cardiac mesoderm (progenitor cells), induces CM proliferation in postnatal and adult mouse hearts. By screening 24 factors enriched in cardiac progenitors or embryonic CMs, we found that only Tbx6 could induce CM proliferation in primary cultured postnatal rat CMs. Intriguingly, it did not induce the proliferation of cardiac fibroblasts. We next generated a recombinant adeno-associated virus serotype 9 vector encoding Tbx6 (AAV9-Tbx6) for transduction into mouse CMs in vivo. The subcutaneous injection of AAV9-Tbx6 into neonatal mice induced CM proliferation in postnatal and adult mouse hearts. Mechanistically, Tbx6 overexpression upregulated multiple cell cycle activators including Aurkb, Mki67, Ccna1, and Ccnb2 and suppressed the tumor suppressor Rb1. Thus, Tbx6 promotes CM proliferation in postnatal and adult mouse hearts by modifying the expression of cell cycle regulators.
KW - AAV9
KW - Cardiomyocyte
KW - Cell cycle
KW - Regeneration
KW - Tbx6
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U2 - 10.1016/j.bbrc.2019.04.087
DO - 10.1016/j.bbrc.2019.04.087
M3 - Article
C2 - 31010673
AN - SCOPUS:85064455844
SN - 0006-291X
VL - 513
SP - 1041
EP - 1047
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -