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TGF-β1 enhances cardiomyogenic differentiation of skeletal muscle-derived adult primitive cells

  • Ahmed Abdel-Latif
  • , Ewa K. Zuba-Surma
  • , Jamie Case
  • , Sumit Tiwari
  • , Greg Hunt
  • , Smita Ranjan
  • , Robert J. Vincent
  • , Edward F. Srour
  • , Roberto Bolli
  • , Buddhadeb Dawn

Producción científica: Articlerevisión exhaustiva

31 Citas (Scopus)

Resumen

The optimal medium for cardiac differentiation of adult primitive cells remains to be established. We quantitatively compared the efficacy of IGF-1, dynorphin B, insulin, oxytocin, bFGF, and TGF-β1 in inducing cardiomyogenic differentiation. Adult mouse skeletal muscle-derived Sca1+/CD45-/c-kit-/Thy-1+ (SM+) and Sca1-/CD45-/c-kit-/Thy-1+ (SM-) cells were cultured in basic medium (BM; DMEM, FBS, IGF-1, dynorphin B) alone and BM supplemented with insulin, oxytocin, bFGF, or TGF-β1. Cardiac differentiation was evaluated by the expression of cardiac-specific markers at the mRNA (qRT-PCR) and protein (immunocytochemistry) levels. BM+TGF-β1 upregulated mRNA expression of Nkx2.5 and GATA-4 after 4 days and Myl2 after 9 days. After 30 days, BM+TGF-β1 induced the greatest extent of cardiac differentiation (by morphology and expression of cardiac markers) in SM- cells. We conclude that TGF-β1 enhances cardiomyogenic differentiation in skeletal muscle-derived adult primitive cells. This strategy may be utilized to induce cardiac differentiation as well as to examine the cardiomyogenic potential of adult tissue-derived stem/progenitor cells.

Idioma originalEnglish
Páginas (desde-hasta)514-524
Número de páginas11
PublicaciónBasic Research in Cardiology
Volumen103
N.º6
DOI
EstadoPublished - 2008

Nota bibliográfica

Funding Information:
We gratefully acknowledge Barbara Turgeon for expert secretarial assistance. This study was supported in part by NIH grants R01 HL-72410, HL-55757, HL-68088, HL-70897, HL-76794, HL-78825, and R21 HL-89737.

Financiación

We gratefully acknowledge Barbara Turgeon for expert secretarial assistance. This study was supported in part by NIH grants R01 HL-72410, HL-55757, HL-68088, HL-70897, HL-76794, HL-78825, and R21 HL-89737.

FinanciadoresNúmero del financiador
National Institutes of Health (NIH)HL-70897, R21 HL-89737, R01 HL-72410, HL-78825, HL-55757, HL-68088
National Heart, Lung, and Blood Institute (NHLBI)R01HL076794

    ASJC Scopus subject areas

    • Physiology
    • Cardiology and Cardiovascular Medicine
    • Physiology (medical)

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