FGF-2 controls the differentiation of resident cardiac precursors into functional cardiomyocytes
J. Clin. Invest. Nathalie Rosenblatt-Velin, et al. 115:1724 doi:10.1172/JCI23418 [Go to this article.]

Figure 1
Sca-1 expression in cardiac tissues from WT (FGF-2^+/+) or FGF-2–deficient (FGF-2^–/–) mice. (A) Sca-1 immunostaining in heart sections from FGF-2^+/+ and FGF-2^–/– neonatal and adult mice with or without renovascular hypertension and cardiac hypertrophy (2-kidney 1-clip model [2K1C]). Original magnification, ×20 and ×63 (insets). (B) Immunodetection of Sca-1 and troponin I in the hearts of adult FGF-2^+/+ mice. Original magnification, ×40 (left panels), ×63 (right panels). (C) Percentage of Sca-1⁺ and c-kit⁺ cells as determined by FACS analysis in total heart cells (Total) and in the cardiomyocyte (CM) and nonmyocyte cell (NMC) fractions from FGF-2^+/+ and FGF-2^–/– mice (n = 5). (D) Percentage of Sca-1⁺ cells as determined by FACS analysis in neonatal or adult NMCs isolated from FGF-2^+/+ (white bars) and FGF-2^–/– mice (black bars). NMCs were either depleted or not depleted of cells expressing CD45, CD31, CD34, Flk-1, CD3, CD4, CD8, B220, TER119, Mac-1, and Gr-1. *P < 0.05; NS, not significant as compared with the corresponding nondepleted group; n = 3–6.