Cardioprotective c-kit⁺ cells are from the bone marrow and regulate the myocardial balance of angiogenic cytokines
J. Clin. Invest. Shafie Fazel, et al. 116:1865 doi:10.1172/JCI27019 [Go to this article.]

Figure 4
c-kit dysfunction increases apoptosis and decreases mitogenesis. (A) Incubation of bone marrow cells from Kit^+/+ mice with 50 ng/ml of recombinant SCF causes cell proliferation. Kit^W/Kit^W–v bone marrow cells had no response to SCF. (B) After coronary ligation, myocardial SCF levels increased in both Kit^+/+ and Kit^W/Kit^W–v mice. Representative immunoblot of 5 independent experiments is shown. (C) Consistent with the in vitro data, the recruited c-kit⁺ cells in Kit^W/Kit^W–v mice had lower index of proliferation as assessed by Ki67 and c-kit staining and visualized by confocal microscopy of 10 random ×400 fields. n =3 per group. *P <0.05. (D) The total number of c-kit⁺ cells in Kit^W/Kit^W–v mice was lower than in Kit^+/+ mice. (E) Quantification of the total number of c-kit–expressing cells in the infarcted myocardium. n =3 per time point per group. (F) The Kit^+/+ mice had more CD45^– c-kit⁺ cells than Kit^W/Kit^W–v mice. n =3 per group. (G) Nonmyocyte mitogenesis was markedly higher in Kit^+/+ mice in the infarct border zone. (H) Quantification of general mitogenesis by region and over a time course. n =3 per time point per group. ^#P <0.01. BZ, border zone. (I) The number of infiltrating c-kit–expressing cells correlated with the number of cycling cells (r =0.78). (J) Differences in apoptotic cell death as quantified in K were smaller than differences in mitogenesis. n =3 per time point per group. *P <0.05 versus Kit^+/+. Magnification, ×200.