Bai Xiaowen, Sadat Sanga, Gehmert Sebastian, Alt Eckhard, Song Yao-Hua
Department of Molecular Pathology, University of Texas, MD Anderson Cancer Center, SCRB2, Box 951, 7435 Fannin Street, Houston, TX 77054, United States.
FEBS Lett. 2007 Oct 2;581(24):4681-4. doi: 10.1016/j.febslet.2007.08.063. Epub 2007 Sep 5.
It is known that c-kit(+) cells are increased in heart after infarction. The exact origins of the cardiac c-kit(+) cells remain to be determined. We asked whether adipose tissue could be a potential source of c-kit(+) cells. Our data show that the number of c-kit(+) cells increased in adipose tissue derived stem cells when cultured with conditioned medium from neonatal cardiomyocytes grown under serum deprivation and hypoxia condition. We also found that VEGF receptor Flk-1 is involved in c-kit up regulation via ERK-mediated pathway.
已知梗死心脏中c-kit(+)细胞会增加。心脏c-kit(+)细胞的确切来源仍有待确定。我们探究了脂肪组织是否可能是c-kit(+)细胞的潜在来源。我们的数据显示，当脂肪组织来源的干细胞与在血清剥夺和缺氧条件下培养的新生心肌细胞的条件培养基一起培养时，c-kit(+)细胞数量增加。我们还发现VEGF受体Flk-1通过ERK介导的途径参与c-kit的上调。
