CD47 Inhibits Self-renewal and Reprogramming by Regulating c-Myc and Other Stem Cell Transcription Factors

ABSTRACT: Signaling through the thrombospondin-1 receptor CD47 broadly limits cell and tissue survival of stress, but the molecular mechanisms are incompletely understood. We now show that loss of CD47 permits sustained proliferation of primary murine endothelial cells and enables these cells to spontaneously reprogram to form multipotent embryoid bodies. c-Myc, Klf4, Oct4, and Sox2 expression is elevated in CD47-null endothelial cells, in several tissues of CD47- or thrombospondin-1-null mice, and in a human T cell line lacking CD47. CD47 knockdown acutely increases mRNA levels of c-Myc and other stem cell transcription factors in cells and in vivo, whereas CD47 ligation by thrombospondin-1 suppresses c-Myc expression. The inhibitory effects of increasing CD47 levels can be overcome by maintaining

ORGANISM(S): Mus musculus

SUBMITTER: abdel elkahloun 

PROVIDER: E-GEOD-43133 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress