PBX1: a novel stage-specific regulator of adipocyte development.

摘要: Although adipocyte terminal differentiation has been extensively studied, the early steps of development and embryonic origin this lineage remain largely unknown. Here we describe a novel role for pre-B-cell leukemia transcription factor one (PBX1) in using both mouse stem cells (mESCs) human multipotent adipose-derived (hMADS) cells. We show that Pbx1(-/-) mESCs are unable to generate adipocytes, despite normal expression neuroectoderm neural crest (NC) markers. Early markers not induced mESCs, suggesting Pbx1 controls generation and/or maintenance progenitors (APs) from NC. further characterize function PBX1 postnatal adipogenesis silencing hMADS reduces their proliferation by preventing entry S phase cell cycle. Furthermore, it promotes into adipocytes partially substitutes glucocorticoids rosiglitazone, two key proadipogenic agents. These effects involve direct modulation PPARγ activity, most likely through regulation biosynthesis natural endogenous ligand(s). Together, our data suggest regulates at multiple levels, promoting NC-derived APs during embryogenesis, while favoring commitment life.