Abstract
Adipocytes arise from distinct progenitor populations during developmental and adult stages but little is known about how developmental progenitors differ from adult progenitors. Here, we investigate the role of platelet-derived growth factor receptor alpha (PDGFRα) in the divergent regulation of the two different adipose progenitor cells (APCs). Using in vivo adipose lineage tracking and deletion mouse models, we found that developmental PDGFRα+ cells are adipogenic and differentiated into mature adipocytes, and the deletion of Pdgfra in developmental adipose lineage disrupted white adipose tissue (WAT) formation. Interestingly, adult PDGFRα+ cells do not significantly contribute to adult adipogenesis, and deleting Pdgfra in adult adipose lineage did not affect WAT homeostasis. Mechanistically, embryonic APCs require PDGFRα for fate maintenance, and without PDGFRα, they underwent fate change from adipogenic to fibrotic lineage. Collectively, our findings indicate that PDGFRα+ cells and Pdgfra gene itself are differentially required for WAT development and adult WAT homeostasis.
Highlights
White adipose tissue (WAT) is a dynamic endocrine organ that controls important physiological processes and mediates various metabolic responses (Kershaw and Flier, 2004; Rosen and Spiegelman, 2006; Rosen and Spiegelman, 2014; Spiegelman and Flier, 2001; Trayhurn and Beattie, 2001)
Our previous work demonstrated that adult but not developmental adipocytes emanate from a vascular smooth cell expressing smooth muscle actin (SMA) and other mural markers (Jiang et al, 2017b; Jiang et al, 2014)
We proposed to test the possibility of using platelet-derived growth factor receptor alpha (PDGFRa) as a fate marker for the developmental adipose progenitor cells (APCs)
Summary
White adipose tissue (WAT) is a dynamic endocrine organ that controls important physiological processes and mediates various metabolic responses (Kershaw and Flier, 2004; Rosen and Spiegelman, 2006; Rosen and Spiegelman, 2014; Spiegelman and Flier, 2001; Trayhurn and Beattie, 2001). The thiazolidinedione (TZD) class of diabetes treatments increases de novo adipogenesis by stimulating stem cell compartment self-renew and proliferation (Tang et al, 2011). Both childhood and adult obesity are caused by uncontrolled expansion of WAT and excessive lipid accumulation, which elevate the risk of metabolic disorders
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