Preadipocytes in the human subcutaneous adipose tissue display distinct features from the adult mesenchymal and hematopoietic stem cells

Abstract

The stroma-vascular fraction (SVF) of human adipose tissue has recently been described to be composed of endothelial cells identified as CD34+/CD31+ cells, infiltrated/resident macrophages defined as CD14+/CD31+ cells, and a new cell population characterized as CD34+/CD31- cells. To elucidate the cell identity of the adipocyte precursor cells, fluorescent activating cell sorter (FACS) analyses were performed on crude SVF cultured under adipogenic conditions, i.e., serum-deprived medium containing insulin, cortisol, triiodothyronine, and supplemented with a PPARgamma agonist for the first 3 days. The progressive accumulation of lipid droplets was associated with a selective enrichment of the CD34+/CD31- cell population whereas control experiments performed in medium supplemented with 10% serum showed an overall downregulation of the three cell markers without adipogenesis. Among the different cell subsets, the CD34+/CD31- subset was the unique cell fraction able to answer to adipogenic culture conditions. Indeed, a time-dependent expression of adipocyte markers as well as acquisition of adipocyte-typical metabolic activities were observed. In parallel, the gene expression of lipogenic and lipolytic enzymes increased. The ability to differentiate into adipocytes was restricted to cells that did not express the mesenchymal stem cell marker CD105. Furthermore, the CD34+/CD31- cells did not respond to culture conditions used for hematopoietic colony assays. Taken together, the present study demonstrates that adipocyte progenitor cells, i.e., the preadipocytes, are included in the CD34+/CD31- cell fraction, which displays distinct features from the adult mesenchymal and hematopoietic stem cells.

Native Adipose Stromal Cells Egress from Adipose Tissue In Vivo: Evidence During Lymph Node Activation

“…S1A-S1C). Based on our previous work on human native ASCs [13,25,26] and in accordance with Rodeheffer et al [27], we identified native murine ASCs as the Sca-1 þ /CD45 À /CD31 À cell population. The further immunophenotyping of Sca-1 þ /CD45 À /CD31 À cells showed that murine native ASCs were positive for CD29, CD34, CD90 (Fig.…”

Functionally Convergent White Adipogenic Progenitors of Different Lineages Participate in a Diffused System Supporting Tissue Regeneration

“…2A). The CD45 À /CD31 À (Lin À )/a 7 À subpopulation, which comprised approximately 14% of the SVF, was then separated based on the expression of stem cell antigen 1 (Sca1), a marker that labels proliferating cells in fat depots [15] and expression of CD34, a marker expressed by stem/ progenitor cells [16] and primary preadipocytes [17]. We found that approximately 27% of the Lin À /a 7 À population was CD34 þ /Sca1 þ , with up to 95% of the Sca1 þ cells expressing CD34 (Fig.…”

Advances in adipose tissue metabolism

“…Nevertheless, particularly in the field of metabolic regulation, the clinical relevance of results obtained with transgenic mice must be questioned. In vitro studies on isolated fat cells 1 or fat cell precursors differentiated into adipocytes in vitro 2,3 have provided a suitable system to explore fat cell biology and a number of regulatory mechanisms at the cell level. AT is not the easiest tissue to study for an integrated approach to its biology and physiology.…”

“…Fat mobilization is potently suppressed by insulin acting through its usual signalling pathway for the control of acute metabolic events, that is, through phosphatidylinositol-3 0 -kinase and protein kinase B activation, which in turn phosphorylates and activates phosphodiesterase 3B, which hydrolyses cAMP to AMP and reduces the lipolytic activity. Several other antilipolytic pathways that involve a 2 -adrenergic receptors, A 1 -adenosine-receptors, EP 3 ) catecholamines (epinephrine and norepinephrine) through b-adrenergic receptor-mediated adenylyl cyclase activation, (ii) inhibitory receptors (that is, a 2 -adrenergic receptors, adenosine, prostaglandin, neuropeptide Y/peptide YY and nicotinic acid) through inhibition of adenylyl cyclase activity and (iii) insulin through cyclic nucleotide phosphodiesterase 3B activation of phosphodiesterase 3B. ANP and B-type natriuretic peptide stimulate NPR-A-dependent guanylyl cyclase activity and cGMP production.…”