西亚试剂：IFATS Series: Adipose Stromal Cell Differentiation is Reduc

发布时间：2025-07-19

Stem Cells First published online July 31, 2008

IFATS Series: Adipose Stromal Cell Differentiation is Reduced by Endothelial Cell Contact and Paracrine Communication: Role of Canonical Wnt-Signaling

Gangaraju Rajashekhar, Dmitry O. Traktuev, Christopher William Roell, Brian H. Johnstone, Stephanie Merfeld-Clauss, Bruce Van Natta, Elliot D. Rosen, Keith L March, Matthias Clauss

Adipose stromal cells (ASC) are multipotential mesenchymal progenitor cells which are readily induced to undergo adipogenic differentiation, and we have recently demonstrated to have functional and phenotypic overlap with pericytes lining microvessels in adipose tissues. In this study we addressed the hypothesis that modulation of ASC fate within this perivascular niche can occur via interaction with endothelial cells (EC) which serve to modulate the adipogenic potential of ASC. To this end, we investigated contact as well as paracrine effects of EC on ASC adipogenesis in 2D-co-culture and via conditioned media, and analyzed mutual gene expression changes by real time RT-PCR. A significant decrease in adipogenic differentiation was observed in ASC when co-cultured with EC but not control fibroblasts. This endothelial cell-specific effect was accompanied by increased expression of factors involved in Wnt signaling; most prominently Wnt1, Wnt4 and Wnt10a, well known inhibitors of adipogenesis. Suppression of Wnt1, but not Wnt 10a or scrambled control siRNA in co-cultures partially reversed the endothelial cell effect, thus increasing adipogenic differentiation, suggesting a plausible role of Wnt1 ligand in modulation of adipogenesis by the vasculature. Furthermore, addition of recombinant Wnt ligand or the Wnt signaling agonist inhibited adipogenic differentiation of ASC in the absence of EC. In conclusion, these data define the relationship in adipose tissue between ASC and EC in the perivascular niche, in which the latter act to repress adipogenesis, thereby stabilizing vasculature. It is tempting to speculate that abnormal endothelial function may be associated with pathologic de-repression of adipogenesis.

 

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