Elena J. Moerman

TL;DR: It is demonstrated that, during aging, the status of mMSC changes with respect to both their intrinsic differentiation potential and production of signaling molecules, which contributes to the formation of a specific marrow microenvironment necessary for maintenance of bone homeostasis.

TL;DR: It is strongly suggested that PPARγ2 negatively regulates stromal cell plasticity by suppressing Osf2/Cbfa1 and osteoblast‐like biosynthetic activity, while promoting terminal differentiation to adipocytes.

TL;DR: It is shown that the naturally occurring PPARγ ligands 9,10-dihydroxyoctadecenoic acid, and 15-deoxy-Δ12,14-PGJ2, also stimulate adipocytes and inhibit osteoblast differentiation of U-33/γ2 cells.

TL;DR: Results indicate that senescence of both WS and normal HDF is accompanied by overexpression of similar sets of diverse genes which may play a role in the senescent arrest of cellular replication and in the genesis of WS, normal biological aging, and attendant diseases.

TL;DR: Molar ratios of IGFBP-3/IGF-II were consistently higher in old and WS cells and increased substantially as all three cell types became quiescent, due to either serum depletion or high cell density, which are consistent with either an adaptive or a causal role for IGF BP-3 protein in the senescent andQuiescent growth arrest of HDFs.