PPARgamma2 gene expression signature in U-33 / gamma2 and U-33/c mouse cell lines
Murine marrow-derived U-33 cells represent a clonal cell line spontaneously immortalized in the long term bone marrow culture conditions.
To study the effect of PPARgamma2 on marrow mesenchymal stem cell (MSC) differentiation, U-33 cells were stably transfected with either the PPARgamma2 expression construct (U-33/gamma2 cells) or an empty vector control (U-33/c cells). The effect of PPARgamma2 on MSC molecular signature was evaluated with respect to the expression of 135 genes that represent markers of either early or lineage committed stem cells. For further details see the supporting manuscript (Shockley et al., 2007).
To compliment biochemical analyses, rosiglitazone treatment (1 µM) of a marrow stromal cell line (UAMS-33) transfected with empty vector (U-33/c) or with PPARgamma2 (U-33/gamma2) were analyzed by microarray. The effect of Rosi stimulated PPARgamma2 on genes related to the insulin-like growth factor system was studied further. For more details see Lecka-Czernik et al., 2006.
In order to identify mechanisms by which PPARgamma2 suppresses osteoblastogenesis and promotes adipogenesis in MSC, we analyzed the PPARgamma2 transcriptome in response to Rosi. The experimental design consisted of 2 levels of rosiglitazone treatment (with/without Rosi), 3 time points (2-, 24- and 72-hr after treatment) in both cell types (U-33/g2 and U-33/c cells). For further details see the supporting manuscript (Shockley et al., 2009)
PPARgamma2 nuclear receptor controls multiple regulatory pathways of osteoblast differentiation from marrow mesenchymal stem cells
PPARgamma2 Regulates a Molecular Signature of Marrow Mesenchymal Stem Cells
Activation of peroxisome proliferator-activated receptor gamma (PPARgamma) by rosiglitazone suppresses components of the insulin-like growth factor regulatory system in vitro and in vivo
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