The PPARgamma-selective ligand BRL-49653 differentially regulates the fate choices of rat calvaria versus rat bone marrow stromal cell populations

Abstract

Background: Osteoblasts and adipocytes are derived from a common mesenchymal progenitor and an inverse relationship between expression of the two lineages is seen with certain experimental manipulations and in certain diseases, i.e., osteoporosis, but the cellular pathway(s) and developmental stages underlying the inverse relationship is still under active investigation. To determine which precursor mesenchymal cell types can differentiate into adipocytes, we compared the effects of BRL-49653 (BRL), a selective ligand for peroxisome proliferators-activated receptor (PPAR)γ, a master transcription factor of adipogenesis, on osteo/adipogeneis in two different osteoblast culture models: the rat bone marrow (RBM) versus the fetal rat calvaria (RC) cell system.

Combination treatment with pioglitazone and fenofibrate attenuates pioglitazone-mediated acceleration of bone loss in ovariectomized rats

“…The latter is consistent with our finding that Pio exacerbated OVX-induced loss of bone and is in accordance with several other studies showing that TZD PPARg agonists suppress osteogenesis (Akune et al 2004) and/or reduce alkaline phosphatase activity (Hasegawa et al 2008). Thus, PPARg may exert direct inhibitory effects on osteogenesis/osteoblast function in addition to its well-established effects through stimulation of adipogenesis from marrow progenitor cells that can reciprocally give rise to adipocytes or osteoblasts (Akune et al 2004).…”

“…sialoprotein and collagen I) in MC3T3-E1 cells (Syversen et al 2009) and inhibited osteoclast formation (Chan et al 2007). In contrast, PPARg activation by high doses of troglitazone and ciglitazone decreased maturation of MC3T3-E1 cells (Jackson & Demer 2000) and rosiglitazone has been shown to decrease the expression of several osteoblast markers in vitro (Hasegawa et al 2008). …”

Superpulsed laser irradiation increases osteoblast activity via modulation of bone morphogenetic factors

“…PPARa and g were examined because they are closely connected with the reduction of cell viability and proliferation and with the increase in differentiation [36,37]. In laser-exposed cells, the strongest increase occurred in the isotype g. The observation regarding the PPARg increase is in disagreement with some reports indicating an anti-osteoblastogenic role for this nuclear receptor [38][39][40][41]; these studies principally analyzed the role of PPARg in determining the destiny of multipotent mesenchymal stem cells in bone marrow.…”

Comparative study of porous hydroxyapatite/chitosan and whitlockite/chitosan scaffolds for bone regeneration in calvarial defects

“…By contrast, less numbers of newly formed bone tissue were found in HAP/chitosan group, with obvious vacancy between implants and preexisting bone. Moreover, in microscopic view, we found more bone ingrowth into the WH/chitosan scaffolds, with more positive area for fluorochrome labeling (for calcium deposition), Van Gieson (for collagen of newly formed bone), 34 and OCN (for secreted protein from mature osteoblast) 35 staining. We mainly attributed the better performance of bone regeneration of WH/chitosan to Mg incorporation, microstructure, and gradual release of Ca and P of the scaffolds.…”