The EP4-ERK-dependent pathway stimulates osteo-adipogenic progenitor proliferation resulting in increased adipogenesis in fetal rat calvaria cell cultures
2012
Minamizaki, Tomoko | Yoshiko, Yuji | Yoshioka, Hirotaka | Kozai, Katsuyuki | Aubin, Jane E. | Maeda, Norihiko
We previously reported that fetal rat calvaria (RC) cells are osteo-adipogenic bipotential and that PGE₂ receptors EP2 and EP4 are involved in bone nodule formation via both common and distinct MAPK pathways in RC cell cultures. Because PGE₂ participates in multiple biological processes including adipogenesis, it is of interest to determine the additional role(s) of PGE₂ in RC cells. PGE₂ increased the number of adipocyte colonies when RC cells were treated during proliferation but not other development stages. Of four EP agonists tested, the EP4 agonist ONO-AE1-437 (EP4A) was the most effective in promoting adipogenesis. Concomitantly, EP4A increased the number of cells with BrdU labeling and gene expression of CCAAT/enhancer binding protein (C/EBP)δ and c-fos but not peroxisome proliferator-activated receptor γ2 and C/EBPα. Amongst MAPK inhibitors, U0126, an inhibitor of MEK1/2, abrogated the EP4A-dependent effects. Our results suggest that the PGE₂–EP4-ERK pathway increases the number of osteo-adipogenic bipotential progenitor cells, with a resultant increase in adipogenesis in RC cell cultures.
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