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Prostaglandins Regulate the Expression of Fibroblast Growth Factor-2 in Bone

Universita degli Studi di Camerino, Departimento Di Scienze (M.G.S., L.M.), Morphologiche E Biochimiche Comparate, Camerino (MC) Italy; University of Connecticut School of Medicine, Division of Endocrinology and Metabolism (C.A., A.M., L.G.R., M.M.H.), Farmington, Connecticut 06030-1850; and University of Connecticut School of Dental Medicine, Department of Pediatric Dentistry (A.R.H.), Farmington, Connecticut 06030-1610

Address all correspondence and requests for reprints to: Marja M. Hurley, M.D., The University of Connecticut Health Center, Department of Medicine, Division of Endocrinology and Metabolism, Farmington, Connecticut 06030-1850.

We examined the effect of PGs, particularly PGF₂, on basic fibroblast growth factor-2 (FGF-2) messenger RNA (mRNA) and protein in the rat osteoblastic cell line Py1a and in fetal rat calvariae. Py1a cells expressed multiple FGF-2 mRNA transcripts. PGF₂ dose-dependently increased the 6-kb transcript at 6 h. The selective PGF₂ agonist, fluprostenol (Flup), was more potent than PGF₂. Phorbol myristate acetate (10^-6 M) also increased a 6-kb mRNA at 6 h. By immunofluorescence microscopy, Flup increased perinuclear staining for FGF-2 protein at 6 h and nuclear labeling at 24 h. Immunogold labeling of calvariae revealed that treatment with Flup for 3 h caused a transition of FGF expression from matrix to cells and an increase in cytoplasmic labeling for FGF-2 protein in periosteal cells and in osteoblasts. After treatment with Flup for 24 h, nuclear labeling was marked in periosteal cells and in osteoblasts, and a further increase in cytoplasmic labeling for FGF-2 was noted in osteocytes, periosteal cells, and osteoblasts. We conclude that PGs can increase FGF-2 mRNA and protein in bone cells. Because the effect of Flup was mimicked by phorbol myristate acetate, we hypothesize that PGs’ regulation of FGF-2 is mediated by a PGF₂-selective receptor acting through protein kinase C. Hence, effects of PGs on bone remodeling may be mediated, in part, by endogenous FGF-2.

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