ABSTRACT
The aims of this study were to determine how Prostaglandin E2 (PGE2) locally applied affected the immunodistribution of latent transforming growth factor-beta 1 (TGF-beta1), and how the eicosanoid modified TGF-beta1 release and TGF-beta receptors gene expression in cultured osteoblasts. PGE2 locally delivered on the rat mandible at doses of 0.1 and 0.05 mg/day, but not 0.025 mg/day, over 20 days significantly increased latent TGF-beta1 immunodistribution (P<0.001), comparing with a placebo-treated group. Cultured osteoblasts stimulated with 10(-5) or 10(-7)M PGE2 significantly varied the level of activated TGF-beta1 released into supernatants at different experimental periods compared with negative and positive controls. TGF-beta receptor type I gene expression was significantly increased in osteoblasts (P<0.01) after 10 days of treatment with 10(-5) and 10(-7)M PGE2, whereas 10(-3) M PGE2 produced the opposite effect. It is concluded that PGE2 may stimulate bone deposition by affecting TGF-beta pathway. This effect on the pathway appears to be dose-dependent.
Subject(s)
Dinoprostone/pharmacology , Gene Expression/drug effects , Receptors, Transforming Growth Factor beta/genetics , Transforming Growth Factor beta/metabolism , Activin Receptors, Type I/genetics , Alkaline Phosphatase/analysis , Animals , Body Weight/drug effects , Cells, Cultured , Core Binding Factor Alpha 1 Subunit/analysis , Culture Media, Conditioned/chemistry , Delayed-Action Preparations/administration & dosage , Dinoprostone/administration & dosage , Dose-Response Relationship, Drug , Female , Implants, Experimental , Osteoblasts/cytology , Osteoblasts/drug effects , Osteoblasts/metabolism , Protein Serine-Threonine Kinases , Rats , Rats, Inbred Lew , Rats, Wistar , Receptor, Transforming Growth Factor-beta Type I , Receptor, Transforming Growth Factor-beta Type II , Transforming Growth Factor beta/analysis , Transforming Growth Factor beta1ABSTRACT
OBJECTIVE: To determine whether treatments with high-density lipoprotein (HDL) may alter the lipopolysaccharide (LPS)-induced alveolar bone resorption in rats. MATERIALS AND METHODS: Rats were injected with 500 microg of LPS from Escherichia coli at the alveolar mucosa of lower right first molar once every 2 days for 8 days. The negative and positive control were injected with phosphate buffered saline (PBS) and LPS alone, respectively. In HDL-treated animals various concentration of HDL were injected immediately before, after the third or the final LPS injection. The bone sections were stained with tartrate-resistant acid phosphatase (TRAP) and the numbers of both osteoclasts and preosteoclasts and the levels of alveolar bone resorption were assessed. RESULTS: The numbers of both osteoclasts and preosteoclasts and the levels of alveolar bone resorption in animals treated with HDL before or during LPS injections were lower than those in the positive control, but higher than those in the negative control, regardless of HDL doses. Similar results were also observed in animals treated with 250 and 500 microg of HDL after the final LPS injection. Only treatments with 1000 microg of HDL after LPS injections completely reduced the number of both osteoclasts and preosteoclasts, but only partially decreased the alveolar bone resorption. CONCLUSION: HDL treatments partially reduced the LPS-induced alveolar bone resorption in vivo in rats, suggesting that HDL may neutralize the ability of LPS to induce alveolar bone resorption.
