OBJECTIVES: Prostaglandin E(2) (PGE(2)) is an important factor in the pathogenesis of periodontal disease because of bone resorbing activity and association with attachment loss. PGE(2) and PGE receptor subtypes (EPs) play an important role in modulating bone metabolism via osteoblasts. However, little is known about the effects of PGE(2) on cementoblasts. The aims of this study were to determine the expression of EPs in mature cementoblasts, and to examine the effect of PGE(2) and EPs on their cellular function. DESIGN: Expression of EPs in immortalized mouse cementoblasts (OCCM-30 cells), which were characterized as mature cementoblasts, was determined using reverse transcriptase polymerase chain reaction (RT-PCR). The effects of PGE(2) and EP agonists on mineralization were examined by studying nodule formation with alizarin red S staining. Alkaline phosphatase (ALP) activity with PGE(2) and EP4 agonist was examined using the Bessey-Lowry enzymologic method. Effects of the PGE(2)-EP4 pathway on expression levels of osteocalcin (OCN) and matrix metalloproteinase-13 (MMP-13) mRNA were examined using real-time RT-PCR. RESULTS: OCCM-30 cells expressed EP1, EP2, EP3 and EP4 mRNA. PGE(2) and EP4 agonist led to downregulation of mineralized nodule formation and ALP activity in OCCM-30 cells. OCN mRNA expression was suppressed and MMP-13 mRNA expression was stimulated via the PGE(2)-EP4 pathway in OCCM-30 cells. CONCLUSIONS: Cementoblasts may downregulate their mineralization ability and upregulate MMP-13 production through the PGE(2)-EP4 pathway, and may contribute to destruction of connective tissue attachment under inflammatory conditions.
OBJECTIVES:Prostaglandin E(2) (PGE(2)) is an important factor in the pathogenesis of periodontal disease because of bone resorbing activity and association with attachment loss. PGE(2) and PGE receptor subtypes (EPs) play an important role in modulating bone metabolism via osteoblasts. However, little is known about the effects of PGE(2) on cementoblasts. The aims of this study were to determine the expression of EPs in mature cementoblasts, and to examine the effect of PGE(2) and EPs on their cellular function. DESIGN: Expression of EPs in immortalized mouse cementoblasts (OCCM-30 cells), which were characterized as mature cementoblasts, was determined using reverse transcriptase polymerase chain reaction (RT-PCR). The effects of PGE(2) and EP agonists on mineralization were examined by studying nodule formation with alizarin red S staining. Alkaline phosphatase (ALP) activity with PGE(2) and EP4 agonist was examined using the Bessey-Lowry enzymologic method. Effects of the PGE(2)-EP4 pathway on expression levels of osteocalcin (OCN) and matrix metalloproteinase-13 (MMP-13) mRNA were examined using real-time RT-PCR. RESULTS: OCCM-30 cells expressed EP1, EP2, EP3 and EP4 mRNA. PGE(2) and EP4 agonist led to downregulation of mineralized nodule formation and ALP activity in OCCM-30 cells. OCN mRNA expression was suppressed and MMP-13 mRNA expression was stimulated via the PGE(2)-EP4 pathway in OCCM-30 cells. CONCLUSIONS: Cementoblasts may downregulate their mineralization ability and upregulate MMP-13 production through the PGE(2)-EP4 pathway, and may contribute to destruction of connective tissue attachment under inflammatory conditions.
Authors: Yubo Sun; David R Mauerhan; Atiya M Franklin; Natalia Zinchenko; Harry James Norton; Edward N Hanley; Helen E Gruber Journal: Arthritis Date: 2014-05-20