title: Expression of cyclooxygenase genes and involvement of endogenous prostaglandin during osteogenesis in the rat tibial bone marrow cavity.
abstract: Many researchers have demonstrated that the administration of prostaglandins (PGs), especially PGE2, increases the bone volume in vivo. It is still not clear how endogenous PG is associated with such bone formation. Cyclooxygenase (COX), which acts in the synthesis of PG from arachidonic acid, has been recently revealed to have two subtypes, a constitutive type (COX-1) and an inducible one (COX-2). We examined the expression of each COX subtype during osteogenesis with the established model of the rat tibial medullary cavity in which osteogenesis can be induced by the injection of colchicine. The expression of both COX-1 and COX-2 genes was enhanced after colchicine injection in the early stage before the start of bone formation. Only the COX-2 gene expression was elevated again later during the beginning of bone formation. Furthermore, the daily administration of indomethacin, COX inhibitor, could reduce the bone mass induced by colchicine in the rat tibiae. These data indicate that endogenous PGs are associated with osteogenesis in this model. Moreover, the present study suggests that COX-2 and COX-1 would both be involved in the early stage of osteogenesis, and COX-2 is likely to be more associated with the maturation of osteoblasts in the later stage.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Tokyo Medical and Dental University, Yushima, Japan. yu-sato.os1@dent.tmd.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Sato
authors.forename: N
authors.initials: N
authors.lastname: Arai
authors.forename: A
authors.initials: A
authors.lastname: Negishi
authors.forename: K
authors.initials: K
authors.lastname: Ohya
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000201:enzymology; D003078:Colchicine / Q000494:pharmacology; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000096:biosynthesis / Q000502:physiology*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007527:Isoenzymes / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008565:Membrane Proteins; D010012:Osteogenesis / Q000187:drug effects / Q000502:physiology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D013977:Tibia
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D012333:RNA, Messenger; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; C496513:Ptgs1 protein, rat; D015232:Dinoprostone; D003078:Colchicine; D007213:Indomethacin