title: Nitric oxide in pulp cell growth, differentiation, and mineralization.
abstract: Dental preparation sometimes causes transient congestion, edema, and necrosis of the pulp. We hypothesized that nitric oxide (NO) is involved in the pathophysiological changes in pulp after preparation. The mRNA and protein expression of the inducible isoform of NO synthase (iNOS) was examined in murine pulp after dental preparation. The effects of NO on the proliferation, mineralization, and apoptosis of pulp cells were also studied in vitro. We found that not only iNOS, but also mRNAs for alkaline phosphatase and plasma membrane glycoprotein-1, were expressed in the pulp after preparation. NOC-18, an NO donor, suppressed the proliferation of pulp cells without inducing cell death, whereas it promoted the mineralization of cells cultured in the presence of beta-glycerophosphate, ascorbic acid, dexamethasone, and KH(2)PO(4). Under these conditions, NOC-18 induced the apoptosis of pulp cells. These results suggest that NO regulates the growth, apoptosis, and mineralization of pulp cells.
authors.affiliation: Department of Biochemistry, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Yasuhara
authors.forename: T
authors.initials: T
authors.lastname: Suzawa
authors.forename: Y
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: M
authors.initials: M
authors.lastname: Takami
authors.forename: A
authors.initials: A
authors.lastname: Yamada
authors.forename: R
authors.initials: R
authors.lastname: Kamijo
mesh_terms: D000469:Alkaline Phosphatase / Q000096:biosynthesis; D000818:Animals; D017209:Apoptosis; D002454:Cell Differentiation; D048708:Cell Growth Processes / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D003737:Dental Cavity Preparation / Q000009:adverse effects*; D003782:Dental Pulp / Q000166:cytology / Q000378:metabolism* / Q000503:physiopathology; D004790:Enzyme Induction; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis*; D009603:Nitroso Compounds / Q000494:pharmacology; D010727:Phosphoric Diester Hydrolases / Q000096:biosynthesis; D011671:Pulpitis / Q000209:etiology; D011755:Pyrophosphatases / Q000096:biosynthesis; D014074:Tooth Calcification
chemical_list: C093285:NOC 18; D020030:Nitric Oxide Donors; D009603:Nitroso Compounds; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D000469:Alkaline Phosphatase; D010727:Phosphoric Diester Hydrolases; C065962:ectonucleotide pyrophosphatase phosphodiesterase 1; D011755:Pyrophosphatases