title: Irreversible inflammation is associated with decreased levels of the alpha1-, beta1-, and alpha2-subunits of sGC in human odontoblasts.
abstract: The nitric oxide (NO) receptor enzyme soluble guanylate cyclase (sGC) contains one prosthetic heme group as an αβ heterodimer, and two heterodimer isoforms (α(1)β(1), α(2)β(1)) were characterized to have enzyme activity. To test the irreversible inflammation-dependent regulation of sGC in odontoblasts, we incubated decalcified frozen sections of healthy and inflamed human third molars with antibodies against β-actin, nitrotyrosine, inducible nitric oxide synthase (iNOS), α(1)-, β(1)-, and α(2)-subunits of sGC and analyzed them at protein levels by quantitative immunohistochemistry. The irreversible inflammation induced an increase in the signal intensities for nitrotyrosine and iNOS and a decrease for the α(1)-, β(1)-, and α(2)-subunits of sGC in odontoblasts. Inflammatory mediators, reactive oxygen, and nitrogen species may impair the expression of the α(1)-, β(1)-, and α(2)-subunits in odontoblasts. The decrease of sGC at the protein level in inflamed odontoblasts is compatible with a critical role for sGC to mediate biological effects of NO in health.
authors.affiliation: Department of Operative Dentistry, Periodontics and Endodontics, Heinrich-Heine-University, Moorenstrasse 5, 40225 Düsseldorf, Germany. yueksel.korkmaz@uni-duesseldorf.de
authors.forename: Y
authors.initials: Y
authors.lastname: Korkmaz
authors.forename: H
authors.initials: H
authors.lastname: Lang
authors.forename: T
authors.initials: T
authors.lastname: Beikler
authors.forename: B
authors.initials: B
authors.lastname: Cho
authors.forename: S
authors.initials: S
authors.lastname: Behrends
authors.forename: W
authors.initials: W
authors.lastname: Bloch
authors.forename: K
authors.initials: K
authors.lastname: Addicks
authors.forename: W H-M
authors.initials: WH
authors.lastname: Raab
mesh_terms: D000199:Actins / Q000032:analysis; D000293:Adolescent; D000328:Adult; D039481:CD11b Antigen / Q000032:analysis; D017252:CD3 Complex / Q000032:analysis; D003731:Dental Caries / Q000201:enzymology* / Q000473:pathology; D003782:Dental Pulp / Q000201:enzymology / Q000473:pathology; D003804:Dentin / Q000201:enzymology / Q000473:pathology; D006162:Guanylate Cyclase / Q000032:analysis*; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D018836:Inflammation Mediators / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D018613:Microscopy, Confocal; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D009804:Odontoblasts / Q000201:enzymology* / Q000378:metabolism; D011671:Pulpitis / Q000201:enzymology* / Q000473:pathology; D026361:Reactive Nitrogen Species / Q000032:analysis; D017382:Reactive Oxygen Species / Q000032:analysis; D018160:Receptors, Cytoplasmic and Nuclear / Q000032:analysis*; D000071756:Soluble Guanylyl Cyclase; D014443:Tyrosine / Q000031:analogs & derivatives / Q000032:analysis; D055815:Young Adult
chemical_list: D000199:Actins; D039481:CD11b Antigen; D017252:CD3 Complex; C000605660:GUCY1A2 protein, human; C509295:ITGAM protein, human; D018836:Inflammation Mediators; D007527:Isoenzymes; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D018160:Receptors, Cytoplasmic and Nuclear; C002744:3-nitrotyrosine; D014443:Tyrosine; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D006162:Guanylate Cyclase; D000071756:Soluble Guanylyl Cyclase