NO-cGMP Signaling Molecules in Cells of the Rat Molar Dentin-Pulp Complex
Y. Korkmaz1,*,
M.A. Baumann2,
D. Steinritz3,
H. Schröder4,
S. Behrends5,
K. Addicks3,
K. Schneider1,
W.H.-M. Raab1, and
W. Bloch6
1 Department of Operative and Preventive Dentistry and Endodontics, Heinrich-Heine-University, Moorenstrasse 5, 40225 Düsseldorf, Germany;
2 Department of Operative Dentistry and Periodontology, University of Cologne, Germany;
3 Department of Anatomy I, University of Cologne;
4 Department of Anatomy II, University of Cologne;
5 Department of Pharmacology, Faculty of Medicine, 1 King’ College Circle, Toronto, ON, Canada; and
6 Department of Molecular and Cellular Sports Medicine, German Sports University, Cologne;
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Figure 1. NO-cGMP signaling molecules in odontoblasts. NOS I in odontoblasts (A) and in their initial processes (B). NOS II in a subpopulation of odontoblasts (C) was undetectable in cells of the control section (pre-absorption of NOS II antibody with appropriate peptide in 4-fold excess) (D). NOS III in dental pulp (p), odontoblasts (o), and their initial processes in predentin (pd) and dentin (d) (E). The sGC ß1-subunit in odontoblasts and their processes (F). The labeled odontoblast processes reveal a peripheral localization of the sGC ß1-subunit located near the dentino-enamel junction (dej) (G). cGMP is localized in odontoblasts (H). The morphometric and statistical analyses revealed a significance for localization of the sGC ß1-subunit in the peripheral odontoblast processes (I). Data analysis was performed by analysis of variance with the Bonferroni post hoc test. The data are presented as mean ± SD; N = 10 for each group. Significance was considered at a p-value < 0.05. Bars: 50 µm.
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Figure 3. Neurovascular localization of NO-cGMP signaling molecules in the dentin-pulp complex. In pulpal blood vessels, NADPH-diaphorase (A) and NOS III (B) are revealed by arrows. The sGC ß1-subunit in endothelium (double arrows) and in the vascular smooth muscle (arrows; C). cGMP in blood vessels (asterisks) and in nerve fibers (arrows; D). Thick (double arrows) and thin nerve fibers (arrows), as well as blood vessels (asterisks), showing staining for NOS I with different intensities (E). The sGC  2-subunit in nerve fibers in the dental pulp (p), subodontoblastic plexus (double arrows), predentin (pd) (arrows; F), and dentin (d) (arrows; G). cGMP in odontoblasts (arrows) and in nerve fibers at the pulpodentinal border (H). Bars: a = 80 µm; b-h = 40 µm.
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Figure 4. Staining intensities of cGMP in odontoblasts and blood vessels after treatment with NONOate and L-NAME. Localization of cGMP in odontoblasts (o) (A) and blood vessels (asterisks; D) in control sections. Higher detectable staining for cGMP in odontoblasts (B) and in blood vessels (asterisks; E) after treatment of rat molars with NO donor NONOate (10–5 M). There is a weaker staining of cGMP in odontoblasts (C) and in blood vessels (asterisks; F) after treatment of molars with NO inhibitor L-NAME (10–4 M). Higher cGMP intensities after NONOate treatment and weak cGMP intensities after L-NAME treatment were found in statistical analyses of densitometric measurements (G). The findings were analyzed statistically by Student’s t tests. Data are mean ± SD; N = 8 for each group. Significant differences were considered at a p-value < 0.05. p = dental pulp, pd = predentin, d = dentin. Bars: 50 µm.
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10.80; N = 20). Bars: a = 3 µm; b = 0.15 µm; c = 0.25 µm; and d = 0.4 µm.