Inflammation of the Human Dental Pulp Induces Phosphorylation of eNOS at Thr495 in Blood Vessels
Özlem Erdek,
Wilhelm Bloch,
Svenja Rink-Notzon,
Hubert C. Roggendorf,
Senem Uzun,
Britta Meul,
Manuel Koch,
Jörg Neugebauer,
James Deschner,
Yüksel Korkmaz
Affiliations
Özlem Erdek
Department of Oral and Maxillofacial Plastic Surgery, University of Cologne, 50931 Cologne, Germany
Wilhelm Bloch
Department of Molecular and Cellular Sport Medicine, German Sport University, 50933 Cologne, Germany
Svenja Rink-Notzon
Department of Prosthetic Dentistry, School of Dental and Oral Medicine, University of Cologne, 50931 Cologne, Germany
Hubert C. Roggendorf
Department of Oral and Maxillofacial Plastic Surgery, University of Cologne, 50931 Cologne, Germany
Senem Uzun
Department of Periodontology and Operative Dentistry, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany
Britta Meul
Department of Molecular and Cellular Sport Medicine, German Sport University, 50933 Cologne, Germany
Manuel Koch
Institute for Experimental Dental Research and Oral Musculoskeletal Biology, Center for Biochemistry, Medical Faculty, University of Cologne, 50931 Cologne, Germany
Jörg Neugebauer
Department of Oral and Maxillofacial Plastic Surgery, University of Cologne, 50931 Cologne, Germany
James Deschner
Department of Periodontology and Operative Dentistry, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany
Yüksel Korkmaz
Department of Periodontology and Operative Dentistry, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany
The activity of endothelial nitric oxide synthase (eNOS) in endothelial cells increased with the phosphorylation of the enzyme at Ser1177 and decreased at Thr495. The regulation of the phosphorylation sites of eNOS at Ser1177 and Thr495 in blood vessels of the healthy and inflamed human dental pulp is unknown. To investigate this, healthy and carious human third molars were immersion-fixed and decalcified. The localization of eNOS, Ser1177, and Thr495 in healthy and inflamed blood vessels was examined in consecutive cryo-sections using quantitative immunohistochemical methods. We found that the staining intensity of Ser1177 in healthy blood vessels decreased in inflamed blood vessels, whereas the weak staining intensity of Thr495 in healthy blood vessels strongly increased in inflamed blood vessels. In blood vessels of the healthy pulp, eNOS is active with phosphorylation of the enzyme at Ser1177. The phosphorylation of eNOS at Thr495 in inflamed blood vessels leads to a decrease in eNOS activity, contributing to eNOS uncoupling and giving evidence for a decrease in NO and an increase in O2− production. Since the formation of the tertiary dentin matrix depends on intact pulp circulation, eNOS uncoupling and phosphorylation of eNOS at Thr495 in the inflamed pulp blood vessels should be considered during caries therapy.
