Article citationsMore>>

Ishii-Yonemoto, T., Masuzaki, H., Yasue, S., Okada, S., Kozuka, C., Tanaka, T., Noguchi, M., Tomita, T., Fujikura, J., Yamamoto, Y., Ebihara, K., Hosoda, K. and Nakao, K. (2010) Glucocorticoid Reamplification within Cells Intensifies NF-κB and MAPK Signaling and Reinforces Inflammation in Activated Preadipocytes. American Journal of Physiology-Endocrinology and Metabolism, 298, E930-E940.
https://doi.org/10.1152/ajpendo.00320.2009

has been cited by the following article:

• TITLE: Increased Expression of 11β-Hydroxysteroid Dehydrogenase Type 1 in Experimental Periodontitis Induced by Lipopolysaccharide from Porphyromonas gingivalis

  AUTHORS: Atsuko Fujita, Takaya Nakata, Makoto Umeda, Hiroaki Masuzaki, Hirofumi Sawai

  KEYWORDS: Chronic Periodontitis, 11β-Hydroxysteroid Dehydrogenase Type 1, Lipopolysaccharide, Porphyromonas gingivalis

  JOURNAL NAME: Open Journal of Stomatology, Vol.7 No.10, September 30, 2017

  ABSTRACT: It has been proposed that 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which activates glucocorticoids, plays a role in chronic inflammatory diseases including metabolic diseases, rheumatoid arthritis, and ulcerative colitis. We have recently reported that the expression of 11β-HSD1 is increased in the gingiva of patients with chronic periodontitis and in that of rats with ligature-induced periodontitis. In this study, to further demonstrate the involvement of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in another rat model of experimental periodontitis induced by intragingival injection of lipopolysaccharide from Porphyromonas gingivalis (LPS-PG). Alveolar bone loss was observed two weeks after intragingival injection of LPS-PG. The level of 11β-HSD1 mRNA assessed by real-time reverse transcriptase-polymerase chain reaction was significantly elevated in LPS-PG-induced periodontitis compared with controls. The expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which inactivates glucocorticoids, was not significantly different between control and LPS-PG-induced periodontitis. The expression of 11β-HSD1 was significantly correlated with that of TNF in LPS-PG-induced periodontitis. The increased expression of 11β-HSD1 protein in LPS-PG-induced periodontitis was confirmed by immunohistochemistry using anti-11β-HSD1 antibody. These results further suggest a role for 11β-HSD1 in the pathogenesis of chronic periodontitis.