Article citationsMore>>
Hermanowski-Vosatka, A., Balkovec, J.M., Cheng, K., Chen, H.Y., Hernandez, M., Koo, G.C., Le Grand, C.B., Li, Z., Metzger, J.M., Mundt, S.S., Noonan, H., Nunes, C.N., Olson, S.H., Pikounis, B., Ren, N., Robertson, N., Schaeffer, J.M., Shah, K., Springer, M.S., Strack, A.M., Strowski, M., Wu, K., Wu, T., Xiao, J., Zhang, B.B., Wright, S.D. and Thieringer, R. (2005) 11β-HSD1 Inhibition Ameliorates Metabolic Syndrome and Prevents Progression of Atherosclerosis in Mice. The Journal of Experimental Medicine, 202, 517-527.
https://doi.org/10.1084/jem.20050119
has been cited by the following article:
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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.
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