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The receptor AT1 appears to be important for the maintenance of bone mass and AT2 receptor function in periodontal bone loss appears to be regulated by AT1 receptor

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Item Type:Article
Title:The receptor AT1 appears to be important for the maintenance of bone mass and AT2 receptor function in periodontal bone loss appears to be regulated by AT1 receptor
Creators Name:Lima, M.L.S., Martins, A.A., Medeiros, C.A.C.X., Guerra, G.C.B., Santos, R., Bader, M., Pirih, F.Q., Araújo Júnior, R.F., Brito, G.A.C., Leitão, R.F.C., Silva, R.A., Barbosa, S.J.A., Melo, R.C.O. and Araújo, A.A.
Abstract:A large number of experimental studies has demonstrated that angiotensin II (Ang II) is involved in key events of the inflammatory process. This study aimed to evaluate the role of Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors on periodontitis. Methods: Experimental periodontitis was induced by placing a 5.0 nylon thread ligature around the second upper left molar of AT1 mice, no-ligature or ligature (AT1-NL and AT1-L), AT2 (AT2-NL or AT2-L) and wild type (WT-NL or L). Alveolar bone loss was scanned using Micro-CT. Cytokines, peptides and enzymes were analyzed from gingival tissues by Elisa and RT-PCR. Results: The blockade of AT1 receptor resulted in bone loss, even in healthy animals. Ang II receptor blockades did not prevent linear bone loss. Ang II and Ang 1-7 levels were significantly increased in the AT2-L (p < 0.01) group compared to AT2-NL and AT1-L. The genic expression of the Mas receptor was significantly increased in WT-L and AT2-L compared to (WT-NL and AT2-NL, respectively) and in AT1-L. Conclusions: Our data suggest that the receptor AT1 appears to be important for the maintenance of bone mass. AT2 receptor molecular function in periodontitis appears to be regulated by AT1.
Keywords:Bone, Micro-Computed Tomography, Periodontal Disease, Molecular, Animals, Mice
Source:International Journal of Molecular Sciences
ISSN:1422-0067
Publisher:MDPI
Volume:22
Number:23
Page Range:12849
Date:27 November 2021
Official Publication:https://doi.org/10.3390/ijms222312849
PubMed:View item in PubMed

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