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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. and Martins, A.A. and Medeiros, C.A.C.X. and Guerra, G.C.B. and Santos, R. and Bader, M. and Pirih, F.Q. and Araújo Júnior, R.F. and Brito, G.A.C. and Leitão, R.F.C. and Silva, R.A. and Barbosa, S.J.A. and 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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