A potential role for the silent information regulator 2 homologue 1 (SIRT1) in periapical periodontitis.

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A potential role for the silent information regulator 2 homologue 1 (SIRT1) in periapical periodontitis.

Int Endod J. 2018 Jan 24;:

Authors: Kudo H, Takeichi O, Hatori K, Makino K, Himi K, Ogiso B

Abstract
AIM: To investigate the role played by silent information regulator 2 homologue 1 (SIRT1) during angiogenesis of periapical periodontitis.
METHODOLOGY: Periapical granulomas were subjected to dual-colour immunofluorescence imaging and real-time polymerase chain reactions assaying the expression levels of SIRT1, vascular endothelial growth factor (VEGF), and VE-cadherin. The association between Ki-67 and SIRT1 expression was also examined. Human umbilical vein endothelial cells (HUVECs) were treated with a combination of lipopolysaccharide and resveratrol (a SIRT1 activator) or sirtinol (a SIRT1 inhibitor); and the levels of mRNAs encoding SIRT1, VEGF, and VE-cadherin were determined. HUVEC tube formation was assayed in the presence of resveratrol or sirtinol. The Mann-Whitney U-test or the Tukey-Kramer test was used for statistical analysis.
RESULTS: Ki-67-expressing cells (including endothelial cells) lay adjacent to SIRT1-expressing cells in periapical granulomas. In addition, SIRT1-expressing cells were detected adjacent to VEGF-expressing cells and VEGF- or VE-cadherin-expressing endothelial cells. SIRT1, VEGF, and VE-cadherin mRNA expression levels in periapical granulomas were significantly higher (p = 0.0054, 0.0090, and 0.0090, respectively) than those of healthy gingival tissues. HUVECs treated with resveratrol exhibited significantly higher expression of mRNAs encoding SIRT1, VEGF, and VE-cadherin (p = 0.0019, 0.00005, and 0.0045, respectively) compared with controls, but sirtinol inhibited such expression. Resveratrol caused HUVECs to form tube-like structures, while sirtinol inhibited this process.
CONCLUSIONS: These findings suggest that SIRT1 may stimulate angiogenesis in periapical granulomas by triggering the proliferation of endothelial cells and inducing VEGF and VE-cadherin expression. This article is protected by copyright. All rights reserved.

PMID: 29363137 [PubMed - as supplied by publisher]

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