Ran Xu1, Guang Zeng2, Shuyong Wang3, Hong Tao1, Le Ren1, Zhe Zhang1, Qingna Zhang1, Jinxiu Zhao1, Jing Gao4, Daxu Li5. 1. Department of Stomatology, The First Affiliated Hospital of Xi'an JiaoTong University, Xi'an 710061, Shaanxi, People's Republic of China. 2. Department of Plastic and Burn Surgery, Tangdu Hospital of the Fourth Military Medical University, Xi'an 710038, Shaanxi, People's Republic of China. 3. Department of Operative Dentistry and Endodontic, School of Stomatology, Fourth Military Medical University, Xi'an 710032, Shaanxi, People's Republic of China. 4. State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi Key Laboratory of Stomatology, Department of Prosthodontics, School of Stomatology, The Fourth Military Medical University, 145 Changle West Road, Xi'an 710032, Shaanxi, People's Republic of China. Electronic address: gaojingg@yeah.net. 5. Department of Stomatology, The First Affiliated Hospital of Xi'an JiaoTong University, Xi'an 710061, Shaanxi, People's Republic of China. Electronic address: daxul2210@163.com.
Abstract
BACKGROUND: Emerging evidence has indicated the bad effect of periodontal inflammation on diabetes control. However, the exact regulatory mechanisms within the association between periodontitis and diabetic development remain unclear. This study aims to investigate the function of microRNAs in regulating periodontitis-induced inflammation in an obese rat model. METHODS: Experimental periodontitis was introduced into OLETF and LETO rat. Intraperitoneal glucose tolerance test was performed to detect diabetic development. Serum cytokines levels and microRNAs expression were detected by ELISA and RT-PCR analysis respectively. And, macrophages were isolated for gain- and loss-of-function studies, to investigate the regulatory mechanism of miR-147 in periodontitis-induced inflammation. RESULTS: Periodontitis induced proinflammatory response with classical activated macrophages in both rats, but distinctively aggravated the impaired glucose tolerance of OLETF rat with spontaneous type 2 diabetes. Analysis for serum microRNAs expression showed the distinctive and synergistic upregulation of miR-147 with periodontitis-induced effects in rats, while further experiments demonstrated the positive regulatory mechanism of miR-147 on classical activated macrophages with overexpressed proinflammatory markers, showing M1 phenotype. CONCLUSION: This study provided new evidence for the positive effect of periodontal inflammation on diabetic development, while the regulatory mechanism of miR-147 on classical macrophage activation, was verified, and presumed to contribute to the impaired glucose tolerance aggravated by periodontitis in obese rats. Besides, this study indicated the application of miR-147 for therapeutic approach in the treatment of diabetes with periodontitis.
BACKGROUND: Emerging evidence has indicated the bad effect of periodontal inflammation on diabetes control. However, the exact regulatory mechanisms within the association between periodontitis and diabetic development remain unclear. This study aims to investigate the function of microRNAs in regulating periodontitis-induced inflammation in an obeserat model. METHODS: Experimental periodontitis was introduced into OLETF and LETO rat. Intraperitoneal glucose tolerance test was performed to detect diabetic development. Serum cytokines levels and microRNAs expression were detected by ELISA and RT-PCR analysis respectively. And, macrophages were isolated for gain- and loss-of-function studies, to investigate the regulatory mechanism of miR-147 in periodontitis-induced inflammation. RESULTS:Periodontitis induced proinflammatory response with classical activated macrophages in both rats, but distinctively aggravated the impaired glucose tolerance of OLETF rat with spontaneous type 2 diabetes. Analysis for serum microRNAs expression showed the distinctive and synergistic upregulation of miR-147 with periodontitis-induced effects in rats, while further experiments demonstrated the positive regulatory mechanism of miR-147 on classical activated macrophages with overexpressed proinflammatory markers, showing M1 phenotype. CONCLUSION: This study provided new evidence for the positive effect of periodontal inflammation on diabetic development, while the regulatory mechanism of miR-147 on classical macrophage activation, was verified, and presumed to contribute to the impaired glucose tolerance aggravated by periodontitis in obeserats. Besides, this study indicated the application of miR-147 for therapeutic approach in the treatment of diabetes with periodontitis.
Authors: Desheng Tang; Feng Cao; Changsheng Yan; Kun Fang; Jiamin Ma; Lei Gao; Bei Sun; Gang Wang Journal: Front Immunol Date: 2022-06-13 Impact factor: 8.786
Authors: Ann-Kathrin Vlacil; Evelyn Vollmeister; Wilhelm Bertrams; Florian Schoesser; Raghav Oberoi; Jutta Schuett; Harald Schuett; Sonja Huehn; Katrin Bedenbender; Bernd T Schmeck; Bernhard Schieffer; Karsten Grote Journal: PLoS One Date: 2020-04-30 Impact factor: 3.240