Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues

التفاصيل البيبلوغرافية
العنوان: Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues
المؤلفون: Xinxin Wang, Saisai Wang, Ang Li, Jing Guo, Chunhui Zhu, Ke Li, Ye Li
المصدر: Cell Proliferation
بيانات النشر: Wiley, 2020.
سنة النشر: 2020
مصطلحات موضوعية: Adult, Male, 0301 basic medicine, Pathology, medicine.medical_specialty, Necrosis, Bone density, Macrophage polarization, Diabetes Mellitus, Experimental, Proinflammatory cytokine, Mice, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Bone Density, Alveolar Process, Animals, Humans, Medicine, Periodontitis, Dental alveolus, Mice, Knockout, Interleukin-6, Tumor Necrosis Factor-alpha, business.industry, Macrophages, Interleukin, Complement C3, Gingival Crevicular Fluid, Original Articles, Cell Biology, General Medicine, Macrophage Activation, Middle Aged, medicine.disease, Mice, Inbred C57BL, 030104 developmental biology, Diabetes Mellitus, Type 2, 030220 oncology & carcinogenesis, Female, Original Article, medicine.symptom, business
الوصف: Objectives Diabetes aggravates the risk and severity of periodontitis, but the specific mechanism remains confused. Complement 3 (C3) is closely related to complications of type 2 diabetes (T2DM). In the present study, we concentrated on whether C3 mediates the development of periodontitis in T2DM. Materials and Methods Levels of C3 in blood and gingival crevicular fluid (GCF) of patients were measured first. A C3‐knockout diabetic mouse model was established, real‐time PCR, Western blotting and histological investigation were performed to evaluate the progress of periodontitis. Microcomputed tomography (micro‐CT) and TRAP staining were performed to detect alveolar bone resorption. Immunofluorescence was performed to detect polarization of macrophages. Results Our data showed that C3 levels were elevated in the blood and GCF of T2DM patients compared with non‐diabetic individuals. Increased C3 was closely related to the upregulation of inflammatory cytokines including interleukin (IL)‐1, IL‐6 and tumour necrosis factor‐alpha (TNF‐α), as well as the decline of the bone volume density (BMD) and bone volume over total volume (BV/TV) of the alveolar bones in diabetic mice. The deletion of C3 inhibited inflammatory cytokines and rescued the decreased BMD and BV/TV of the alveolar bones. C3‐mediated polarization of macrophages was responsible for the damage. Conclusion T2DM‐related upregulation of C3 contributes to the development of periodontitis by promoting macrophages M1 polarization and inhibiting M2 polarization, triggering a pro‐inflammatory effect on periodontal tissues.
T2DM led to an increase in C3 levels, which affected the macrophages in periodontal tissues by promoting macrophages to polarize to M1 and inhibiting M2 polarization, thus triggering a pro‐inflammatory effect on periodontal tissues. C3‐related osteoclasts increase potentially promoted alveolar bone resorption.
تدمد: 1365-2184
0960-7722
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::68f3d97654568bf0947c061aeed98a2eTest
https://doi.org/10.1111/cpr.12886Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....68f3d97654568bf0947c061aeed98a2e
قاعدة البيانات: OpenAIRE