Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues. (14th August 2020)
- Record Type:
- Journal Article
- Title:
- Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues. (14th August 2020)
- Main Title:
- Complement 3 mediates periodontal destruction in patients with type 2 diabetes by regulating macrophage polarization in periodontal tissues
- Authors:
- Li, Ye
Wang, Xinxin
Wang, Saisai
Zhu, Chunhui
Guo, Jing
Li, Ke
Li, Ang - Abstract:
- Abstract: 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 promotingAbstract: 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. Abstract : 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. … (more)
- Is Part Of:
- Cell proliferation. Volume 53:Number 10(2020)
- Journal:
- Cell proliferation
- Issue:
- Volume 53:Number 10(2020)
- Issue Display:
- Volume 53, Issue 10 (2020)
- Year:
- 2020
- Volume:
- 53
- Issue:
- 10
- Issue Sort Value:
- 2020-0053-0010-0000
- Page Start:
- n/a
- Page End:
- n/a
- Publication Date:
- 2020-08-14
- Subjects:
- Cell proliferation -- Periodicals
571.84 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2184 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1111/cpr.12886 ↗
- Languages:
- English
- ISSNs:
- 0960-7722
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3097.854000
British Library DSC - BLDSS-3PM
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- 22020.xml