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MicroRNA-138 Inhibits Periodontal Progenitor Differentiation under Inflammatory Conditions
1Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago, IL, USA Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, IL, USA.
Journal of Dental Research
|November 1, 2015
Summary
MicroRNA-138 (miR-138) is upregulated in periodontal disease, inhibiting bone formation. Inhibiting miR-138 may prevent bone loss in advanced periodontal disease.
Area of Science:
- Oral biology
- Molecular biology
- Biomedical engineering
Background:
- Periodontal disease causes alveolar bone loss and connective tissue imbalance.
- MicroRNAs (miRNAs) are emerging regulators in cellular homeostasis.
- MicroRNA-138 (miR-138) role in periodontal disease is not well understood.
Purpose of the Study:
- To investigate the role of miR-138 in periodontal stem cells during inflammation.
- To determine miR-138's effect on bone homeostasis and osteoblast differentiation.
- To evaluate miR-138 as a therapeutic target for periodontal disease.
Main Methods:
- Utilized a periodontal disease animal model.
- Assessed miR-138 expression and its interaction with osteocalcin (OC) promoter.
- Overexpressed/knocked down miR-138 in periodontal progenitor and ligament cells.
- Measured expression of OC, Runx2, collagen I, and alkaline phosphatase activity.
- Treated cells with interleukin-6 (IL-6) and lipopolysaccharide (LPS).
Main Results:
- miR-138 was significantly upregulated in the periodontal disease model.
- miR-138 overexpression inhibited OC, Runx2, and collagen I.
- Inflammatory mediators (IL-6, LPS) increased miR-138 expression and decreased OC/Runx2.
- miR-138 knockdown partially reversed LPS-induced downregulation of OC.
- miR-138 inhibition or OC addition enhanced alkaline phosphatase activity.
Conclusions:
- miR-138 plays a critical role in regulating osteoblast differentiation and bone homeostasis during periodontal disease.
- miR-138 inhibition shows potential as a therapeutic strategy to prevent bone loss in periodontal disease.
- Targeting miR-138 may restore OC-mediated mineralization and counteract inflammatory effects.
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