| Autor: |
Yang, Yang, Ren, Dongping, Zhao, Duo, Zhang, Bo, Ye, Rui |
| Předmět: |
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| Zdroj: |
Oral Diseases; May2023, Vol. 29 Issue 4, p1715-1725, 11p, 1 Chart, 5 Graphs |
| Abstrakt: |
Aim: In this study, we aimed to explore the effects of microRNA‐203 (miR‐203) on Porphyromonas gingivalis lipopolysaccharide (P.g. LPS)‐stimulated periodontal ligament cells (PDLCs) and identify potential molecular targets for periodontitis treatment. Methods: Periodontal ligament cells were stimulated by P.g. LPS, followed by quantification of miR‐203 and AP‐1 expression. Next, loss‐ and gain‐of‐function experiments were applied in P.g. LPS‐induced PDLCs. The proliferation, apoptosis, and differentiation of PDLCs were determined, and mineralized nodule numbers were counted. Functional assays were used to identify interactions among miR‐203, activator protein‐1 (AP‐1), and intercellular adhesion molecule‐1 (ICAM‐1). In addition, expression of osteogenesis‐related genes and release of proinflammatory factors were analyzed. Results: miR‐203 was found to be downregulated while AP‐1 was upregulated in PDLCs stimulated by P.g. LPS. The overexpression of miR‐203 promoted P.g. LPS‐stimulated PDLC proliferation and differentiation, inhibited apoptosis, and increased the number of mineralized nodules. miR‐203 was verified to downregulate AP‐1/ICAM‐1 axis. miR‐203 overexpression reduced the secretion of proinflammatory factors while increasing the expression of osteogenesis‐related genes in P.g. LPS‐stimulated PDLCs, which was reversed by overexpressing AP‐1 and ICAM‐1. Conclusion: These experimental data demonstrated the potential inhibitory effects of overexpressed miR‐203 on periodontitis development by promoting PDLC differentiation and suppressing inflammatory responses through AP‐1/ICAM‐1 axis. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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