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Long non-coding RNA FOXD2-AS1 promotes inflammation but suppresses osteogenesis in pulpitis via miR-338-3p/THBS1 axis
Huawen Cui1, Yanmei Guo2, Yajun Zhang3
1Department of Stomatology, Heilongjiang University Hospital, Harbin, 150080, China.
Odontology
|June 21, 2026
Summary
Long noncoding RNA FOXD2-AS1 promotes pulpitis by upregulating THBS1 via the miR-338-3p axis. Targeting FOXD2-AS1 may offer a therapeutic strategy for pulpitis by restoring normal cell function.
Area of Science:
- Molecular Biology
- Dental Research
- Biochemistry
Background:
- The molecular mechanisms underlying pulpitis pathogenesis are not fully understood.
- Investigating the role of long noncoding RNAs (lncRNAs) in dental pulp inflammation is crucial for developing targeted therapies.
Purpose of the Study:
- To elucidate the role of lncRNA FOXD2-AS1 in pulpitis pathogenesis.
- To investigate the regulatory axis involving FOXD2-AS1, miR-338-3p, and THBS1 in dental pulp inflammation and differentiation.
Main Methods:
- Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot to detect gene and protein expression.
- Cell Counting Kit-8 (CCK-8) assay, enzyme-linked immunosorbent assay (ELISA), and alkaline phosphatase (ALP) activity assays to assess cell viability, inflammation, and osteogenesis.
- RNA immunoprecipitation (RIP) and dual luciferase reporter assays to confirm molecular interactions.
Main Results:
- FOXD2-AS1 and THBS1 were upregulated, while miR-338-3p was downregulated in pulpitis tissues.
- FOXD2-AS1 promoted inflammation and inhibited osteogenic differentiation in human dental pulp stem cells (hDPSCs).
- The FOXD2-AS1/miR-338-3p/THBS1 axis was identified, where FOXD2-AS1 sponges miR-338-3p, leading to increased THBS1 expression.
Conclusions:
- FOXD2-AS1 exacerbates pulpitis by promoting inflammation and impairing odontogenic differentiation through the miR-338-3p/THBS1 pathway.
- Modulating the FOXD2-AS1/miR-338-3p/THBS1 axis presents a potential therapeutic strategy for pulpitis.
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