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FOXA1基因敲低通过STAT3信号通路减轻炎症并增强牙周膜干细胞的成骨分化。

FOXA1 knockdown alleviates inflammation and enhances osteogenic differentiation of periodontal ligament stem cells via STAT3 pathway.

作者信息

Wang Jin, Zhu Yanru

机构信息

Department of Stomatology, The Second People's Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical University, No.68 Gehu Middle Road, Wujin District, Changzhou City, Jiangsu Province, People's Republic of China.

出版信息

J Orthop Surg Res. 2024 Dec 2;19(1):814. doi: 10.1186/s13018-024-05286-7.

DOI:10.1186/s13018-024-05286-7
PMID:39623394
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11613586/
Abstract

BACKGROUND

Evidence has confirmed that forkhead box protein A1 (FOXA1) inhibits the osteogenic differentiation of bone marrow mesenchymal stem cells. However, whether FOXA1 regulates the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) to participate in periodontitis process is unclear.

METHODS

Lipopolysaccharide (LPS) was used to treat hPDLSCs to mimic inflammation environments. FOXA1 expression was examined by quantitative real-time PCR and western blot. The levels of IL-6 and TNF-α were evaluated by quantitative real-time PCR, ELISA and immunohistochemistry staining. hPDLSCs osteogenic differentiation was assessed by measuring alkaline phosphatase activity, alizarin red S intensity and the levels of osteogenic differentiation-related markers. Besides, the expression of signal transducer and activator of transcription 3 (STAT3) pathway-related markers were examined by western blot and immunofluorescence staining.

RESULTS

FOXA1 was upregulated in the periodontal ligament tissues of periodontitis patients, and its knockdown enhanced osteogenic differentiation of hPDLSCs. Besides, downregulation of FOXA1 suppressed inflammation levels in LPS-induced hPDLSCs. Also, FOXA1 silencing promoted the osteogenic differentiation of LPS-induced hPDLSCs by the inactivation of STAT3 pathway.

CONCLUSION

Our data confirmed that knockdown of FOXA1 attenuated inflammation and enhanced osteogenic differentiation of LPS-induced hPDLSCs by regulating STAT3 pathway, indicating that FOXA1 might be a target for periodontitis treatment.

摘要

背景

已有证据证实叉头框蛋白A1（FOXA1）可抑制骨髓间充质干细胞的成骨分化。然而，FOXA1是否调节人牙周膜干细胞（hPDLSCs）的成骨分化以参与牙周炎进程尚不清楚。

方法

使用脂多糖（LPS）处理hPDLSCs以模拟炎症环境。通过定量实时PCR和蛋白质印迹法检测FOXA1表达。通过定量实时PCR、酶联免疫吸附测定（ELISA）和免疫组织化学染色评估白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）水平。通过测量碱性磷酸酶活性、茜素红S染色强度和成骨分化相关标志物水平评估hPDLSCs的成骨分化。此外，通过蛋白质印迹法和免疫荧光染色检测信号转导和转录激活因子3（STAT3）信号通路相关标志物的表达。

结果

FOXA1在牙周炎患者的牙周膜组织中上调，其敲低增强了hPDLSCs的成骨分化。此外，FOXA1的下调抑制了LPS诱导的hPDLSCs中的炎症水平。而且，FOXA1沉默通过STAT3信号通路的失活促进了LPS诱导的hPDLSCs的成骨分化。

结论

我们的数据证实，FOXA1敲低通过调节STAT3信号通路减轻了LPS诱导的hPDLSCs的炎症并增强了其成骨分化，表明FOXA1可能是牙周炎治疗的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/0cfa70c4b8e1/13018_2024_5286_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/1c2b3796cd91/13018_2024_5286_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/2fcda605fdba/13018_2024_5286_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/73bee35aee84/13018_2024_5286_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/0cfa70c4b8e1/13018_2024_5286_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/1c2b3796cd91/13018_2024_5286_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/2fcda605fdba/13018_2024_5286_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/73bee35aee84/13018_2024_5286_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/90ea/11613586/0cfa70c4b8e1/13018_2024_5286_Fig4_HTML.jpg

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PRMT5 inhibition ameliorates inflammation and promotes the osteogenic differentiation of LPS‑induced periodontal stem cells via STAT3/NF‑κB signaling.
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