m6Am 甲基转移酶 PCIF1 调控牙周炎。

IF 5.7 1区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Journal of Dental Research Pub Date : 2024-09-18 DOI:10.1177/00220345241271078

W Song,L Liu,H Liang,H Cheng,W He,Q Yin,Z Zhang,W Lin,H Li,Q Li,W Liu,D Zhang,D Chen,Q Yuan

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引用次数: 0

摘要

N6,2'-O-二甲基腺苷（m6Am）是真核生物带帽 mRNA 中常见的一种 mRNA 修饰，在细胞功能和疾病进展中起着关键作用。然而，它在宿主炎症中的参与仍然难以捉摸。在这里，我们证明了 m6Am 甲基转移酶磷酸化 CTD 交互因子 1（PCIF1）的缺失会在全身和髓系特异性基因敲除小鼠模型中减轻牙周炎症。Pcif1 基因缺失会通过 m6Am-Csf1r 信号抑制巨噬细胞的吞噬和迁移。此外，集落刺激因子-1 受体（CSF1R）被确定为治疗牙周炎的潜在靶点。因此，我们揭示了 PCIF1 介导的 m6Am 修饰在调控巨噬细胞反应和牙周炎症中的作用，这种作用以前从未被认识到。

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m6Am Methyltransferase PCIF1 Regulates Periodontal Inflammation.

N6,2'-O-dimethyladenosine (m6Am), a common mRNA modification in eukaryotic capped mRNAs, plays a pivotal role in cellular functions and disease progression. However, its involvement in host inflammation remains elusive. Here, we demonstrate that loss of m6Am methyltransferase phosphorylated CTD interacting factor 1 (PCIF1) attenuates periodontal inflammation in whole-body and myeloid lineage-specific knockout mouse models. Pcif1 deletion inhibits macrophage phagocytosis and migration through m6Am-Csf1r signaling. In addition, colony-stimulating factor-1 receptor (CSF1R) is identified as a potential target for the treatment of periodontitis. We thus reveal a previously unrecognized role for PCIF1-mediated m6Am modification in governing macrophage responses and periodontal inflammation.

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来源期刊

Journal of Dental Research 医学-牙科与口腔外科

CiteScore

15.30

自引率

3.90%

发文量

155

审稿时长

3-8 weeks

期刊介绍： The Journal of Dental Research (JDR) is a peer-reviewed scientific journal committed to sharing new knowledge and information on all sciences related to dentistry and the oral cavity, covering health and disease. With monthly publications, JDR ensures timely communication of the latest research to the oral and dental community.