2025/06/09 更新

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写真a

ザカリア エムエイチデイーフオアド
ZAKARIA MHD FOUAD
ZAKARIA MHD FOUAD
所属
歯学研究院 歯学部門 助教
歯学部 歯学科(併任)
歯学府 歯学専攻(併任)
職名
助教
連絡先
メールアドレス

研究分野

  • ライフサイエンス / 応用分子細胞生物学

学位

  • PhD of dental science ( 2024年9月 九州大学 )

学歴

  • 九州大学   Periodontology   PhD

    2020年4月 - 2024年9月

      詳細を見る

    国名:日本国

研究テーマ・研究キーワード

  • 研究テーマ: 38 / 5,000 間葉系幹細胞におけるSCN1Aの役割

    研究キーワード: 幹細胞、電位依存性ナトリウムチャネル Kan saibō, den'i isonsei natoriumuchaneru

    研究期間: 2020年4月 - 現在

論文

  • NaV1.1 contributes to the cell cycle of human mesenchymal stem cells by regulating AKT and CDK2

    Zakaria, MF; Kato, H; Sonoda, S; Kato, K; Uehara, N; Kyumoto-Nakamura, Y; Sharifa, MM; Yu, LT; Dai, LS; Yamaza, H; Kajioka, S; Nishimura, F; Yamaza, T

    JOURNAL OF CELL SCIENCE   137 ( 19 )   2024年10月   ISSN:0021-9533 eISSN:1477-9137

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    記述言語:英語   出版者・発行元:Journal of Cell Science  

    Non-excitable cells express sodium voltage-gated channel alpha subunit 1 gene and protein (known as SCN1A and NaV1.1, respectively); however, the functions of NaV1.1 are unclear. In this study, we investigated the role of SCN1A and NaV1.1 in human mesenchymal stem cells (MSCs). We found that SCN1A was expressed in MSCs, and abundant expression of NaV1.1 was observed in the endoplasmic reticulum; however, this expression was not found to be related to Na+ currents. SCN1A-silencing reduced MSC proliferation and delayed the cell cycle in the S phase. SCN1A silencing also suppressed the protein levels of CDK2 and AKT (herein referring to total AKT), despite similar mRNA expression, and inhibited AKT phosphorylation in MSCs. A cycloheximide-chase assay showed that SCN1A-silencing induced CDK2 but not AKT protein degradation in MSCs. A proteolysis inhibition assay using epoxomicin, bafilomycin A1 and NH4Cl revealed that both the ubiquitin–proteasome system and the autophagy and endo-lysosome system were irrelevant to CDK2 and AKT protein reduction in SCN1A-silenced MSCs. The AKT inhibitor LY294002 did not affect the degradation and nuclear localization of CDK2 in MSCs. Likewise, the AKT activator SC79 did not attenuate the SCN1A-silencing effects on CDK2 in MSCs. These results suggest that NaV1.1 contributes to the cell cycle of MSCs by regulating the post-translational control of AKT and CDK2.

    DOI: 10.1242/jcs.261732

    Web of Science

    Scopus

    PubMed

  • Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease

    Zakaria, MF; Sonoda, S; Kato, H; Ma, L; Uehara, N; Kyumoto-Nakamura, Y; Sharifa, MM; Yu, LT; Dai, LS; Yamauchi-Tomoda, E; Aijima, R; Yamaza, H; Nishimura, F; Yamaza, T

    SCIENTIFIC REPORTS   14 ( 1 )   6719   2024年3月   ISSN:2045-2322

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    記述言語:英語   出版者・発行元:Scientific Reports  

    Alveolar bone loss caused by periodontal disease eventually leads to tooth loss. Periodontal ligament stem cells (PDLSCs) are the tissue-specific cells for maintaining and repairing the periodontal ligament, cementum, and alveolar bone. Here, we investigated the role of erythropoietin receptor (EPOR), which regulates the microenvironment-modulating function of mesenchymal stem cells, in PDLSC-based periodontal therapy. We isolated PDLSCs from patients with chronic periodontal disease and healthy donors, referred to as PD-PDLSCs and Cont-PDLSCs, respectively. PD-PDLSCs exhibited reduced potency of periodontal tissue regeneration and lower expression of EPOR compared to Cont-PDLSCs. EPOR-silencing suppressed the potency of Cont-PDLSCs mimicking PD-PDLSCs, whereas EPO-mediated EPOR activation rejuvenated the reduced potency of PD-PDLSCs. Furthermore, we locally transplanted EPOR-silenced and EPOR-activated PDLSCs into the gingiva around the teeth of ligament-induced periodontitis model mice and demonstrated that EPOR in PDLSCs participated in the regeneration of the periodontal ligament, cementum, and alveolar bone in the ligated teeth. The EPOR-mediated paracrine function of PDLSCs maintains periodontal immune suppression and bone metabolic balance via osteoclasts and osteoblasts in the periodontitis model mice. Taken together, these results suggest that EPOR signaling is crucial for PDLSC-based periodontal regeneration and paves the way for the development of novel options for periodontal therapy.

    DOI: 10.1038/s41598-024-57361-y

    Web of Science

    Scopus

    PubMed

教育活動概要

  • 組織学と口腔解剖学