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      Peroxisome proliferator activated receptor γ promotes mineralization and differentiation in cementoblasts via inhibiting Wnt/β‐catenin signaling pathway

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      https://www.riss.kr/link?id=O113187276

      • 저자
      • 발행기관
      • 학술지명
      • 권호사항
      • 발행연도

        2020년

      • 작성언어

        -

      • Print ISSN

        0730-2312

      • Online ISSN

        1097-4644

      • 등재정보

        SCI;SCIE;SCOPUS

      • 자료형태

        학술저널

      • 수록면

        3700-3710   [※수록면이 p5 이하이면, Review, Columns, Editor's Note, Abstract 등일 경우가 있습니다.]

      • 소장기관
      • 구독기관
        • 전북대학교 중앙도서관  
        • 성균관대학교 중앙학술정보관  
        • 부산대학교 중앙도서관  
        • 전남대학교 중앙도서관  
        • 제주대학교 중앙도서관  
        • 중앙대학교 서울캠퍼스 중앙도서관  
        • 인천대학교 학산도서관  
        • 숙명여자대학교 중앙도서관  
        • 서강대학교 로욜라중앙도서관  
        • 계명대학교 동산도서관  
        • 충남대학교 중앙도서관  
        • 한양대학교 백남학술정보관  
        • 이화여자대학교 중앙도서관  
        • 고려대학교 도서관  
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      부가정보

      다국어 초록 (Multilingual Abstract)

      Peroxisome proliferator activated receptor γ (PPARγ) is a member of the nuclear receptor family of transcription factors, which involved in inflammation regulating and bone remodeling. Rare studies explored the effects of PPARγ on mineralization an...

      Peroxisome proliferator activated receptor γ (PPARγ) is a member of the nuclear receptor family of transcription factors, which involved in inflammation regulating and bone remodeling. Rare studies explored the effects of PPARγ on mineralization and differentiation in cementoblasts. To explore the potential approaches to repair the damaged periodontal tissues especially for cementum, the present study aims to investigate the effects and the regulating mechanism of PPARγ on mineralization and differentiation in cementoblasts. Murine cementoblast cell lines (OCCM‐30) were cultured in basic medium for 24 hours/48 hours or in mineralization medium for 3/7/10 days, respectively at addition of dimethyl sulphoxide, rosiglitazone (PPARγ agonist), GW9662 (PPARγ antagonist), lithium chloride (LiCl), tumor necrosis factor‐α (TNF‐α), or respective combination. Expression of mineralization genes alkaline phosphatase (ALP), runt related transcription factors 2 (RUNX2), and osteocalcin (OCN) were detected by quantitative real‐time polymerase chain reaction or/and Western blot. ALP staining and alizarin red staining were used to evaluate the mineralization in OCCM‐30 cells. The change of β‐catenin expression and translocation in cytoplasm/nucleus was analyzed by Western blot and immunofluorescence. The results showed that PPARγ agonist rosiglitazone improved the expression of ALP, RUNX2, and OCN, deepened ALP staining, increased mineralized nodules formation, and decreased β‐catenin expression in the nucleus. LiCl, an activator of the Wnt signaling pathway, inhibited the expression of mineralization genes and reversed the upregulated expression of mineralization genes resulted from rosiglitazone. Under inflammatory microenvironment, rosiglitazone not only suppressed the expression of interleukin‐1β caused by TNF‐α, but improved the expression of mineralization genes in OCCM‐30 cells. In conclusion, PPARγ could promote mineralization and differentiation in cementoblasts via inhibiting the Wnt/β‐catenin signaling pathway, which would shed new light on the treatment of periodontitis and periodontal tissue regeneration.
      Peroxisome proliferator activated receptor γ (PPARγ) promotes mineralization and differentiation in cementoblasts by inhibiting the Wnt/β‐catenin signaling, and PPARγ not only inhibits the expression of inflammatory cytokines but also promotes the expression of mineralization genes under inflammatory condition in cementoblasts.

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