Vitamin C induces periodontal ligament progenitor cell differentiation via activation of ERK pathway mediated by PELP1

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• 作者：Yan Yan (13030) (33030)
  Wenfeng Zeng (23030)
  Shujun Song (43030)
  Fayun Zhang (23030)
  Wenxi He (13030)
  Wei Liang (23030)
  Zhongying Niu (13030) (33030)
  
• 关键词：periodontal ligament progenitor cells ; Vitamin C ; PELP1 ; ERK signaling pathway ; osteogenic differentiation
• 刊名：Protein & Cell
• 出版年：2013
• 出版时间：August 2013
• 年：2013
• 卷：4
• 期：8
• 页码：620-627
• 全文大小：580KB
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• 作者单位：Yan Yan (13030) (33030)
  Wenfeng Zeng (23030)
  Shujun Song (43030)
  Fayun Zhang (23030)
  Wenxi He (13030)
  Wei Liang (23030)
  Zhongying Niu (13030) (33030)
  
  13030. Department of Endodontics, School of Stomatology, Fourth Military Medical University, Xi鈥檃n, 710032, China
  33030. Treatment Center of Oral Diseases, the 306th Hospital of People鈥檚 Liberation Army, Beijing, 100101, China
  23030. Protein and Peptide Pharmaceutical Laboratory, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China
  43030. Department of Pathology and Experimental Medicine, the 306th Hospital of People鈥檚 Liberation Army, Beijing, 100101, China
  

文摘

The differentiation of periodontal ligament (PDL) progenitor cells is important for maintaining the homeostasis of PDL tissue and alveolar bone. Vitamin C (VC), a water-soluble nutrient that cannot be biosynthesized by humans, is vital for mesenchymal stem cells differentiation and plays an important role in bone remodeling. Therefore, the objective of this study was to determine the function and mechanism of VC in PDL progenitor cells osteogenic differentiation at the molecular level. We demonstrated that VC could induce the osteogenic differentiation and maturation of PDL progenitor cell without other osteogenic agents. During the process, VC preferentially activated ERK1/2 but did not affect JNK or p38. Co-treatment with ERK inhibitor effectively decreased the Vitamin C-induced expression of Runx2. ERK inhibitor also abrogated Vitamin C-induced the minimized nodules formation. PELP1, a nuclear receptor co-regulator, was up-regulated under VC treatment. PELP1 knockdown inhibited ERK phosphorylation. The overexpression of PELP1 had a positive relationship with Runx2 expression. Taken together, we could make a conclude that VC induces the osteogenic differentiation of PDL progenitor cells via PELP1-ERK axis. Our finding implies that VC may have a potential in the regeneration medicine and application to periodontitis treatment.