Vitamin C induces periodontal ligament progenitor cell differentiation via activation of ERK pathway mediated by PELP1.
10.1007/s13238-013-3030-0
- Author:
Yan YAN
1
;
Wenfeng ZENG
;
Shujun SONG
;
Fayun ZHANG
;
Wenxi HE
;
Wei LIANG
;
Zhongying NIU
Author Information
1. Department of Endodontics, School of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
- Publication Type:Journal Article
- MeSH:
Ascorbic Acid;
pharmacology;
Butadienes;
pharmacology;
Cell Differentiation;
drug effects;
Cells, Cultured;
Co-Repressor Proteins;
antagonists & inhibitors;
genetics;
metabolism;
Core Binding Factor Alpha 1 Subunit;
genetics;
metabolism;
Humans;
MAP Kinase Signaling System;
drug effects;
Mitogen-Activated Protein Kinase 1;
antagonists & inhibitors;
metabolism;
Mitogen-Activated Protein Kinase 3;
antagonists & inhibitors;
metabolism;
Nitriles;
pharmacology;
Periodontal Ligament;
cytology;
Phosphorylation;
drug effects;
RNA Interference;
RNA, Small Interfering;
metabolism;
Stem Cells;
cytology;
Transcription Factors;
antagonists & inhibitors;
genetics;
metabolism;
Up-Regulation;
drug effects
- From:
Protein & Cell
2013;4(8):620-627
- CountryChina
- Language:English
-
Abstract:
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.
