Pleiotrophin inhibited chondrogenic differentiation potential of dental pulp stem cells

Author:

Liu Chang1,Zhang Lili2ORCID,Zheng Xiaoyu3,Zhu Jiaman1,Jin Luyuan2ORCID,Gao Runtao1ORCID

Affiliation:

1. Department of Stomatology Beijing Friendship Hospital, Capital Medical University Beijing China

2. Department of General Dentistry and Integrated Emergency Dental Care Beijing Stomatological Hospital, Capital Medical University Beijing China

3. Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Capital Medical University School of Stomatology Beijing China

Abstract

AbstractObjectiveStudies have shown that the levels of pleiotrophin (PTN) are greatly elevated in the synovial fluid and cartilage in osteoarthritis. Therefore, the purpose of this study was to investigate the effect and mechanism of PTN on the chondrogenic differentiation of DPSCs in inflammatory and normal microenvironments.Materials and MethodsA lentiviral vector was used to deplete or overexpress PTN in DPSCs. The inflammatory microenvironment was simulated in vitro by the addition of IL‐1β to the culture medium. The chondrogenic differentiation potential was assessed using Alcian Blue staining and the main chondrogenic markers. A dual‐luciferase reporter assay was used to explore the relationship between miR‐137 and PTN.ResultsThe results showed that 0.1 ng/mL IL‐1β treatment during chondrogenic induction greatly impaired the chondrogenic differentiation of DPSCs. Supplementation with PTN and PTN overexpression inhibited chondrogenic differentiation of DPSCs, while PTN depletion promoted chondrogenic differentiation. MiR‐137 negatively regulated the expression of PTN by binding to the 3′UTR of its mRNA. Moreover, miR‐137 promoted chondrogenic differentiation of DPSCs in normal and inflammatory microenvironments.ConclusionOur results suggest that PTN may play an inhibitory role in the chondrogenic differentiation of DPSCs in normal and inflammatory microenvironments, which is regulated by miR‐137.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

General Dentistry,Otorhinolaryngology

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