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Related Experiment Video

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Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
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Delta-like 2 negatively regulates chondrogenic differentiation.

Weifeng Xu1, Yexin Wang1, Haoming Zhao1

  • 1Shanghai Key Laboratory of Stomatology, Department of Oral Surgery, Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China.

Journal of Cellular Physiology
|October 24, 2017
PubMed
Summary

Delta-like 2 (Dlk2) regulates chondrogenic differentiation by activating the p38 pathway. This finding offers potential strategies for treating cartilage diseases like osteoarthritis.

Keywords:
ATDC5 cellsDelta-like 2chondrogenesismitogen-activated protein kinasep38

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Biochemistry

Background:

  • Delta-like 2 (Dlk2) is homologous to Dlk1 and part of the Notch/Delta/Serrata family.
  • Dlk2 is known to regulate adipogenesis, but its role in other differentiation processes is unclear.

Purpose of the Study:

  • To investigate the role of Dlk2 in chondrogenic differentiation.
  • To elucidate the molecular mechanisms underlying Dlk2's function in chondrogenesis.

Main Methods:

  • Overexpression and silencing of Dlk2 in ATDC5 cells.
  • Assessment of chondrogenic differentiation markers (matrix formation, gene expression).
  • Analysis of mitogen-activated protein kinase (MAPK) pathway activation (p38, ERK1/2, JNK).
  • Detection of Dlk2 expression in developing mouse epiphyseal cartilage.

Main Results:

  • Dlk2 overexpression promoted ATDC5 cell growth but inhibited chondrogenesis, reducing cartilage matrix and key gene expression (aggrecan, collagen II, X).
  • Dlk2 silencing inhibited proliferation but enhanced chondrogenic differentiation.
  • Dlk2 modulated the p38 MAPK pathway, promoting its activation during overexpression and inhibiting it during silencing, with no effect on ERK1/2 or JNK.
  • Dlk2 expression was detected in embryonic mouse limb buds, decreasing in superficial zones of epiphyseal cartilage.

Conclusions:

  • Dlk2 is a key regulator of chondrogenesis, primarily acting through the p38 MAPK pathway.
  • These findings suggest potential therapeutic strategies for cartilage-related disorders, including osteoarthritis.