Inhibition of Chondrocyte Hypertrophy of Osteoarthritis by Disruptor Peptide

Abstract

The goals of this research project is to characterize how disruptor peptide blocks beta-catenin interaction with PTH receptor, inhibits chondrocyte hypertrophy and prevents osteoarthritis (OA) progression. In the first year, we completed the most work in the Aim 1 and initiated some work in Aim 2. We designed a disruptor peptide corresponding to the carboxyl-terminal region of PTH receptor, and found this disruptor peptide inhibited beta-catenin binding to PTH receptor by GST-pull down assay. We also confirmed that disruptor peptide conjugated to penetratin can enter cells. Importantly, disruptor peptide can reverse the beta-catenin-mediated PTH receptor signaling switch by increasing Gs/cAMP signaling and inhibiting Gq/PLC activation in chondrocytes. In addition, we successfully induced ATDC5 cell differentiation from proliferating chondrocytes to the hypertrophic stage, and generated mouse OA model surgically induced by destabilization of the medial meniscus. These results provide the foundation for further studies whether disruptor peptide can inhibit chondrocyte hypertrophy in vitro and protect cartilage damage in a mouse OA model.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2017
Accession Number
AD1046225

Entities

People

  • Bin Wang

Organizations

  • Thomas Jefferson University

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Arthritis
  • Biological Staining And Labeling
  • Biomedical Research
  • Cartilage
  • Cell Physiological Processes
  • Cells
  • Confocal Microscopy
  • Connective Tissue Cells
  • Hypertrophy
  • Inhibition
  • Joints (Anatomy)
  • Medical Personnel
  • Orthopedics
  • Peptides
  • Proteins
  • Terminals

Fields of Study

  • Biology

Readers

  • Immunology
  • Neurotoxicology
  • Neurotrauma and Rehabilitation Medicine.