Inhibition of cartilage degradation: a combined tissue engineering and gene therapy approach

Arthritis Rheum. 2003 Mar;48(3):709-18. doi: 10.1002/art.10842.

Abstract

Objective: To determine if tissue-engineered cartilage can be protected from cytokine-induced degradation using a gene therapy approach.

Methods: Chemical and pantropic retroviral gene transfer methodologies were compared for their ability to introduce a luciferase reporter gene into adult bovine cartilage chondrocytes grown in monolayer. Pantropic retrovirus was then used to transduce these cells with human tissue inhibitor of metalloproteinases 1 (TIMP-1), and the stability of expression in monolayer or pellet culture was monitored for 6 weeks. Untransduced and TIMP-1-transduced cells were also used to tissue engineer 3-dimensional cartilage constructs that were then challenged with interleukin-1 (IL-1) for 4 weeks. Conditioned media and residual cartilage were collected for analysis of matrix components, including type II collagen and proteoglycans, and for TIMP-1 production and matrix metalloproteinase (MMP) activity.

Results: Chemical transfection of adult bovine chondrocytes gave rise to short-lived reporter expression that was virtually undetectable after 4 weeks of culture. In contrast, pantropic retroviral transduction gave rise to stable expression that persisted at a high level for at least 6 weeks. Pantropic transduction of the cells with TIMP-1 gave rise to similar long-term expression, both in monolayer and pellet cultures. TIMP-1-transduced tissue-engineered cartilage also retained TIMP-1 expression for an additional 4 weeks of culture in the presence of IL-1. Compared with control samples, TIMP-1-transgenic cartilage resisted the catabolic effects of IL-1, with MMP activity reduced to basal levels and a decreased loss of type II collagen.

Conclusion: Pantropic retroviral transduction permits long-term expression of potentially therapeutic transgenes in adult tissue-engineered cartilage. While TIMP-1 transduction could be used to prevent collagen breakdown, alternative transgenes may be necessary to protect cartilage proteoglycans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bioreactors*
  • Cartilage / cytology
  • Cartilage / drug effects*
  • Cartilage / metabolism*
  • Cattle
  • Cell Aggregation
  • Cell Transformation, Viral
  • Cells, Cultured
  • Chondrocytes / cytology
  • Chondrocytes / drug effects
  • Chondrocytes / metabolism
  • Extracellular Matrix / chemistry
  • Extracellular Matrix / metabolism
  • Gene Transfer Techniques
  • Genetic Therapy / methods*
  • Genetic Vectors
  • Interleukin-1 / pharmacology
  • Moloney murine leukemia virus / genetics
  • Organoids
  • Osteoarthritis / therapy*
  • Polyglycolic Acid
  • Tissue Engineering / methods*
  • Tissue Inhibitor of Metalloproteinase-1 / pharmacology

Substances

  • Interleukin-1
  • Tissue Inhibitor of Metalloproteinase-1
  • Polyglycolic Acid