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The Notochord, Notochordal cell and CTGF/CCN-2: ongoing activity from development through maturation
1Division of Orthopaedic Surgery, University of Toronto, Toronto Western Hospital, 399 Bathurst St., McLaughlin Pavilion Rm 13-415, Toronto, ON, M5T 2S8, USA, mark.erwin@utoronto.ca.
Journal of Cell Communication and Signaling
|November 13, 2008
Summary
Connective tissue growth factor (CTGF/CCN-2) is vital for skeletal development and cartilage formation. Non-chondrodystrophic dogs, with notochordal cells secreting CTGF/CCN-2, are protected from degenerative disc disease.
Area of Science:
- Developmental Biology
- Connective Tissue Biology
- Veterinary Science
Background:
- Connective tissue growth factor (CTGF/CCN-2) is crucial for growth, development, and tissue repair.
- CTGF/CCN-2 plays a significant role in early embryonic development, particularly in notochord formation.
- Mutant mice lacking CTGF/CCN-2 exhibit severe skeletal and cartilage defects, highlighting its essential function.
Purpose of the Study:
- To investigate the role of CTGF/CCN-2 in notochordal cell biology and its potential protective effect against degenerative disc disease (DDD).
- To explore the use of non-chondrodystrophic canines as a natural model for studying CTGF/CCN-2's function in disc health.
Main Methods:
- Detection of CTGF/CCN-2 in conditioned medium from notochordal cells of non-chondrodystrophic canines (NCCM).
- Assessing proteoglycan production in response to NCCM.
- Evaluating aggrecan gene expression in bovine nucleus pulposus (NP) cells treated with recombinant human CTGF/CCN-2 and NCCM.
Main Results:
- NCCM significantly increased proteoglycan production.
- Recombinant human CTGF/CCN-2 replicated the effects of NCCM, robustly increasing aggrecan gene expression in bovine NP cells.
- Non-chondrodystrophic canines retain notochordal cells that secrete CTGF/CCN-2, correlating with protection from DDD, unlike chondrodystrophic canines.
Conclusions:
- CTGF/CCN-2 is essential for notochordal cell biology and proteoglycan synthesis within the disc nucleus.
- Non-chondrodystrophic canines serve as a valuable natural model for understanding CTGF/CCN-2's role in preventing DDD.
- Differential notochordal cell survival and CTGF/CCN-2 secretion may explain protection against degenerative disc disease.
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