The distribution of cartilage oligomeric matrix protein (COMP) in tendon and its variation with tendon site, age and load.

This study investigates the distribution, variation, and role of the protein Cartilage Oligomeric Matrix Protein (COMP) in tendon tissues, highlighting how it varies with tendon location, age, and load. It suggests that COMP is essential for tendons to resist load.

Research Methodology

• The researchers confirmed the presence of COMP in adult bovine and equine digital flexor tendons through several laboratory techniques, including reducing and non-reducing SDS-PAGE, Western blots, trypsin digestion followed by HPLC on a C2/C18 column, and Northern blots.
• Immunohistochemistry and Western blots of extracts were used to identify COMP across all regions of digital flexor tendons, indicating that the protein was uniformly distributed.
• The researchers also quantified COMP in equine digital flexor tendons at different ages, and in other tendons and ligaments, using a method known as heterologous inhibition ELISA. They purified equine tendon COMP through ion exchange chromatography and gel filtration for this purpose.

Findings

• The mean COMP levels in digital flexor tendon were approximately 2-5mg/g wet weight, but exhibited a large variation.
• Levels were low in neonatal tendon and increased rapidly during growth, reaching the highest levels in the metacarpal (tensional) superficial digital flexor tendon. The levels then declined in this area, while COMP concentrations in areas subject to variable compression increased less but then remained constant.
• Extensor tendons and collateral ligaments, with less loading experienced during living conditions, had COMP levels similar to those in neonatal tendon.
• COMP was found in scarred skin and granulation tissue but was not present in normal skin, chronic fibrosis, or a fibrosarcomatous skin growth.
• A unilateral non-weight-bearing growing animal contained three to six times more COMP in the weight-bearing digital flexor tendons compared to the paralyzed limb, while the extensor tendons had similar amounts in both limbs.

Conclusion

• The discovery of a COMP gene mutation causing pseudoachondroplasia, a condition characterized by lax tendons and ligaments, supports the researchers’ suggestion that COMP is synthesized in response to and is necessary for tendon to resist load.