Versican splice variant messenger RNA expression in normal human Achilles tendon and tendinopathies

• Published in: Rheumatology (Oxford, England) Vol. 43; no. 8; pp. 969 - 972
• Main Authors: Corps, A. N., Robinson, A. H. N., Movin, T., Costa, M. L., Ireland, D. C., Hazleman, B. L., Riley, G. P.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-08-2004; Oxford Publishing Limited (England)
• Subjects: Achilles Tendon - physiology; Adult; Aged; Aged, 80 and over; Base Sequence; Biological and medical sciences; Chondroitin Sulfate Proteoglycans - genetics; Collagen Type I - genetics; Diseases of the osteoarticular system; Humans; Juxtaarticular diseases. Extraarticular rhumatism; Lectins, C-Type; Medical sciences; Medicin och hälsovetenskap; Middle Aged; Pain - genetics; Proteoglycan; Proteoglycans - genetics; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA Splicing - genetics; RNA, Messenger - analysis; Tendinopathy; Tendinopathy - genetics; Tendon; Tendon Injuries - genetics; Versican; Versicans; Juxtaarticular disease; Human; Proteoglycan; Tendo calcaneus; Diseases of the osteoarticular system; Rheumatology; Tendinopathy; Normal; Variant; Messenger RNA; Tendinitis; Tendon; Versican
• ISSN: 1462-0324; 1462-0332
• DOI: 10.1093/rheumatology/keh222

Objectives. Versican is the principal large proteoglycan expressed in mid-tendon, but its role in tendon pathology is unknown. Our objective was to define the expression of versican isoform splice variant messenger ribonucleic acid (mRNA) in normal Achilles tendons, in chronic painful tendinopathy and in ruptured tendons. Methods. Total RNA isolated from frozen tendon samples (normal n = 14; chronic painful tendinopathy n = 10; ruptured n = 8) was assayed by relative quantitative reverse transcriptase polymerase chain reaction (RT-PCR) for total versican, versican variants V0, V1, V2, V3 and type I collagen α1 mRNA, normalized to glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Differences between sample groups were tested by Wilcoxon statistics. Results. Painful and ruptured tendons showed a significant decrease (median 2-fold) in the expression of versican mRNA, in contrast to an increased expression (median 8-fold) of type I collagen α1 mRNA in painful tendons. Versican splice variants V0 and V1 mRNA were readily detected in normal samples, V3 levels were substantially lower, and V2 levels were more variable. Each of V1, V2 and V3 mRNA showed significant decreases in expression in painful and ruptured tendons, but V0 was not significantly changed. Conclusions. Changes in versican expression relative to that of collagen, and alterations in the balance of versican splice variants, may contribute to changes in matrix structure and function in tendinopathies.