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Rheumatology Advance Access originally published online on September 24, 2008
Rheumatology 2008 47(11):1655-1658; doi:10.1093/rheumatology/ken378
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Lack of association between Tenascin-C gene and spondyloarthritis

E. Zinovieva1, N. Lebrun1, F. Letourneur1, F.-X. Laurent1, R. Said-Nahal2, G. Chiocchia1 and M. Breban1,2,3

1Institut Cochin, INSERM U567, CNRS UMR8104 and Université Paris Descartes IFR116, Paris 2Rheumatology Division, Ambroise Paré Hospital, AP-HP and 3Université Versailles Saint-Quentin en Yvelines, Boulogne-Billancourt, France.

Correspondence to: M. Breban, Rheumatology Division, Hôpital Ambroise Paré, 9 ave Charles de Gaulle, 92100, Boulogne, France. E-mail: maxime.breban{at}apr.aphp.fr


  Abstract

Objectives. We previously identified a new susceptibility region linked to SpA in 9q31–34. Tenascin-C (TNC) appears as one of the best positional and functional candidate genes lying within this SPA2 locus. The objectives of the present study were to identify TNC polymorphisms, and to examine their putative association with SpA.

Methods. We first performed variants screening in 20 independent SpA patients from families with high linkage score to the SPA2 locus, and three unrelated controls: TNCs coding regions (28 exons), intron–exon boundaries and 5'- and 3'-flank regions were fully re-sequenced to identify polymorphisms. Then we genotyped selected variants in 183 independent trios, and assessed their intrafamilial association with SpA by transmission disequilibrium test.

Results. Variants screening allowed us to identify 26 polymorphisms, 7 of which were selected for further study, in addition to an intronic polymorphism previously reported as associated with Achilles tendon injuries. In intrafamilial association test, none of the variants showed significant transmission disequilibrium. Results from analysis restricted to AS were not different from those obtained on the whole SpA group.

Conclusions. TNC was one of the best positional and functional candidate genes within the SPA2 locus. Nevertheless, we found no association between polymorphisms in this gene and SpA. However, we cannot exclude that variants located in intronic regions or in the vicinity of TNC, which were not tested in the present study, could be implicated in the predisposition to SpA.

KEY WORDS: Ankylosing spondylitis, Spondyloarthritis, Association study, Tenascin-C, Genetics

Submitted 27 June 2008; revised version accepted 19 August 2008.
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