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Mol. Hum. Reprod. Advance Access published online on January 29, 2004
Molecular Human Reproduction, doi:10.1093/molehr/gah026
© 2004 by Oxford University Press
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Received August 1, 2003
Revised November 17, 2003
Accepted November 19, 2003

Article

Analysis of the involvement of CCR5-{Delta}32 and CCR2-V64I variants in the development of endometriosis

G. Antiñolo 1*, R.M. Fernández 1, J.A. Noval 2, J.L. Moliní 1, S. Borrego 1

1 Unidad Clínica de Genética y Reproducción, Hospitales Universitarios Virgen del Rocío, Avda. Manuel Siurot s/n., 41013, Seville, Spain
2 Servicio de Ginecología, Hospitales Universitarios Virgen del Rocío, Avda. Manuel Siurot s/n., 41013, Seville, Spain

* To whom correspondence should be addressed. E-mail: guillermo.antinolo.sspa{at}juntadeandalucia.es.


  Abstract

Several arguments support the proposal that the cytokine network plays a critical role in the aetiology of endometriosis. Among various chemokines, regulated-on-activation, normal-T-cell-expressed and -secreted (RANTES) and monocyte chemotactic protein 1 (MCP-1) concentrations have been shown to be increased in the peritoneal fluid of women with endometriosis. Some studies have demonstrated that, in the context of endometriosis, these chemokines are involved in apoptosis, angiogenesis and/or chemotaxis. Since the chemokines exert their effects by binding to their receptors, it would be plausible that factors affecting such interactions might play a role in the pathogenesis of endometriosis. Thus we postulated that the genes encoding CCR5 and CCR2, which are the receptors for RANTES and MCP-1 respectively, could be good candidate genes for the disease. We have used real-time PCR and FRET technologies to genotype and evaluate the variants CCR5-{Delta}32 and CCR2-V64I, as susceptibility factors in a cohort of Spanish women with endometriosis. No differences have been found in the frequencies of the two polymorphisms nor in the haplotype/genotype distribution between cases and controls. These data would suggest the lack of association between these polymorphisms and endometriosis in our population, although they do not permit us to discard completely a possible role of other variants within CCR5 and CCR2 genes in this pathology.

Key Words: Key words: CCR5-{Delta}32/CCR2-V64I/endometriosis/genetics/polymorphisms


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[Abstract] [Full Text] [PDF]


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