Laser capture microdissection and cDNA array analysis of endometrium identify CCL16 and CCL21 as epithelial-derived inflammatory mediators associated with endometriosis

doi:10.1186/1477-7827-5-18

Reproductive Biology and Endocrinology

Volume 5

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Chand AL
Murray AS
Jones RL
Hannan NJ
Salamonsen LA
Rombauts L

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Murray AS
Jones RL
Hannan NJ
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Rombauts L
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Research

Laser capture microdissection and cDNA array analysis of endometrium identify CCL16 and CCL21 as epithelial-derived inflammatory mediators associated with endometriosis

Ashwini L Chand¹^* , Andrew S Murray²^,4^* , Rebecca L Jones¹^,3 , Natalie J Hannan¹ , Lois A Salamonsen¹ and Luk Rombauts²

¹Prince Henry's Institute of Medical Research, PO Box 5152, Clayton, Victoria 3168, Australia

²Department of Obstetrics and Gynaecology, Monash University, Clayton, Victoria 3168, Australia

³Division of Human Development, Academic Unit of Child Health, University of Manchester, St Mary's Hospital Research Floor, Hathersage Road, Manchester M13 OJH, UK

⁴Wellington School of Medicine, Otago University, Wellington, New Zealand

author email corresponding author email* Contributed equally

Reproductive Biology and Endocrinology 2007, 5:18doi:10.1186/1477-7827-5-18


Published:	17 May 2007

Abstract

Background

Understanding the pathophysiology of chemokine secretion in endometriosis may offer a novel area of therapeutic intervention. This study aimed to identify chemokines differentially expressed in epithelial glands in eutopic endometrium from normal women and those with endometriosis, and to establish the expression profiles of key chemokines in endometriotic lesions.

Methods

Laser capture microdissection isolated epithelial glands from endometrial eutopic tissue from women with and without endometriosis in the mid-secretory phase of their menstrual cycles. Gene profiling of the excised glands used a human chemokine and receptor cDNA array. Selected chemokines were further examined using real-time PCR and immunohistochemistry.

Results

22 chemokine/receptor genes were upregulated and two downregulated in pooled endometrial epithelium of women with endometriosis compared with controls. CCL16 and CCL21 mRNA was confirmed as elevated in some women with endometriosis compared to controls on individual samples. Immunoreactive CCL16 and CCL21 were predominantly confined to glands in eutopic and ectopic endometrium: leukocytes also stained. Immunoreactive CCL16 was overall higher in glands in ectopic vs. eutopic endometrium from the same woman (P < 0.05). Staining for CCL16 and CCL21 was highly correlated in individual tissues.

Conclusion

This study provides novel candidate molecules and suggests a potential local role for CCL16 and CCL21 as mediators contributing to the inflammatory events associated with endometriosis.