
Laser Capture Microdissection and cDNA Array Analysis of Endometrium Identify CCL16 and CCL21
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.
Reproductive Biology and Endocrinology 2007 
 
 An 
 Published 17 May 2007 
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.
References:
Article available in 
Reproductive Biology and Endocrinology 2007, 5:18 doi:10.1186/1477-7827-5-18The electronic version of this article is the complete one and can be found online at: 
© 2007 Chand et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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