Implication of the RAGE–EN-RAGE axis in endometriosis

Sharma, Indu; Dhawan, Veena; Saha, Subhash Chand; Rashmi, Bagga; Dhaliwal, Lakhbir Kaur

doi:10.1016/j.ijgo.2010.03.037

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Volume 110, Issue 3 , Pages 199-202, September 2010

Implication of the RAGE–EN-RAGE axis in endometriosis

Indu Sharma
- Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
Veena Dhawan
- Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
- Corresponding author. Department of Experimental Medicine & Biotechnology, Research Block ‘B’, Postgraduate Institute of Medical Education & Research (PGIMER), Chandigarh-160012, India. Tel.: +91 172 2747585x5235; fax: +91 172 2744401.
Subhash Chand Saha
- Department of Obstetrics and Gynecology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
Bagga Rashmi
- Department of Obstetrics and Gynecology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
Lakhbir Kaur Dhaliwal
- Department of Obstetrics and Gynecology, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India

Received 22 January 2010; received in revised form 30 March 2010; accepted 27 April 2010. published online 01 June 2010.

Abstract

Objective

To investigate the involvement of the receptor gene for advanced glycation (RAGE), its ligand EN-RAGE, and COX-2 in endometriosis.

Methods

The mRNA and protein expression of the corresponding genes were determined from endometriotic cells from 28 study patients and healthy endometrial stromal cells from 20 controls by semiquantitative RT-PCR and Western blot analysis, respectively, using β-actin as an invariant control.

Results

The expression of COX-2, RAGE, and EN-RAGE was significantly increased, as evidenced by the significantly greater mRNA and protein expression in the cells of the study patients (P<0.001). Previous treatment for endometriosis did not lessen mRNA and protein expression (P<0.001).

Conclusion

Our findings strengthen the hypothesis of an underlying inflammation in the pathophysiology of endometriosis and suggest exploring anti-inflammatory therapies as adjunct treatment.

Keywords: Endometriosis, Inflammation, Endometriotic stromal cells, COX-2, RAGE, EN-RAGE