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LOX family enzymes expression in vaginal tissue of premenopausal women with severe pelvic organ prolapse

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Abstract

Introduction and Hypothesis

The extracellular matrix proteins collagen and elastin provide tissue strength and resilience, whereas lysyl oxidase enzymes play a major role in their stabilization. This study examines the expression and tissue localization of lysyl oxidase family proteins in the anterior vaginal wall of premenopausal women with advanced pelvic organ prolapse (POP, n = 15) and asymptomatic controls (n = 11). All women were in the proliferative phase of menstrual cycle.

Methods

Total mRNAs and proteins extracted from the vaginal tissue were examined by real-time polymerase chain reaction and immunoblotting, and tissue specimens were analyzed by immunohistochemistry.

Results

The expression of LOX, LOXL1, and LOXL3 genes as well as LOX and LOXL3 proteins were significantly reduced in POP patients (P < 0.05). Immunolocalization of LOX family proteins was confirmed in all vaginal specimens.

Conclusion

We proposed that reduced expression of LOX enzymes may result in defective assembly of pelvic tissues and development of POP.

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Acknowledgements

The study funding was provided by the Research Fund, Department of Obstetrics and Gynecology, Mount Sinai Hospital, Toronto. There is no conflict of interest to be disclosed.

We thank Dr. V. Miranda for assisting us in the statistical analysis.

Conflicts of interest

None.

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Correspondence to May Alarab.

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Supplemental Fig. 1

Double immunostaining for CD68 and LOXL1 proteins. Immunofluorescence microscopy stained with antibodies against LOXL1 (C, red color), CD68 (B, green color), and nuclear staining (A, blue color). Coexpression of LOXL1 and CD68 by the same cell is indicated by yellow color (overlap of green and red). Magnification is ×400; scale bar = 25 μm (GIF 22 kb)

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Alarab, M., Bortolini, M.A., Drutz, H. et al. LOX family enzymes expression in vaginal tissue of premenopausal women with severe pelvic organ prolapse. Int Urogynecol J 21, 1397–1404 (2010). https://doi.org/10.1007/s00192-010-1199-9

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  • DOI: https://doi.org/10.1007/s00192-010-1199-9

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