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Updated: Apr 5, 2026
08:20
A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
Published on: October 2, 2018
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Failure of podocalyxin suppression and HOXA10/HOXA11 activation characterizes endometrial dysfunction in
Nilufer Celik1, Onder Celik2, Ulun Ulug3
1Department of Biochemistry, Behcet Uz Children's Hospital, 35210, Izmir, Turkey.
Molecular and Cellular Endocrinology
|February 19, 2026
Summary
Polycystic ovary syndrome (PCOS) with hyperandrogenemia disrupts endometrial receptivity by altering key gene expressions, impacting implantation. This study reveals testosterone
Area of Science:
- Reproductive Endocrinology
- Molecular Biology
- Gynecology
Background:
- Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenemia (HA).
- Endometrial receptivity is crucial for successful implantation and is often impaired in women with PCOS.
- The role of HA in modulating endometrial receptivity regulators in PCOS requires further elucidation.
Purpose of the Study:
- To investigate the impact of hyperandrogenemia in PCOS on the expression of PCX, HOXA10, and HOXA11, key regulators of endometrial receptivity.
- To compare these regulators across different PCOS phenotypes and with healthy controls.
- To identify predictors of PCX, HOXA10, and HOXA11 expression in the context of PCOS and HA.
Main Methods:
- Analysis of endometrial samples from 54 women with PCOS (classified into four phenotypes) and 25 controls.
- Quantification of PCX mRNA and protein levels, and HOXA10/HOXA11 mRNA expression.
- Immunohistochemical analysis of PCX and comparison of H-score values between groups.
- Statistical analysis to identify predictors of gene expression and protein levels.
Main Results:
- PCX mRNA and protein levels were significantly elevated in PCOS patients compared to controls.
- HOXA10 and HOXA11 mRNA expression were significantly reduced in PCOS patients.
- Hyperandrogenic PCOS phenotypes showed lower HOXA10/HOXA11 and higher PCX expression compared to normoandrogenic PCOS.
- Testosterone, insulin resistance, and progesterone levels were identified as significant predictors of PCX, HOXA10, and HOXA11 expression.
Conclusions:
- Hyperandrogenemia in PCOS disrupts the normal mid-luteal phase regulation of endometrial receptivity markers.
- Elevated PCX and reduced HOXA10/HOXA11 expression in PCOS patients contribute to impaired endometrial receptivity.
- These molecular changes likely displace the implantation window, potentially explaining infertility in women with PCOS.
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