Abstract

Pten (phosphatase and tensin homolog deleted on chromosome 10), a kind of tumor suppressor gene, plays important roles in female reproductive system. But its expression and roles in the formation of polycystic ovaries are yet to be known. In this study, we constructed a rat model of PCOS using norethindrone and HCG injections and found the expressions of pten mRNA and PTEN protein increased significantly in the polycystic ovary tissue by immunohistochemistry, RT-PCR, and western blot. Furthermore, the results showed that in vivo ovaries could be effectively transfected by lentiviral vectors through the ovarian microinjection method and indicated that pten shRNA may inhibit the formation of polycystic ovaries by pten down-regulation. Our study provides new information regarding the role of PTEN in female reproductive disorders, such as polycystic ovary syndrome.

Highlights

  • Pten, a kind of tumor suppressor gene, plays important roles in female reproductive system

  • Our study provides new information regarding the role of PTEN in female reproductive disorders, such as polycystic ovary syndrome

  • Due to the difficulties of acquirement of clinical patient samples, the construction of Polycystic ovary syndrome (PCOS) animal models seemed to be very important to the study of the pathogenic mechanisms of PCOS

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Summary

Introduction

Pten (phosphatase and tensin homolog deleted on chromosome 10), a kind of tumor suppressor gene, plays important roles in female reproductive system. Its expression and roles in the formation of polycystic ovaries are yet to be known. The results showed that in vivo ovaries could be effectively transfected by lentiviral vectors through the ovarian microinjection method and indicated that pten shRNA may inhibit the formation of polycystic ovaries by pten down-regulation. Our study provides new information regarding the role of PTEN in female reproductive disorders, such as polycystic ovary syndrome. Further studies are needed to explore whether pten expression is related to abnormal follicular development (e.g., early excessive follicular growth and impeded dominant follicular formation) in PCOS. We used an animal model of PCOS to study the expression of PTEN in polycystic ovaries and to investigate its role in the formation of polycystic ovaries. Our research will provide a better understanding of the pathogenic mechanisms involved in PCOS and of the molecular mechanisms necessary for the diagnosis of related female reproductive disorders

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