Expression of Prokineticin-2 Gene in Ovaries of PCOS Rat Models Induced by Testosterone or Estradiol

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 554-573-Ovarian & Uterine Function I
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-555
Gustavo Arantes Maciel*1, Rodrigo Rodrigues Marcondes1, Katia Candido Carvalho2, Cecilia Ferreira2, Natalia Garcia2, Daniele Coelho Duarte2, Thiago Hideki Goncalves2, Vinicius Cestari Amaral2, Alvaro Anzai3, Manuel Jesus Simoes4 and Edmund Chada Baracat5
1Faculdade de Medicina Universidade de Sao Paulo, Sao Paulo, Brazil, 2Faculdade de Medicina Universidade de Sao Paulo, 3Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil, 4Universidade Federal de Sao Paulo - Escola Paulista de Medicina, Brazil, 5Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo, Brazil
Introduction: Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects 5-10 % of women at reproductive age. Its etiology remains unknown, but environmental factors have been associated to the origins of this syndrome. In rodents, exposure to androgen or estrogen excess in early life induces to abnormalities in female endocrinology that mimics PCOS in women. Ovaries of women with PCOS present hyperplasia of theca cells and excessive production of androgens. Prokineticin-2 (Prok2) gene activity is thought to be related to Leydig cells differentiation in males. Theca cells and Leydig cells are counterparts, but the role of Prok2 in theca cells is not clear. In this sense, we proposed to investigate whether Prok2 might be associated with ovarian dysfunction in PCOS rat models Objective: The aim of this study was to analyze the impact of the sex steroids excess in neonatal period on the expression of apoptosis genes, especially, prokineticin-2 gene in the ovary of adult female rats submitted to sex steroids during neonatal life. Methods: Thirty rats aged between 0-3 days of age were used in this study. These animals were sorted in three groups according with sc administration of the following compounds: testosterone propionate (1.25 mg) (Testosterone Group, TG; n=10), estradiol benzoate (0.5 mg) (Estradiol Group, EG; n=10) and vehicle (0.1 mL) (Control Group, CG; n=10). With 90 days of life, the animals were euthanized and the ovaries were removed to evaluation of prokineticin-2 gene expression by quantitative Real Time PCR. Statistical analysis was performed using SABiosciences PCR array data analysis software available online. Results: Testosterone Group exhibited an increase in fold expression of Prok2, which was 36.3 times overexpressed in comparison to CG. EG also exhibited an increased fold change in Prok2 expression, and was 2.1 times more expressed than Control Group. Both results were statistically significant (P<0.05). Conclusion: Our data showed that ovarian expression of prokineticin-2 gene seems to be programmed by sex steroids, mainly testosterone, exposure in early life. This event might be related to ovarian dysfunction in the rat models used in this study.

Nothing to Disclose: GAM, RRM, KCC, CF, NG, DCD, THG, VCA, AA, MJS, ECB

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