Grant number: | 12/11069-9 |
Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
Start date: | June 01, 2013 |
End date: | May 31, 2016 |
Field of knowledge: | Health Sciences - Medicine - Maternal and Child Health |
Principal Investigator: | Rosana Maria dos Reis |
Grantee: | Cristiana Libardi Miranda Furtado |
Host Institution: | Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
Abstract Premature ovarian failure (POF) is a heterogeneous disorder, clinically defined by permanent cessation of ovarian function before the age of 40 years, causing infertility. POF is a common condition affecting 1% of the female population and the diagnosis is established by amenorrhea, hypoestrogenism, and elevated FSH levels. The exact etiology is still unknown and may arise as secondary complications to order diseases or iatrogenic mechanisms, but in most cases it is idiopathic. Genetic and chromosome abnormalities are one of the most well known causes of POF, especially in X chromosome due to presence of essential genes for ovarian function. The Androgen Receptor gene (AR), located on the Xq11, is suggested as a marker for POF, because of its physiological role in ovarian development. The AR has a polymorphic repetitive DNA motif (CAGn) which is directly related to its expression, which has been inversely correlated with the AR function. Longer CAG repeat length can reduce the activity of the AR or even can silence the gene. The AR is proposed to have an association with telomeric proteins, playing a role in telomere stability, which is an important marker for cellular senescence that is lost with each cell division. In order to investigate the role of AR and telomere shortening in POF phenotype, and a possible correlation between these events, the present study aims to assess the repeat CAG polymorphism in the AR gene and telomere length in POF patients. | |
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