Progesterone Enhances Transthyretin Expression in the Rat Choroid Plexus In Vitro and In Vivo via Progesterone Receptor

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• 作者：Telma Quintela (1)
  Isabel Gon?alves (1)
  Ana Martinho (1)
  Celso Henrique Alves (1)
  Maria Jo?o Saraiva (2)
  Pedro Rocha (3)
  Cecília Reis Alves Santos (1) (4)
  
• 关键词：Cerebrospinal fluid ; Choroid plexus ; Estradiol ; Progesterone ; Progesterone receptor ; Transthyretin
• 刊名：Journal of Molecular Neuroscience
• 出版年：2011
• 出版时间：July 2011
• 年：2011
• 卷：44
• 期：3
• 页码：152-158
• 全文大小：161KB
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• 作者单位：Telma Quintela (1)
  Isabel Gon?alves (1)
  Ana Martinho (1)
  Celso Henrique Alves (1)
  Maria Jo?o Saraiva (2)
  Pedro Rocha (3)
  Cecília Reis Alves Santos (1) (4)
  
  1. Health Sciences Research Centre—CICS, University of Beira Interior, Av. Infante D. Henrique, 6200-506, Covilh?, Portugal
  2. Molecular Neurobiology, Institute of Molecular and Cellular Biology—IBMC, Porto and ICBAS, University of Porto, Rua do Campo Alegre, 823, 4150-180, Porto, Portugal
  3. Chemistry Department, University of Beira Interior, 6201-001, Covilh?, Portugal
  4. Centre of Investigation in Health Sciences—CICS, University of Beira Interior, Av. Infante D. Henrique, 6200-506, Covilh?, Portugal
  

文摘

Depletion of ovarian hormones 17β-estradiol (E2) and progesterone (P) after menopause may contribute to the decline in cognitive performance and increases the risk of Alzheimer’s disease (AD) in women, striking the importance of understanding the regulation of pivotal proteins involved in AD pathogenesis by ovarian hormones. Transthyretin (TTR) is now recognized as one of such proteins due to its ability to sequester and degrade amyloid β (Aβ) into less harmful peptides and preventing their aggregation. We have previously demonstrated that E2 enhances TTR expression. In this study, we investigate the effects of P on TTR expression in primary cultures of rat choroid plexus epithelial cells and in adult ovariectomized female rats. The results obtained demonstrate that, in vitro and in vivo, TTR is up-regulated by P. In addition, the mechanism underlying the response of TTR to P was investigated, and we provide evidence that this response is achieved through a progesterone receptor-mediated mechanism. Our results reinforce the importance of ovarian hormones on the regulation of TTR, which may reflect on the processing of Aβ peptides and consequently on AD onset and progression.