June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
The hormone prolactin: a novel endogenous trophic factor able to limit retinal degeneration
Author Affiliations & Notes
  • Stephanie Thebault
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Edith Arnold
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Andrés Quintanar-Stéphano
    Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, Aguascalientes, Mexico
  • Gerardo Rojas-Piloni
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Miguel Condés-Lara
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Nadine Binart
    INSERM, Unit 845, University Paris-Descartes, Faculty of Medicine, Paris, France
  • Gonzalo Martinez de la Escalera
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Carmen Clapp
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Footnotes
    Commercial Relationships Stephanie Thebault, None; Edith Arnold, None; Andrés Quintanar-Stéphano, None; Gerardo Rojas-Piloni, None; Miguel Condés-Lara, None; Nadine Binart, None; Gonzalo Martinez de la Escalera, None; Carmen Clapp, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 1271. doi:
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      Stephanie Thebault, Edith Arnold, Andrés Quintanar-Stéphano, Gerardo Rojas-Piloni, Miguel Condés-Lara, Nadine Binart, Gonzalo Martinez de la Escalera, Carmen Clapp; The hormone prolactin: a novel endogenous trophic factor able to limit retinal degeneration. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1271.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Retinal degeneration is characterized by the progressive destruction of retinal cells, causing deterioration and eventual loss of vision. We explored whether the hormone prolactin (PRL) provides trophic support to retinal cells, thus protecting the retina from degeneration.

Methods: Retinal function, apoptosis, gliosis, and neurotrophin expression were assessed by electroretinogram, TUNEL, GFAP immunohistochemistry, and real-time pcr, respectively, in knock-out mice for PRL receptor and in a rat model of photoreceptor degeneration that consists in bright continuous light (1500 lux) exposure for 48 hours. These rats were either normoprolactinemic or rendered hyperprolactinemic by placing two anterior pituitary glands under the kidney capsule for 15 days.

Results: Retinas from PRL receptor-deficient mice exhibited photoresponsive dysfunction and gliosis that correlate with the down-regulation of neurotrophins (bFGF, GNDF, and BDNF) and antioxidant glutathione S-transferase µ-type 2. Most of these effects were exacerbated in aged (9 month-old) compared with young (3 month-old) mice. Also, PRL receptors were up-regulated in retinal glia of rats exposed to bright continuous light. In this model of photoreceptor degeneration, inducing hyperprolactinemia limited photoreceptor apoptosis, prevented gliosis and changes in neurotrophin expression, and restored photoresponse.

Conclusions: This study unveils PRL as a trophic factor regulating glial-neuronal cell interactions in the retina, and a potential therapeutic molecule against retinal degeneration.

Keywords: 615 neuroprotection • 603 Muller cells • 695 retinal degenerations: cell biology  
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