May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Prolactin Protects Photoreceptors From Light Damage in vivo
Author Affiliations & Notes
  • E. Arnold Hernandez
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • J. Rivera
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • J. Aranda
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • C. Vega
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • A. Quintanar-Stephano
    Basic Sciences Center, University of Aguascalientes, Aguascalientes, Mexico
  • G. Martinez de la Escalera
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • C. Clapp
    Neurobiology Institute, National University of Mexico, Queretaro, Mexico
  • Footnotes
    Commercial Relationships E. Arnold Hernandez, None; J. Rivera, None; J. Aranda, None; C. Vega, None; A. Quintanar-Stephano, None; G. Martinez de la Escalera, None; C. Clapp, None.
  • Footnotes
    Support The National Council of Science and Technology, grants SALUD–2004–C02–16.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 1344. doi:https://doi.org/
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    • Get Citation

      E. Arnold Hernandez, J. Rivera, J. Aranda, C. Vega, A. Quintanar-Stephano, G. Martinez de la Escalera, C. Clapp; Prolactin Protects Photoreceptors From Light Damage in vivo. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1344. doi: https://doi.org/.

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

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Abstract

Purpose:: Prolactin (PRL) is a survival factor for various cell types, and both PRL and the PRL receptor (PRLR) are expressed in retinal tissue. Here, we determined whether PRL exhibits neuroprotective activity in vivo for photoreceptor cells.

Methods:: Wistar rats were injected intravitreally with 1 µg of PRL in 2 µl of phosphate-buffered saline (PBS) or subjected to endogenous hyperprolactinemia induced by pituitary grafts placed under the kidney capsule for 15 days. Animals were then exposed to white light (1200 lux) for 48 hours. DNA fragmentation evaluated by the TUNEL and the ELISA methods measured apoptosis of photoreceptors.

Results:: Intravitreal injection of PRL or chronic exposure to increased circulating levels of PRL (18.4 ± 0.8 vs. 12.9 ± 1.0 ng/ml for the grafted and control rats, respectively) resulted in a 6- and 3-fold inhibition of photoreceptor cell apoptosis in the retina of light-damaged rats as determined by TUNEL and ELISA, respectively.

Conclusions:: Intraocular and systemic PRL significantly increase photoreceptor cell survival following excessive light exposure. The mechanism(s) underlying this protection are under current investigation and may lead to the development of therapeutic strategies to prevent and treat degenerative diseases of the retina

Keywords: apoptosis/cell death • neuroprotection • photoreceptors 
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