The hormone prolactin is a novel, endogenous trophic factor able to regulate reactive glia and to limit retinal degeneration
Edith Arnold, Stéphanie Thebault, German Baeza-Cruz, David Arredondo Zamarripa, Norma Adán, Andrés Quintanar-Stéphano, Miguel Condés-Lara, Gerardo Rojas-Piloni, Nadine Binart, Gonzalo Martínez de la Escalera, Carmen Clapp, Edith Arnold, Stéphanie Thebault, German Baeza-Cruz, David Arredondo Zamarripa, Norma Adán, Andrés Quintanar-Stéphano, Miguel Condés-Lara, Gerardo Rojas-Piloni, Nadine Binart, Gonzalo Martínez de la Escalera, Carmen Clapp
Abstract
Retinal degeneration is characterized by the progressive destruction of retinal cells, causing the deterioration and eventual loss of vision. We explored whether the hormone prolactin provides trophic support to retinal cells, thus protecting the retina from degenerative pressure. Inducing hyperprolactinemia limited photoreceptor apoptosis, gliosis, and changes in neurotrophin expression, and it preserved the photoresponse in the phototoxicity model of retinal degeneration, in which continuous exposure of rats to bright light leads to retinal cell death and retinal dysfunction. In this model, the expression levels of prolactin receptors in the retina were upregulated. Moreover, retinas from prolactin receptor-deficient mice exhibited photoresponsive dysfunction and gliosis that correlated with decreased levels of retinal bFGF, GDNF, and BDNF. Collectively, these data unveiled prolactin as a retinal trophic factor that may regulate glial-neuronal cell interactions and is a potential therapeutic molecule against retinal degeneration.
Keywords: gliosis; prolactin; retinal degeneration; trophic factor.
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Source: PubMed