The Hormone Prolactin Is a Novel, Endogenous Trophic Factor Able to Regulate Reactive Glia and to Limit Retinal Degeneration

被引:41
作者
Arnold, Edith [1 ]
Thebault, Stephanie [1 ]
Baeza-Cruz, German [1 ]
Arredondo Zamarripa, David [1 ]
Adan, Norma [1 ]
Quintanar-Stephano, Andres [2 ]
Condes-Lara, Miguel [1 ]
Rojas-Piloni, Gerardo [1 ]
Binart, Nadine [3 ]
Martinez de la Escalera, Gonzalo [1 ]
Clapp, Carmen [1 ]
机构
[1] Univ Nacl Autonoma Mexico, Inst Neurobiol, Queretaro 76230, Qro, Mexico
[2] Univ Autonoma Aguascalientes, Ctr Ciencias Basicas, Aguascalientes 20100, Mexico
[3] Univ Paris 11, Fac Med Paris Sud, Inst Natl Sante & Rech Med, U693, F-94270 Le Kremlin Bicetre, France
关键词
gliosis; prolactin; retinal degeneration; trophic factor; FIBRILLARY ACIDIC PROTEIN; NITRIC-OXIDE SYNTHASE; OSCILLATORY POTENTIALS; LIGHT DAMAGE; MULLER CELLS; VISUAL PIGMENTS; PITUITARY-GLAND; GROWTH-HORMONE; ACUTE-PHASE; IN-VITRO;
D O I
10.1523/JNEUROSCI.2452-13.2014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:1868 / 1878
页数:11
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