The hormone prolactin is a novel, endogenous trophic factor able to regulate reactive glia and to limit retinal degeneration.
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.
Instituto de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM-Juriquilla, 76230 Querétaro, México, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, 20100 Aguascalientes, México, and Institut National de la Santé et de la Recherche Médicale, U693, Université Paris-Sud, Faculté de Médecine Paris-Sud, Le Kremlin-Bicêtre 94270, France.
Edith
E
Arnold
Stéphanie
S
Thebault
German
G
Baeza-Cruz
David
D
Arredondo Zamarripa
Norma
N
Adán
Andrés
A
Quintanar-Stéphano
Miguel
M
Condés-Lara
Gerardo
G
Rojas-Piloni
Nadine
N
Binart
Gonzalo
G
Martínez de la Escalera
Carmen
C
Clapp
D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D004195:Disease Models, Animal; D004596:Electroretinography; D005260:Female; D005786:Gene Expression Regulation / Q000235:genetics; D005904:Glial Fibrillary Acidic Protein / Q000235:genetics / Q000378:metabolism; D005911:Gliosis / Q000209:etiology; D006966:Hyperprolactinemia / Q000139:chemically induced / Q000503:physiopathology; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008027:Light / Q000009:adverse effects; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009457:Neuroglia / Q000502:physiology*; D011388:Prolactin / Q000097:blood*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011981:Receptors, Prolactin / Q000235:genetics / Q000378:metabolism; D012162:Retinal Degeneration / Q000150:complications / Q000209:etiology / Q000235:genetics / Q000517:prevention & control*; D012164:Retinal Diseases / Q000235:genetics
D005904:Glial Fibrillary Acidic Protein; D036341:Intercellular Signaling Peptides and Proteins; D012333:RNA, Messenger; D011981:Receptors, Prolactin; D011388:Prolactin
gliosis; prolactin; retinal degeneration; trophic factor