IQUIBICEN   23947
INSTITUTO DE QUIMICA BIOLOGICA DE LA FACULTAD DE CIENCIAS EXACTAS Y NATURALES
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Why is the macula particularly susceptible to non-exudative age-related macular degeneration? Lessons from the mouse.
Autor/es:
ROMEO, HORACIO E; ARANDA ML; DEVOUASSOUX, JULIÁN D; SANDE PABLO H; ALAIMO, AGUSTINA; IAQUINANDI A; KELLER SARMIENTO MI; ROSENSTEIN RE; DIEGUEZ HH; GONZÁLEZ FLEITAS MF; ALTSCHULER, FLORENCIA; CHIANELLI MS; DORFMAN, DAMIÁN
Lugar:
Mardel Plata
Reunión:
Congreso; LXIII Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2018
Institución organizadora:
Sociedad Argentina de Investigación Clínica (SAIC)
Resumen:
AWARDSWHY IS THE MACULA PARTICULARLY SUSCEPTIBLE TO NON-EXUDATIVE AGE-RELATED MACULARDEGENERATION? LESSONS FROM THE MOUSEDieguez Hernan, Romeo Horacio, Alaimo Agustina, Fleitas González Florencia María, Aranda Marcos L, IaquinandiAgustina, Altschuler Florencia, Devouassoux Julian, Keller Ines S., Chianelli Mónica, Sande Pablo H.,Rosenstein Ruth E., Dorfman Damian.Laboratorio de Neuroquímica Retiniana y Oftalmología Experimental, Departamento de Bioquímica Humana, Facultad de Medicina-CEFYBO, UBA. Facultad de Ingeniería y Ciencias Agrarias, Pontificia Universidad Católica Argentina, BIOMED, UCA-CONICET.Laboratorio Interdisciplinario de Dinámica Celular y Nanotools, Departamento de Química Biológica, Facultad de CienciasExactas y Naturales. IQUIBICEN, Universidad de Buenos Aires-CONICETNon-exudative age-related macular degeneration (NEAMD)represents the leading cause of blindness in theelderly. The macular retinal pigment epithelium (RPE)lies in a high oxidative environment because its highmetabolic demand, mitochondria concentration, reactiveoxygen species levels, and macular blood flow. It hasbeen suggested that oxidative stress-induced damage tothe RPE plays a key role in NE-AMD pathogenesis. Thefact that the disease limits to the macular region raisesthe question as to why this area is particularly susceptible.We have developed a NE-AMD model induced bysuperior cervical ganglionectomy (SCGx) in C57BL/6Jmice, which reproduces the disease hallmarks exclusivelycircumscribed to the temporal region of the RPE/outerretina. The aim of this work was analyzing RPE regionaldifferences that could explain AMD localized susceptibility.Adult male C57Bl/6J mice were used. Histological,ultrastructural and biochemical parameters were studied.Lower melanin content, thicker basal infoldings, highermitochondrial mass, and higher levels of antioxidant enzymes,were found in the temporal RPE compared withthe nasal region (*P < 0.05 vs. nasal RPE, by Student´st-test). Moreover, SCGx induced a decrease in the antioxidantsystem, and in mitochondria mass, as well as anincrease in mitochondria superoxide, lipid peroxidationproducts, nuclear factor erythroid 2?related factor (Nrf2)and heme oxygenase-1 levels, and in the occurrence ofdamaged mitochondria exclusively at the temporal RPE(**P < 0.01 vs. nasal RPE from sham-treated eyes; a:P < 0.01 vs. temporal RPE from sham-treated eyes, byTukey´s test (F=4.53)). These findings suggest that despitethe well-known differences between the human andmouse retina, it might not be NE-AMD pathophysiologywhich conditions the localization of the disease, but themacular RPE histologic and metabolic specific attributesthat make it more susceptible to choroid alterations leadinginitially to a localized RPE dysfunction/damage, andsecondarily to macular degeneration.