CELLULAR AND MOLECULAR ABNORMALITIES OF MULLER GLIAL CELLS IN THE RD MICE

POLITI, L.E.; VOLONTÉ Y.; GERMAN O.L.; SIMON M.V.; ROTSTEIN N.P.

San Francisco

Congreso; XXI Biennial Meeting International Society for Eye Research (ISER); 2014

ISER

CELLULAR AND MOLECULAR ABNORMALITIES OF MULLER GLIAL CELLS IN THE ?RD? MICE Luis Politi, Yanel Volonté, Lorena Germán, Victoria Simón, and Nora Rotstein Instituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB) and Universidad Nacional del Sur. 8000 Bahía Blanca, Argentina The molecular basis of retinitis pigmentosa (RP) and of photoreceptor degeneration in ?rd? mice is largely known, however a cure for these diseases is not yet available. The use of stem cells to regenerate the damaged retinas may be useful to reach a suitable treatment for RP. Müller glial cells (MGC) have multiple roles in the eye, providing nutrients and trophic factors essential for neuronal survival. Recent work from several laboratories has shown that MGC are also stem cells, which may replace physiological neuronal losses occurring in the normal eye. In spite of these crucial roles of MGC, up to now there is little or no information about MGC in the ?rd? mice. Since in ?rd? retinas there are no evidences of neuronal regeneration, we hypothesize that, in addition to the already known molecular abnormalities of retina photoreceptors, MGC may present alterations that affect their regenerative capacity. We here investigated whether MGC in ?rd? retinas presented morphological or molecular abnormalities. We analyzed MGC obtained from newborn ?rd? and normal (WT) retinas growing in mixed neuron-glial cultures. WT cultures presented about 2 progenitor photoreceptors per MGC; by contrast, in ?rd? cultures, the number of photoreceptors per MGC was up to 3 times higher. This suggests that there is a decrease in the amount of MGC in ?rd? retinas, which might lead to their inability to adequately furnish neurons with essential . In addition, we found that ?rd? MGC decreased nestin expression and showed abnormal nuclei morphology. Therefore, we suggest that in addition to the photoreceptor failure, the abnormalities in ?rd? MGC may impair the regenerative capacity in these mice. Grants: FONCyT, CONICET and Universidad Nacional del Sur