March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
TUDCA Prevents Microglia Activation In The P23H Rat Retina
Author Affiliations & Notes
  • Laura Fernandez-Sanchez
    Physiology, Genetics & Microbiology, University of Alicante, Alicante, Spain
  • Agustina Noailles
    Physiology, Genetics & Microbiology, University of Alicante, Alicante, Spain
  • Isabel Pinilla
    Ophthalmology, Universitary Hospital Lozano Blesa. Aragon Health Sciences Institute, Zaragoza, Spain
  • Jose Martin-Nieto
    Physiology, Genetics & Microbiology, University of Alicante, Alicante, Spain
  • Pedro Lax
    Physiology, Genetics & Microbiology, University of Alicante, Alicante, Spain
  • Nicolas Cuenca
    Physiology, Genetics & Microbiology, University of Alicante, Alicante, Spain
  • Footnotes
    Commercial Relationships  Laura Fernandez-Sanchez, None; Agustina Noailles, None; Isabel Pinilla, None; Jose Martin-Nieto, None; Pedro Lax, None; Nicolas Cuenca, None
  • Footnotes
    Support  MICINN (BFU2009-07793/BFI), MSyC RETICS RD07/0062/0012, FUNDALUCE, ONCE, Fundación Médica Mutua Madrileña.
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6430. doi:
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      Laura Fernandez-Sanchez, Agustina Noailles, Isabel Pinilla, Jose Martin-Nieto, Pedro Lax, Nicolas Cuenca; TUDCA Prevents Microglia Activation In The P23H Rat Retina. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6430.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Chronic microglia activation is associated with various neurodegenerative diseases including retinitis pigmentosa. Retinal microglial cells are activated to release inflammatory cytokines and neurotoxins that may contribute significantly to retinal tissue damage and pro-apoptotic events. The objective of this study is to quantify microglia activation in the P23H rat retina and to evaluate the effects of TUDCA (Tauroursodeoxycholic acid), which has been described as a good neuroprotective compound.

Methods: : For this study, homozygous P23H line 3 rats were used. Animals from 20 days to 4 months were injected weekly with TUDCA (500 mg/kg, i.p.). Vertical retinal cryostat sections were immunostained for specific markers of microglia (anti-CD11b). Microglia morphology was analyzed in wholemount retinas and the number of microglial cells located in both plexiform layers and in the ganglion cell layer was quantified.

Results: : Microglial cells in the SD rat retina were distributed in plexus located at the inner and outer plexiform and ganglion cell layers. In the ganglion cell layer immunostained cells with macrophage morphology were also found. In the P23H rat retina, an increase in microglia cells numbers was found in all layers compared with control rat retinas. In addition, microglial cells with macrophage-like morphology were observed in the P23H subretinal space, but not present in SD. Retinas of TUDCA-treated animals showed lower cell numbers in all layers and absence of microglia in the subretinal space.

Conclusions: : This work suggests that, besides its neuroprotective effect of on photoreceptor cells, TUDCA prevents microglial activation in retinitis pigmentosa. Therefore, TUDCA could be potentially useful for the future treatment of retinitis pigmentosa.

Keywords: retinitis • neuroprotection • microglia 
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