Anasagasti, A. 1, 7 , Barandika, O. . 1, 7 , Irigoyen, C. 1, 2 , Egiguren, G. 1, 7 , Sánchez, C. 3 , López de Munain, A. 1, 4, 5, 6 & Ruiz, J. 1, 7
1 Department of Neurosciences, Instituto Biodonostia, San Sebastián, Gipuzkoa, Spain
2 Department of Ophthalmology Hospital Universitario Donostia, San Sebastián, Spain
3 Viral Vector Platform,Fundación Inbiomed, San Sebastián, Spain
4 Department of Neurology, Hospital Universitario Donostia, San Sebastián, Spain
5 CIBERNED, Centro de Investigaciones Biomédicas en Red sobre Enfermedades Neurodegenerativas, Instituto Carlos III, Ministerio de Economía y Competitividad, Spain
6 Department of Neurology Hospital Universitario Donostia, San Sebastián, Spain
7 Euskampus, University of the Basque Country UPV/EHU, Spain
Purpose: Retinitis pigmentosa (RP) is the most common form of inherited retinal degeneration associated with progressive dysfunction of rod cells and/or cones. Currently there is no standardized and effective treatment for this eye disease that affects about 1 million people worldwide. Here we propose that an alteration in the expression of microRNAs (miRs) is involved in the pathogenesis of RP.
Methods: Using PCR-based expression microarrays we analyzed the expression of miRs in retinas from an RP mouse model, with photoreceptors death related to an alteration of intracellular Ca2+.
Results: We found 3 miRs with a 5 to 15-fold decreased expression and one miR with a 44-fold increased expression.
Conclusions: Our results support the implication of miRs in RP. Overexpression of one of the altered miRs we found has been linked to increased release of Ca2+. This miR has been reported to target among other genes: PIK3CA, expressed in photoreceptors; connexin 43 and the potassium channel Kir2.1, both expressed in retinal glial cells. Interestingly overexpression of these glial components have been involved in retinal damage induced in experimental models and therefore might be also involved in the mechanism of cell death that takes place in our RP model.