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BioMed Central, Genome Biology, 11(8), p. R248

DOI: 10.1186/gb-2007-8-11-r248

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Altered retinal microRNA expression profile in a mouse model of retinitis pigmentosa.

Journal article published in 2007 by Carol J. Loscher, Karsten Hokamp, Paul F. Kenna, Alasdair C. Ivens ORCID, Peter Humphries, Arpad Palfi, G. Jane Farrar, G. Jane Farrar
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Abstract Background The role played by microRNAs (miRs) as common regulators in physiologic processes such as development and various disease states was recently highlighted. Retinitis pigmentosa (RP) linked to RHO (which encodes rhodopsin) is the most frequent form of inherited retinal degeneration that leads to blindness, for which there are no current therapies. Little is known about the cellular mechanisms that connect mutations within RHO to eventual photoreceptor cell death by apoptosis. Results Global miR expression profiling using miR microarray technology and quantitative real-time RT-PCR (qPCR) was performed in mouse retinas. RNA samples from retina of a mouse model of RP carrying a mutant Pro347Ser RHO transgene and from wild-type retina, brain and a whole-body representation (prepared by pooling total RNA from eight different mouse organs) exhibited notably different miR profiles. Expression of retina-specific and recently described retinal miRs was semi-quantitatively demonstrated in wild-type mouse retina. Alterations greater than twofold were found in the expression of nine miRs in Pro347Ser as compared with wild-type retina ( P