Abstract
MicroRNA expression profiling showed that the retina of mice carrying a rhodopsin mutation that leads to retinitis pigmentosa have notably different microRNA profiles from wildtype mice; further in silico analyses identified potential retinal targets for differentially regulated microRNAs.
Highlights
The role played by microRNAs as common regulators in physiologic processes such as development and various disease states was recently highlighted
Comparison of the retina versus brain samples (Figure 1a) or the retina versus mouse platform samples resulted in large differences in miR expression profiles (Additional data file 1)
Expression of miR-96 and miR-183 decreased by more than 2.5-fold (P < 0.001) in mutant retinas, whereas miR-1 and miR-133 increased by more than 3fold (P < 0.001), as measured using quantitative realtime RT-PCR (qPCR). These results provide the first evidence for an altered miR expression profile in retinal disease
Summary
The role played by microRNAs (miRs) as common regulators in physiologic processes such as development and various disease states was recently highlighted. MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression at the post-transcriptional level in animals, plants, and viruses [1,2]. The end product is a mature miR (about 22 nucleotides) that, via incorporation into the RNA-induced silencing complex [5], appears to play crucial roles in eukaryotic gene regulation, primarily by post-transcriptional silencing. Perfect or near perfect complementarity of the miR to the target usually results in cleavage of the mRNA [8,9], whereas imperfect base pairing leads to translational repression by various mechanisms, including stalling translation, altering mRNA stability or moving mRNAs into specific, translationally inactive cytoplasmic sites called 'P-bodies' [1,10]. RNA-directed transcriptional silencing may guide interference at the nuclear DNA level by promoting heterochromatin formation [1,10,11]
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