Oxidative stress represents one of the principal inductors of lifestyle-related and
genetic diseases. Among them, inherited
retinal dystrophies, such as
age-related macular degeneration and
retinitis pigmentosa, are well known to be susceptible to oxidative stress. To better understand how high
reactive oxygen species levels may be involved in
retinal dystrophies onset and progression, we performed a whole
RNA-Seq experiment. It consisted of a comparison of transcriptomes' profiles among human retinal pigment epithelium cells exposed to the
oxidant agent
N-retinylidene-N-retinylethanolamine (A2E), considering two time points (3h and 6h) after the basal one. The treatment with A2E determined relevant differences in gene expression and splicing events, involving several new pathways probably related to
retinal degeneration. We found 10 different clusters of pathways involving differentially expressed and differentially alternative
spliced genes and highlighted the sub- pathways which could depict a more detailed scenario determined by the oxidative-stress-induced condition. In particular, regulation and/or alterations of angiogenesis, extracellular matrix integrity,
isoprenoid-mediated reactions, physiological or pathological autophagy, cell-death induction and
retinal cell rescue represented the most dysregulated pathways. Our results could represent an important step towards discovery of unclear molecular mechanisms linking oxidative stress and etiopathogenesis of
retinal dystrophies.