12:00 – 12:30 Sheyla Velasco: Anti-inflammatory therapies for the treatment of retinitis pigmentosa

Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by the progressive and irreversible loss of vision due to photoreceptor cell death. Several studies suggest an important inflammatory component in the progression of RP. Activation of microglia, a common event present in retinal degenerations, or increased inflammatory mediators such as the tumor necrosis factor alpha (TNFα) have been described in patients and murine models of RP. In models of RP, microglial activation precedes or coincides with the peak of photoreceptor death and with elevated levels of TNFα. We previously found that intraperitoneal or intravitreal administration of Adalimumab (ADA), a monoclonal anti-TNFα antibody, slowed down retinal degeneration in the murine model of RP, the rd10 mice. In recent years, Drug Delivery Systems (DDS) have emerged as an alternative to conventional dosage forms and have proven to be promising candidates for drug encapsulation and application in ocular diseases. DDS are having a huge impact on medical technology by improving the mode of drug delivery. The aim of this study is to achieve a most effective, specific and economic therapy for RP using DDS.

12:30 – 13:00 Arantxa Martínez:  Role of the polyamine-hypusine-eIF5A in cancer progression

The polyamines are essential metabolites for eukaryotic cell growth, and their metabolism is frequently deregulated in cancer. One key target of polyamines is the translation factor eIF5A, the only known protein that undergoes a post-translational modification named ‘hypusination’. This modification generates the hypusine residue, which is derived from polyamine spermidine, and is essential for the activity of eIF5A on the ribosome. The highly selective modification by hypusination is susceptible of pharmacological inhibition and made this pathway a very attractive therapeutic target. Our research project aims the characterization of the pathogenic role of the eIF5A2 isoform and the polyamine-hypusine pathway in the progression of non-small cell lung cancer. Our results show that the expression of eIF5A2 and hypusinated eIF5A2 is induced by TGFβ1, suggesting that eIF5A2 is a mediator of TGFβ1 signaling. TGF β1-induced expression of eIF5A2 promotes the expression of proteins involved in the epithelial-mesenchymal transition, cell migration and invasion. Also, we show that genetic inactivation of eIF5A2 in cancer cells results in the disorganization of actin cytoskeleton and inhibition of cell proliferation. Modulation of the enzymatic activities by which eIF5A2 is activated and functional will reveal potential therapeutic targets for the prevention of cancer progression.