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Santonicola, P.

Publications and source records attributed to Santonicola, P..

2 recordsLinked to original sources

Microalgae as a novel biofactory for biocompatible and bioactive extracellular vesicles

Nanoalgosomes are extracellular vesicles (EVs) released by microalgal cells that can mediate intercellular and cross-kingdom communication. In the present study, starting from the optimized nanoalgosome manufacturing from cultures of marine microalgae, we evaluated their innate biological properties in preclinical models. Our investigation of nanoalgosome biocompatibility included toxicological analyses, starting from studies on the invertebrate model organism Caenorhabditis elegans, proceeding to hematological and immunological evaluations in mice and immune-compatibility ex vivo. Nanoalgosome biodistribution was evaluated in mice with accurate space-time resolution, and in C. elegans at cellular and subcellular levels. Further examination highlighted the antioxidant and anti-inflammatory bioactivities of nanoalgosomes. This holistic approach to nanoalgosome functional characterization showcases that nanoalgosomes are innate effectors and potential drug delivery system for novel cosmetic formulations and EV-based therapies.

cell biology↗

TGS1 controls snRNA 3' end processing, prevents neurodegeneration and ameliorates SMN-dependent neurological phenotypes in vivo

Trimethylguanosine synthase 1 (TGS1) is a highly conserved enzyme that converts the 5 mono-methylguanosine cap of snRNAs to a trimethylguanosine cap. Here, we show that loss of TGS1 in C. elegans, D. melanogaster and D. rerio results in neurological phenotypes similar to those caused by Survival Motor Neuron (SMN) deficiency. Importantly, expression of human TGS1 ameliorates the SMN-dependent neurological phenotypes in both flies and worms, revealing that TGS1 can partly counteract the effects of SMN deficiency. TGS1 loss in HeLa cells leads to the accumulation of immature U2 and U4atac snRNAs with long 3 tails that are often uridylated. snRNAs with defective 3 terminations also accumulate in Drosophila Tgs1 mutants. Consistent with defective snRNA maturation, TGS1 and SMN mutant cells also exhibit partially overlapping transcriptome alterations that include aberrantly spliced and readthrough transcripts. Together, these results identify a neuroprotective function for TGS1 and reinforce the view that defective snRNA maturation affects neuronal viability and function.

genetics↗