In Vitro and In Vivo Biocompatibility Studies on Engineered Fabric with Graphene Nanoplatelets.

To produce clothes made with engineered fabrics to monitor the physiological parameters of workers, strain sensors were produced by depositing two different types of water-based inks (P1 and P2) suitably mixed with graphene nanoplatelets (GNPs) on a fabric. We evaluated the biocompatibility of fabrics with GNPs (GNP fabric) through in vitro and in vivo assays. We investigated the effects induced on human keratinocytes by the eluates extracted from GNP fabrics by the contact of GNP fabrics with cells and by seeding keratinocytes directly onto the GNP fabrics using a cell viability test and morphological analysis. Moreover, we evaluated in vivo possible adverse effects of the GNPs using the model system Caenorhabditis elegans. Cell viability assay, morphological analysis and Caenorhabditis elegans tests performed on smart fabric treated with P2 (P2GNP fabric) did not show significant differences when compared with their respective control samples. Instead, a reduction in cell viability and changes in the membrane microvilli structure were found in cells incubated with smart fabric treated with P1. The results were helpful in determining the non-toxic properties of the P2GNP fabric. In the future, therefore, graphene-based ink integrated into elastic fabric will be developed for piezoresistive sensors.

Modulation of autophagy by RTN-1C: role in autophagosome biogenesis.

The endoplasmic reticulum (ER) is a key organelle fundamental for the maintenance of cellular homeostasis and to determine the cell's fate under stress conditions. Among the known proteins that regulate ER structure and function there is Reticulon-1C (RTN-1C), a member of the reticulon family localized primarily on the ER membrane. We previously demonstrated that RTN-1C expression affects ER function and stress condition. ER is an essential site for the regulation of apoptotic pathways and it has also been recently recognized as an important component of autophagic signaling. Based on these evidences, we have investigated the impact of RTN-1C modulation on autophagy induction. Interestingly we found that reticulon overexpression is able to activate autophagic machinery and its silencing results in a significative inhibition of both basal and induced autophagic response. Using different experimental approaches we demonstrated that RTN-1C colocalizes with ATG16L and LC3II on the autophagosomes. Considering the key role of reticulon proteins in the control of ER membrane shaping and homeostasis, our data suggest the participation of RTN-1C in the autophagic vesicle biogenesis at the level of the ER compartment. Our data indicate a new mechanism by which this structural ER protein modulates cellular stress, that is at the basis of different autophagy-related pathologies.

Reticulon protein-1C is a key component of MAMs.

The endoplasmic reticulum (ER) is a key organelle fundamental for the maintenance of cellular homeostasis and the determination of cell fate under stress conditions. Reticulon-1C (RTN-1C) is a member of the reticulon family proteins localized primarily on the ER membrane and known to regulate ER structure and function. Several cellular processes depend on the structural and functional crosstalk between different organelles, particularly on the endoplasmic reticulum and mitochondria. These dynamic contacts, called mitochondria-associated ER membranes (MAMs), are essential for the maintenance of mitochondrial structure and participate in lipid and calcium exchanges between the two organelles. In this study we investigated the impact of RTN-1C modulation on mitochondrial dynamics. We demonstrate that RTN-1C controls mitochondrial structure and function affecting intracellular Ca2+ homeostasis and lipid exchange between ER and mitochondria. We propose that these events depend on RTN-1C involvement in the regulation of ER-mitochondria cross-talk and define a role for RTN-1C in maintaining the function of contacts between the two organelles.