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Biology subjects

Cannavale, G.

Publications and source records attributed to Cannavale, G..

2 recordsLinked to original sources

Spatiotemporal atlas of pro-inflammatory (NF-kB) and anti-inflammatory (STAT6) signalling using reporter mice during mRNA vaccination

The immunization process unfolds through a precisely orchestrated sequence of innate and adaptive events across distinct anatomical sites. Although many mechanisms underlying vaccination are well described, most vaccines have been developed empirically, partly due to the lack of tools enabling rapid, organ-specific analysis of immune activation. To address this gap, we developed and validated a novel STAT6 reporter mouse enabling dynamic in vivo whole-body imaging and ex vivo analysis of STAT6-mediated anti-inflammatory signalling, and combined it with an established NF-{kappa}B reporter model to dissect immune activation induced by two LNP-encapsulated mRNA vaccines encoding the same antigen but differing in RNA chemistry (unmodified versus N{superscript 1}-methyl-pseudouridine (m{superscript 1}{Psi})-modified). This dual-reporter system enabled the creation of a spatiotemporal atlas of vaccine-induced signalling, revealing chemistry-dependent immune dynamics and identifying the liver as a predominant early hub for both NF-{kappa}B and STAT6 activity following systemic administration. Integration with antibody measurements demonstrated that early STAT6 activation followed by rapid signal resolution--rather than prolonged NF-{kappa}B-mediated inflammation--correlated with robust humoral responses, suggesting that monitoring NF-{kappa}B and STAT6 dynamics could provide predictive insight into vaccine immunogenicity. Together, these findings establish NF-{kappa}B and STAT6 reporter mice as rapid in vivo screening tools for the early assessment of vaccine immunogenicity and performance. By enabling dynamic, organ-resolved immune profiling, this approach paves the way for more rational, mechanism-driven design of mRNA vaccines and underscores the importance of further investigating the effects of vaccines on the liver, both as a primary LNP target and as an immunologically tolerogenic organ.

immunology↗

Metformin antiproliferative activity is exclusively mediated by the membrane functional expression of the Chloride Intracellular Channel 1 in glioblastoma stem cells

Metformin is the first-line drug for type-2 diabetes. Retrospective analyses, based on diabetic patients clinical data, demonstrate that daily assumption of metformin reduces the incidence of several kinds of solid tumors. Even though it is widely agreed that metformin must be internalized to accomplish its pharmacological activity, direct evidence about metformin membrane permeability and/or the presence of a specific membrane receptor in cancer cells is still missing. Here, we show that the transmembrane form of Chloride Intracellular Channel 1 (tmCLIC1) works as a privileged metformin receptor in glioblastoma stem-like cells. We found that metformin impairs tmCLIC1 activity by a specific binding coordinated by arginine 29. Its mutation, preventing metformin to bind and block tmCLIC1, abolishes the biguanide inhibition of glioblastoma cell proliferation in 2D and 3D models and metformin dependent effect on mitochondrial respiration. In addition, we demonstrate the direct binding between the drug and its target, and by in vivo experiments on zebrafish embryos and mice orthotopically engrafted with glioblastoma cells and treated with metformin, we prove that metformin binding to tmCLIC1 is crucial for metformin antineoplastic effect. Considering tmCLIC1s contribution to glioblastoma progression, the present work provides the fundaments for future development of strategies aimed at improving metformin-tmCLIC1 interaction to further increase metformin therapeutic potential.

cancer biology↗