Publication 2026

Mimouni et al. Journal of Translational Medicine 2026

Leroy et al. Antioxidants 2026

Revel et al. Emerging Microbes & Infections 2026

En ce début d’année 2026, l’équipe BC2M a publié trois articles scientifiques dans des revues internationales de premier plan, témoignant du dynamisme et de l’excellence de ses activités de recherche.

Mimouni M, Darlet S, Jover B, Gayrard N, Jeanson L, Blanchard MP, Lajoix AD, Desmetz C. Involvement of Fibulin-5 in endothelial to mesenchymal transition leading to cardiac fibrosis during metabolic syndrome. J Transl Med. 2026 Jul 7. doi: 10.1186/s12967-026-08589-x. Epub ahead of print. PMID: 42415085.

« Cardiac fibrosis is a hallmark of metabolic syndrome, a condition linked to Western lifestyles and high cardiovascular risk. We previously demonstrated that dietary sodium restriction prevents cardiac fibrosis and remodeling in a rat model of metabolic syndrome through reduced macrophage infiltration. Here, we investigate genes involved in endothelial-to-mesenchymal transition (EndoMT), a key process in cardiac fibrosis. »

Leroy J, Mezghenna K, Tousch D, Canovas J, Laune D, Pugnière M, Azay-Milhau J, Lajoix AD. PIN (Protein Inhibitor of Neuronal Nitric Oxide Synthase) Modulates Glucose Uptake Through NO-Dependent and Independent Mechanisms in Rat Muscle Cells. Antioxidants (Basel). 2026 Mar 31;15(4):436. doi: 10.3390/antiox15040436. PMID: 42072078; PMCID: PMC13114162.

« Protein inhibitor of neuronal NO synthase (PIN) or dynein light chain 8 (LC8) is a highly conserved protein interacting with multiple partners, like neuronal NO synthase (nNOS) or myosin Va to modulate a variety of cellular functions. As PIN is expressed in skeletal muscle, our aim was to investigate a possible role of PIN in glucose uptake in L6 and primary muscle cells. PIN overexpression resulted into a decrease in glucose uptake with reduced GLUT4 expression and translocation at the plasma membrane, similarly to the pharmacological blockade of nNOS with L-NAME. PIN effect is mediated by a reduction in nNOS protein level and a direct interaction with nNOS leading to a reduced NO production in L6 myocytes. Surprisingly, a siRNA targeting PIN decreased glucose uptake and GLUT4 translocation, suggesting the involvement of nNOS-independent effects. We therefore focused on myosin Va which interacts with PIN in L6 myocytes. Myosin Va silencing provoked a decrease in glucose uptake. As PIN siRNA also reduced myosin Va expression, this confirms the essential role of myosin Va in the observed effects of PIN silencing on glucose uptake. We conclude that PIN modulates glucose uptake and GLUT4 translocation in rat muscle cells, through NO-dependent and -independent mechanisms. »

Revel J, Leroy J, Delbecq S, Constant O, Henry Marty F, Naili C, Barthès A, Nagy A, Schmidt-Chanasit J, Cadar D, Abd Rahaman NY, Lajoix AD, Desmetz C, Simonin Y. Differential properties of NS1 glycoproteins in West Nile and Usutu viruses. Emerg Microbes Infect. 2026 Dec;15(1):2667565. doi: 10.1080/22221751.2026.2667565. Epub 2026 May 29. PMID: 42054312; PMCID: PMC13224725.

« West Nile virus (WNV) and Usutu virus (USUV) are neurotropic orthoflaviviruses of the Flaviviridae family, transmitted primarily by Culex mosquitoes and maintained in enzootic cycles involving birds. While WNV is a well-established human pathogen causing hundreds of neuroinvasive cases annually in Europe, USUV has emerged more recently, with fewer documented human infections but increasing evidence of neurovirulence. The viral nonstructural protein 1 (NS1) plays a central role in orthoflavivirus pathogenesis by modulating host immune responses, disrupting endothelial barrier integrity, and facilitating viral dissemination. However, the functional and biochemical properties of NS1 from WNV and USUV remain poorly characterized. We combined in vitro, in vivo, and clinical approaches to compare NS1 secretion, stability, and its impact on blood-brain barrier. Our results show that WNV NS1 is secreted at significantly higher levels, exhibits greater thermal stability, and disrupts brain endothelial barrier integrity in vitro. In contrast, USUV NS1 is secreted less efficiently, is slightly less stable, and does not compromise blood-brain barrier integrity, despite inducing distinct transcriptional responses in brain endothelial cells. In mice, WNV infection led to higher serum NS1 levels and stronger systemic inflammation than USUV. Clinically, WNV NS1 was detected mainly in patients with neurological symptoms, whereas USUV NS1 remained undetectable in all cases. Altogether, these findings reveal differential NS1 properties between these closely related viruses, with key implications for orthoflavivirus diagnosis and neurovirulence mechanisms. »