RECHERCHER DANS LES SHORT NOTES

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DERNIÈRES SHORT NOTES

Kassandra Kobon, David Pereira, Atef Asniacios, Pascal Maire, Voahangy Randrianarison-Huetz, Athanassia Sotiropoulos

Posted on Wednesday November 13, 2024

Abstract

Repair of muscle tissue and growth of multinucleated myofibers depend on adult muscle stem cells (muSCs) and their ability to fuse. In this study, we took advantage of two genetic models of fusion-defective muSCs (both deleted for Serum response factor (Srf Mut), and one overexpressing alpha-actin (Srf Mut/Act+)) to decipher pathways and cellular properties that can restore fusion and gain insight into the mechanisms of mammalian muscle cell fusion. We first showed that Srf is involved in the fusion process after membrane mixing (hemifusion). Furthermore, Srf Mut and Srf Mut/Act+ muSCs were less rigid than control cells, and increasing apparent cell stiffness, presumably by increasing membrane and cortical tension, by hypotonic osmotic shock partially restored their fusion capacity, with a better efficacy when actin was overexpressed. These findings identify membrane and cortical tension/cell stiffness as a potential new player in myoblast fusion that may control Srf-dependent fusion in concert with the formation of actin structures at the fusion site.

Alexandre Faisant, Sandra Carignon, Arnaud Menuet, Nicolas Riteau, Marc Le Bert

Posted on Thursday February 29, 2024

Abstract

This study aimed to establish an experimental model of Guillain-Barré Syndrome (GBS), a peripheral inflammatory neuropathy in humans, using the Experimental Autoimmune Neuritis (EAN) model in C57BL/6 mice. This approach was informed by a comprehensive bibliographic analysis. While this experimental model has been developed successfully in rabbits, rats, and the SJL mouse strain, the literature on its application in C57BL/6 mice is limited. Our protocol analysis encompassed twenty-one articles utilizing the P0180-199 neurogenic peptide to induce EAN in this genetic background. Based on this literature, we selected one protocol for replication and made three adaptations. Despite using high-quality P0(180-199) peptide, we were unable to reproduce the selected EAN protocol or induce any pathological signs, even under optimized conditions. As a control to validate our reagents and methodology, we replicated a different model of inflammatory neuropathy targeting the central nervous system: the well-established Experimental Autoimmune Encephalitis (EAE) protocol. This replication was successful using the same C57BL/6 mouse genetic background and reagents, with the sole exception of the neurogenic peptide employed (MOG(35-55)).