Fabien LE GRAND
DR2 CNRS, HDR
0000-0002-7843-3899
Pauline GARCIA
PhD Student
0000-0002-4673-8583
William JARASSIER
IE CDD, Bioinformaticien
0000-0002-9454-2358
Sidy FALL
IE CDD, Bioinformaticien
Fany AGOSTINI
Assistante Ingénieur
0000-0001-5569-4917
Jade RAVENT
Technicienne supérieur
0000-0002-5023-4230
Figure legend :
To characterize the cellular diversity of the skeletal muscle, we performed mass cytometry (CyTOF) on mononuclear cell suspensions obtained from adult mouse hindlimb muscles. Shown here is the analysis of the CyTOF dataset using the X-shift algorithm paired with single-cell force-directed layout visualization. Each cluster was annotated based on the expression of marker genes in the different major cell types. Clusters sharing the same canonical markers are depicted with the same color.
Skeletal muscle regeneration relies on the subtly orchestrated interplay between muscle stem cells and other cells that reside in or invade the wounded tissue after injury. Cell-to-cell interactions mediated by extracellular signaling cascades affect major cell functions and cause phenotypic transformations as an integral part of the response to environmental cues.
Perturbations in the architecture of this hypernetwork usually lead to defects in tissue repair. However, the environmental cues creating the transitory “regenerative” stem cell niche are poorly known.The team SPaSM assembles expertise in skeletal muscle basic cell biology and translational research to understand muscle tissue repair using an integrated multi-scale approach. We focus on signaling pathways deployed during skeletal muscle regeneration and aim to develop novel pharmacological therapies for muscular dystrophies.
Our research revolves around three aims:
i/ Using single-cell technologies, we map striated muscles cell type composition (RNA-sequencing; Mass Cytometry) during development, regeneration, ageing and in disease.
ii/ We study intracellular cytoskeleton dynamics as an endpoint of extracellular signaling pathways and decipher the cues that regulate skeletal myoblasts fusion.
iii/ We found aberrant activation of Wnt/ß-catenin and Tgfß signalings in both ageing and muscle dystrophies. We decipher the functional consequences of these mis-regulations in muscle cells.
Institut NeuroMyoGène UCBL – CNRS UMR 5261 – INSERM U1315
Faculté de Médecine et de Pharmacie –
3ème étage – Aile B
8 avenue Rockefeller
69008 Lyon France