Dr. Morten Ritso
I have been a stem cell and muscle biologist since starting my graduate studies under Hanns Lochmüller’s supervision at Newcastle University. My PhD project investigated cardiac hypertrophy in Duchenne muscular dystrophy (DMD). I observed that DMD cardiomyocytes could be used to model pathological hypertrophy in culture and used adeno-associated viruses to deliver a micro-dystrophin construct to rescue the dystrophic phenotype in these cells.
I subsequently joined Michael Rudnicki’s laboratory at the Ottawa Hospital Research Institute as a postdoctoral fellow, to study skeletal muscle stem cell (MuSC) subpopulation dynamics in tissue regeneration. MuSCs have a remarkable capacity to rapidly activate and proliferate upon tissue injury. These cells go on to rebuild damaged muscle, while maintaining a functional stem cell pool in vivo. However, when removed from their niche for ex vivo culture and expansion, MuSCs have a finite capacity to proliferate, eventually exhausting the stem cell population. To create an abundant source of MuSCs I reprogrammed healthy human donor and DMD patient cells into iPSCs, which I then differentiated into myogenic MuSC-like populations, to support the cause of finding a universal therapy for all DMD patients.
In the Rossi Lab, I am building on my previous translational expertise in skeletal and cardiac muscle to investigate the convergence and compartmentalisation of interactions between muscle resident cell populations. We have only recently gained technological capabilities to explore muscle regeneration at a level of detail allowing us to reliably assess cell population dynamics and key regulatory signalling. Harnessing single cell and spatial transcriptomics, we have identified novel factors at play in muscle-resident mesenchymal stromal cell (fibro-adipogenic progenitor) and MuSC response to damage.
These datasets provide an abundant resource which I am using to identify biological repair mechanisms with potential for therapeutic intervention in muscular dystrophies. Furthermore, our improved understanding of muscle stem and progenitor cell behaviour does not only reveal information about muscle biology. These findings can also be applied to investigate pathways with potential to facilitate efficient regeneration of other tissues in a range of degenerative and pathologically fibrotic conditions.
I cycle, ski and hike, participate in beer runs and pub trivia competitions. I’m a huge fan of live music and still enjoy listening to albums as an art form.
https://pubmed.ncbi.nlm.nih.gov/?term=morten+ritso&sort=date
I subsequently joined Michael Rudnicki’s laboratory at the Ottawa Hospital Research Institute as a postdoctoral fellow, to study skeletal muscle stem cell (MuSC) subpopulation dynamics in tissue regeneration. MuSCs have a remarkable capacity to rapidly activate and proliferate upon tissue injury. These cells go on to rebuild damaged muscle, while maintaining a functional stem cell pool in vivo. However, when removed from their niche for ex vivo culture and expansion, MuSCs have a finite capacity to proliferate, eventually exhausting the stem cell population. To create an abundant source of MuSCs I reprogrammed healthy human donor and DMD patient cells into iPSCs, which I then differentiated into myogenic MuSC-like populations, to support the cause of finding a universal therapy for all DMD patients.
In the Rossi Lab, I am building on my previous translational expertise in skeletal and cardiac muscle to investigate the convergence and compartmentalisation of interactions between muscle resident cell populations. We have only recently gained technological capabilities to explore muscle regeneration at a level of detail allowing us to reliably assess cell population dynamics and key regulatory signalling. Harnessing single cell and spatial transcriptomics, we have identified novel factors at play in muscle-resident mesenchymal stromal cell (fibro-adipogenic progenitor) and MuSC response to damage.
These datasets provide an abundant resource which I am using to identify biological repair mechanisms with potential for therapeutic intervention in muscular dystrophies. Furthermore, our improved understanding of muscle stem and progenitor cell behaviour does not only reveal information about muscle biology. These findings can also be applied to investigate pathways with potential to facilitate efficient regeneration of other tissues in a range of degenerative and pathologically fibrotic conditions.
I cycle, ski and hike, participate in beer runs and pub trivia competitions. I’m a huge fan of live music and still enjoy listening to albums as an art form.
https://pubmed.ncbi.nlm.nih.gov/?term=morten+ritso&sort=date
