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Caroline E. Brun

Researcher at Ottawa Hospital Research Institute

Publications -  21
Citations -  1303

Caroline E. Brun is an academic researcher from Ottawa Hospital Research Institute. The author has contributed to research in topics: Stem cell & Skeletal muscle. The author has an hindex of 9, co-authored 15 publications receiving 855 citations. Previous affiliations of Caroline E. Brun include University of Ottawa.

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Dystrophin expression in muscle stem cells regulates their polarity and asymmetric division

TL;DR: It is concluded that dystrophin has an essential role in the regulation of satellite cell polarity and asymmetric division, and muscle wasting in DMD not only is caused by myofiber fragility, but also is exacerbated by impaired regeneration owing to intrinsic satellite cell dysfunction.
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The myogenic regulatory factors, determinants of muscle development, cell identity and regeneration.

TL;DR: Application of combined functional genomics technologies along with single cell lineage tracing strategies will allow a deeper understanding of the mechanisms mediating myogenic determination, cell differentiation and muscle regeneration.
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Orienting Muscle Stem Cells for Regeneration in Homeostasis, Aging, and Disease

TL;DR: The relationship of satellite cell heterogeneity and the establishment of polarity to asymmetric division is discussed, as well as how these processes are impacted in homeostasis, aging, and disease.
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Concise Review: Epigenetic Regulation of Myogenesis in Health and Disease

TL;DR: Recent findings on epigenetic regulation in satellite stem cells and committed myoblasts are described and the potential of epigenetic drugs, such as HDAC inhibitors, as well as their molecular mechanism of action in muscle cells, will be addressed.
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The Dystrophin Glycoprotein Complex Regulates the Epigenetic Activation of Muscle Stem Cell Commitment.

TL;DR: Dysregulation of p38γ/Carm1 results in altered epigenetic gene regulation in Duchenne muscular dystrophy and the resulting progenitors exhibit reduced Carm1 binding to Pax7, reduced H3K4-methylation of chromatin, and reduced transcription of Myf5 and other Pax7 target genes.