Regulation of stress granule formation in human oligodendrocytes

Florian Pernin, Qiao-Ling Cui, Abdulshakour Mohammadnia, Milton G. F. Fernandes, Jeffery A. Hall, Myriam Srour, Roy W. R. Dudley, Stephanie E. J. Zandee, Wendy Klement, Alexandre Prat, Hannah E. Salapa, Michael C. Levin, G. R. Wayne Moore, Timothy E. Kennedy, Christine Vande Velde and Jack P. Antel ()
Additional contact information
Florian Pernin: McGill University
Qiao-Ling Cui: McGill University
Abdulshakour Mohammadnia: McGill University
Milton G. F. Fernandes: McGill University
Jeffery A. Hall: McGill University Health Centre
Myriam Srour: Montreal Children’s Hospital
Roy W. R. Dudley: Montreal Children’s Hospital
Stephanie E. J. Zandee: Centre de Recherche Hospitalier de l’Université de Montréal
Wendy Klement: Centre de Recherche Hospitalier de l’Université de Montréal
Alexandre Prat: Centre de Recherche Hospitalier de l’Université de Montréal
Hannah E. Salapa: University of Saskatchewan
Michael C. Levin: University of Saskatchewan
G. R. Wayne Moore: McGill University
Timothy E. Kennedy: McGill University
Christine Vande Velde: Centre de Recherche Hospitalier de l’Université de Montréal
Jack P. Antel: McGill University

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Oligodendrocyte (OL) injury and subsequent loss is a pathologic hallmark of multiple sclerosis (MS). Stress granules (SGs) are membrane-less organelles containing mRNAs stalled in translation and considered as participants of the cellular response to stress. Here we show SGs in OLs in active and inactive areas of MS lesions as well as in normal-appearing white matter. In cultures of primary human adult brain derived OLs, metabolic stress conditions induce transient SG formation in these cells. Combining pro-inflammatory cytokines, which alone do not induce SG formation, with metabolic stress results in persistence of SGs. Unlike sodium arsenite, metabolic stress induced SG formation is not blocked by the integrated stress response inhibitor. Glycolytic inhibition also induces persistent SGs indicating the dependence of SG formation and disassembly on the energetic glycolytic properties of human OLs. We conclude that SG persistence in OLs in MS reflects their response to a combination of metabolic stress and pro-inflammatory conditions.

Date: 2024
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DOI: 10.1038/s41467-024-45746-6

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