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Mitochondrial Microprotein MOCCI Controls Neuroinflammation by Altering Glial Activation States [scRNA-seq]

ABSTRACT: MOCCI, discovered in a screen for mitochondrial peptides that modify inflammatory outcomes, has emerged as a significant regulator of neuroinflammation. Here, we show that MOCCI is upregulated in microglia and astrocytes in both the mouse and human brain upon neuroinflammation, and is required for orchestrating proper, complete, and beneficial activation of microglia and astrocytes. Induction of MOCCI triggers the transition of glial into a neuroprotective state and promotes the resolution of inflammation. In vitro, MOCCI deficiency leads to reduced migration, phagocytosis and cytokine secretion in glia. In the cuprizone mouse model of Multiple Sclerosis, MOCCI plays a role in both demyelination and remyelination: MOCCI deficiency protects against cuprizone-induced oligodendrocyte death and prevents remyelination by inhibiting the clearance of cellular debris.

ORGANISM(S): Mus musculus

PROVIDER: GSE305874 | GEO | 2025/12/31

REPOSITORIES: GEO

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Dynamics of reactive astrocytes fosters tissue regeneration after cuprizone-induced demyelination [RNA-seq II]

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