ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2026
DPSCs-Exos promote OPCs differentiation and white matter repair via Myl9-mediated PRMT5 nucleation after ischemic stroke.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Neuroimmune-oligovascular signaling shapes oligodendrocyte precursor cell fate and repair after ischemic stroke.Cell communication and signaling : CCS · 2026Review
- TNF-α/PAD4 axis drives hyperhomocysteine-induced white matter injury after acute ischemic stroke.Acta pharmacologica Sinica · 2026Article
- Microglial handling of myelin debris and remyelination after ischaemic stroke: recognition, intracellular processing, lipid fate, and oligodendroglial repair.Frontiers in cellular neuroscience · 2026Review
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7 authors.
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Abstract
Ischemic stroke often leads to white matter damage due to impaired oligodendrocyte precursor cells (OPCs) differentiation, hindering post-stroke recovery. While dental pulp stem cells-derived exosomes (DPSCs-Exos) have shown promise in stroke recovery, the underlying mechanisms remain unclear. Toward this aim, we investigated the therapeutic potential of DPSCs-Exos for promoting OPCs differentiation and white matter repair after ischemic stroke using in vivo (middle cerebral artery occlusion, MCAO) and in vitro (oxygen-glucose deprivation/reoxygenation, OGD/R) models. Intracerebroventricular DPSCs-Exos were administered on days 1, 3, and 5 post-MCAO, with functional (sensory-motor and cognitive), morphological, and biochemical assessments performed at 7, 14, and 28 days. Our results demonstrated that DPSC-Exos treatment significantly improved functional outcomes, promoted OPCs proliferation and differentiation, and facilitated white matter repair. Mechanistically, DPSC-Exos-mediated OPCs differentiation involves protein arginine methyltransferase 5 (PRMT5) and inhibitor of differentiation 2 (ID2). Specifically, exosomal myosin regulatory light polypeptide 9 (Myl9) interacts with PRMT5 in OPCs, driving PRMT5 nucleation, subsequent CpG island methylation, and ID2 downregulation, ultimately leading to OPCs differentiation into oligodendrocytes (OLs). These findings identify a novel mechanism by which DPSC-Exos promote white matter repair and suggest their potential as a therapeutic strategy for ischemic stroke.
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