ArticleTranslational stroke research2025
Inhibition of GPR17/ID2 Axis Improve Remyelination and Cognitive Recovery after SAH by Mediating OPC Differentiation in Rat Model.
Article in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- GPR17 Suppresses Triple-Negative Breast Cancer Progression and Serves as an Independent Prognostic Biomarke.World journal of surgical oncology · 2026Article
- DPSCs-Exos promote OPCs differentiation and white matter repair via Myl9-mediated PRMT5 nucleation after ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Exerkine irisin mitigates cognitive impairment by suppressing gut-brain axis-mediated inflammation.Journal of advanced research · 2025Article
- Characterisation of GPR17-expressing oligodendrocyte precursors in human ischaemic lesions and correlation with reactive glial responses.The Journal of pathology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Myelin sheath injury contributes to cognitive deficits following subarachnoid hemorrhage (SAH). G protein-coupled receptor 17 (GPR17), a membrane receptor, negatively regulates oligodendrocyte precursor cell (OPC) differentiation in both developmental and pathological contexts. Nonetheless, GPR17's role in modulating OPC differentiation, facilitating remyelination post SAH, and its interaction with downstream molecules remain elusive. In a rat SAH model induced by arterial puncture, OPCs expressing GPR17 proliferated prominently by day 14 post-onset, coinciding with compromised myelin sheath integrity and cognitive deficits. Selective Gpr17 knockdown in oligodendrocytes (OLs) via adeno-associated virus (AAV) administration revealed that reduced GPR17 levels promoted OPC differentiation, restored myelin sheath integrity, and improved cognitive deficits by day 14 post-SAH. Moreover, GPR17 knockdown attenuated the elevated expression of the inhibitor of DNA binding 2 (ID2) post-SAH, suggesting a GPR17-ID2 regulatory axis. Bi-directional modulation of ID2 expression in OLs using AAV unveiled that elevated ID2 counteracted the restorative effects of GPR17 knockdown. This resulted in hindered differentiation, exacerbated myelin sheath impairment, and worsened cognitive deficits. These findings highlight the pivotal roles of GPR17 and ID2 in governing OPC differentiation and axonal remyelination post-SAH. This study positions GPR17 as a potential therapeutic target for SAH intervention. The interplay between GPR17 and ID2 introduces a novel avenue for ameliorating cognitive deficits post-SAH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.