ArticleiScience2024
SENP1 facilitates OM-MSC differentiation through activating OPTN-mediated mitophagy to mitigate the neurologic impairment following ICH.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Olfactory Mucosal Mesenchymal Stem Cell-Derived Exosomal LncA2M-AS1 Ameliorates Parkinson's Disease by Regulating Microglial Glucose Metabolic Reprogramming and Neuroinflammation via the CFL1/ROCK1 Axis.CNS neuroscience & therapeutics · 2026Article
- RBM15 affects mitophagy in intracerebral hemorrhage by promoting E2F1 nuclear translocation via NXF1.Frontiers in immunology · 2026Article
- Emerging Therapeutic Strategies in Intracerebral Hemorrhage: Enhancing Neurogenesis and Functional Recovery.MedComm · 2025Review
- Mitochondrial Quality Control: Insights into Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2025Review
- Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.Molecular neurobiology · 2025Review
- DeSUMOylation of IGF2BP2 Promotes Neuronal Differentiation of OM-MSCs by Stabilizing SOX11 to Ameliorate Brain Injury After Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
- Rewiring the seizing brain: stem cell grafts as neuromodulatory architects in epilepsy therapy.Frontiers in neurologyReview
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have indicated the neuroprotective effect of olfactory mucosa mesenchymal stem cells (OM-MSCs) on brain injury. Intracerebral hemorrhage (ICH) models were established in rats by injecting autologous blood. SENP1 expression was enhanced in neurons but decreased in astrocytes compared to that in OM-MSCs. Overexpression of SENP1 promoted the proliferation and neuronal differentiation, while inhibiting the astrocytic differentiation of OM-MSCs. Conversely, its knockdown had the opposite effect. Moreover, OM-MSCs reduced neurological dysfunction in rats after ICH, and the neuroprotective effect of OM-MSCs could be further enhanced by SENP1 overexpression. In addition, SENP1 promoted mitophagy, which might be related to SENP1-mediated OPTN deSUMOylation. Furthermore, SENP1 promoted neuronal differentiation of OM-MSCs through mitophagy mediated by OPTN. Similar to SENP1, OPTN transfection further enhanced the remission effect of OM-MSC on ICH rats. SENP1 promoted neuronal differentiation of OM-MSCs through OPTN-mediated mitophagy to improve neurological deficits in ICH rats.
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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 Socratic graph.