ArticleMolecular neurobiology2020
PPAR-γ Is Critical for HDAC3-Mediated Control of Oligodendrocyte Progenitor Cell Proliferation and Differentiation after Focal Demyelination.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- ACSS2 maintains oligodendrocyte progenitor cell pool and is required for myelination during development and aging.Nature aging · 2026Article
- Combined therapeutic effects of Renshenguben and swimming on knee osteoarthritis associated with the gut-joint axis and HDAC3/PPAR-Frontiers in microbiology · 2026Article
- Targeting astrocytic CLC2(CLCN2) restores myelin regeneration through inhibition of SPP1/CD44 signaling pathway in leukoencephalopathy.Molecular psychiatry · 2026Article
- Spinal Cord Injury Remyelination: Pathways to Therapies.International journal of molecular sciences · 2025Review
- Targeting HDAC3 Suppresses Ferroptosis and Demyelination in White Matter Injury by Restoring PDK4-Mediated Iron Homeostasis.CNS neuroscience & therapeutics · 2025Article
- Identification, Clinical Values, and Prospective Pathway Signaling of Lipid Metabolism Genes in Epilepsy and AED Treatment.Molecular neurobiology · 2025Article
- Impact of Histone Acetyltransferases and Histone Deacetylases on Adult Brain Myelin Plasticity.Results and problems in cell differentiation · 2025Review
- Orchestrating the frontline: HDAC3-miKO recruits macrophage reinforcements for accelerated myelin debris clearance after stroke.Theranostics · 2025Article
- The Neuroprotective Mechanisms of PPAR-γ: Inhibition of Microglia-Mediated Neuroinflammation and Oxidative Stress in a Neonatal Mouse Model of Hypoxic-Ischemic White Matter Injury.CNS neuroscience & therapeutics · 2024Article
- SIRT6 modulates lesion microenvironment in LPC induced demyelination by targeting astrocytic CHI3L1.Journal of neuroinflammation · 2024Article
- Therapeutic effects of combining curcumin and swimming in osteoarthritis using a rat model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- L-serine: Neurological Implications and Therapeutic Potential.Biomedicines · 2023Review
- Klotho Upregulation via PPARγ Contributes to the Induction of Brain Ischemic Tolerance by Cerebral Ischemic Preconditioning in Rats.Cellular and molecular neurobiology · 2023Article
- DL-3-n-butylphthalide alleviates motor disturbance by suppressing ferroptosis in a rat model of Parkinson's disease.Neural regeneration research · 2023Article
- Neuroinflammation aggravated by traumatic brain injury at high altitude is reversed by L-serineFrontiers in cellular neuroscience · 2023Article
- CBX4-dependent regulation of HDAC3 nuclear translocation reduces Bmp2-induced osteoblastic differentiation and calcification in adamantinomatous craniopharyngioma.Cell communication and signaling : CCS · 2022Article
- Article
- Effect of β-hydroxybutyrate on behavioral alterations, molecular and morphological changes in CNS of multiple sclerosis mouse model.Frontiers in aging neuroscience · 2022Article
- Histone deacetylase inhibitors regulate vitamin C transporter functional expression in intestinal epithelial cells.The Journal of nutritional biochemistry · 2021Article
- L-Serine, an Endogenous Amino Acid, Is a Potential Neuroprotective Agent for Neurological Disease and Injury.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Disruption of remyelination contributes to neurodegeneration and cognitive impairment in chronically disabled patients. Valproic acid (VPA) inhibits histone deacetylase (HDAC) function and probably promotes oligodendrocyte progenitor cell (OPC) proliferation and differentiation; however, the relevant molecular mechanisms remain unknown. Here, focal demyelinating lesions (FDLs) were generated in mice by two-point stereotactic injection of lysophosphatidylcholine (LPC) into the corpus callosum. Cognitive functions, sensorimotor abilities and histopathological changes were assessed for up to 28 days post-injury with or without VPA treatment. Primary OPCs were harvested and used to study the effect of VPA on OPC differentiation under inflammatory conditions. VPA dose-dependently attenuated learning and memory deficits and robustly protected white matter after FDL induction, as demonstrated by reductions in SMI-32 and increases in myelin basic protein staining. VPA also promoted OPC proliferation and differentiation and increased subsequent remyelination efficiency by day 28 post-FDL induction. VPA treatment did not affect HDAC1, HDAC2 or HDAC8 expression but reduced HDAC3 protein levels. In vitro, VPA improved the survival of mouse OPCs and promoted their differentiation into oligodendrocytes following lipopolysaccharide (LPS) stimulation. LPS caused OPCs to overexpress HDAC3, which translocated from the cytoplasm into the nucleus, where it directly interacted with the nuclear transcription factor PPAR-γ and negatively regulated PPAR-γ expression. VPA decreased the expression of HDAC3 and promoted remyelination and functional neurological recovery after FDL. These findings may support the use of strategies modulating HDAC3-mediated regulation of protein acetylation for the treatment of demyelination-related cognitive dysfunction.
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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.