ArticleOxidative medicine and cellular longevity2019
HDAC6 Inhibition Protects against OGDR-Induced Golgi Fragmentation and Apoptosis.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- Selective HDAC6 inhibition protects against blood-brain barrier dysfunction after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Cdk1 protects against oxygen-glucose deprivation and reperfusion-induced Golgi fragmentation and apoptosis through mediating GM130 phosphorylation.Journal of molecular histology · 2023Article
- Role of Nanoparticle-Conjugates and Nanotheranostics in Abrogating Oxidative Stress and Ameliorating Neuroinflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Protective effects of histone deacetylase 6 specific inhibitor tubastatin A on subarachnoid hemorrhage in rats and the underlying mechanisms.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- Article
- Study on the protective effect of OM-MSCs on Golgi apparatus after intracerebral hemorrhage in Sprague-Dawley rats.American journal of stem cells · 2023Article
- How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia.Metabolic brain disease · 2021Review
- Article
- PAQR3 protects against oxygen-glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells.Journal of molecular histology · 2020Article
- Olfactory Mucosa Mesenchymal Stem Cells Alleviate Cerebral Ischemia/Reperfusion InjuryFrontiers in cell and developmental biology · 2020Article
- Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke.Disease markers · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Golgi apparatus (GA) is a pivotal organelle, and its fragmentation is an essential process in the development of apoptosis. GA is a potential target in the treatment of cerebral ischemia-reperfusion injury. Histone deacetylase 6 (HDAC6) catalyzes the removal of functional acetyl groups from proteins and plays an important role in cell homeostasis. In this study, the neuroprotective effects and the underlying mechanisms of HDAC6 inhibition were assessed in an ischemia-reperfusion injury model. Mouse neuroblastoma N2a cells and cultured neurons were subjected to oxygen-glucose deprivation/reperfusion (OGDR) insult. OGDR induces Golgi fragmentation and reduces tubulin acetylation in N2a cells and cultured neurons. Golgi fragmentation is prior to nuclear chromatin condensation after OGDR injury. Overexpression of GBF1 not only protects against OGDR-induced Golgi fragmentation but also protects against OGDR-induced apoptosis, suggesting that Golgi fragmentation is not secondary to apoptosis but plays a causal role for subsequent apoptosis. HDAC6 inhibition suppresses OGDR-induced tubulin deacetylation, p115 cleavage, and caspase 3 activation and protects against OGDR-induced Golgi fragmentation and apoptosis. This work opens a new avenue for potential clinical application of HDAC6 inhibitors for cerebral ischemia-reperfusion-related disorders.
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