ArticleChild's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery2019
Panobinostat, a histone deacetylase inhibitor, rescues the angiogenic potential of endothelial colony-forming cells in moyamoya disease.
Article in Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Mapping Trends in Moyamoya Angiopathy Research: A 10-Year Bibliometric and Visualization-Based Analyses of the Web of Science Core Collection (WoSCC).Frontiers in neurology · 2021Pooled it
- Plasma extracellular vesicle-associated miR-512-3p modulates angiogenesis in pediatric Moyamoya disease by targeting ARHGEF3.Scientific reports · 2025Article
- Insights into the regulatory role of epigenetics in moyamoya disease: Current advances and future prospectives.Molecular therapy. Nucleic acids · 2024Review
- Recent advances in endothelial colony-forming cells: from the transcriptomic perspective.Journal of translational medicine · 2024Review
- Cyclin-Dependent Kinase Inhibitor 2A is a Key Regulator of Cell Cycle Arrest and Senescence in Endothelial Colony-Forming Cells in Moyamoya Disease.Journal of Korean Neurosurgical Society · 2023Article
- Therapeutic Potential of Endothelial Colony-Forming Cells in Ischemic Disease: Strategies to Improve their Regenerative Efficacy.International journal of molecular sciences · 2020Review
- Vascular Remodeling in Moyamoya Angiopathy: From Peripheral Blood Mononuclear Cells to Endothelial Cells.International journal of molecular sciences · 2020Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMoyamoya disease (MMD) is one of the most common causes of pediatric stroke. We found defective angiogenic function and downregulation of retinaldehyde dehydrogenase 2 (RALDH2) in MMD endothelial colony-forming cells (ECFCs). Downregulation of RALDH2 mRNA was caused by decreased binding of acetyl-histone H3 (Ac-H3) to the RALDH2 promoter. In this study, we evaluated the feasibility of using a histone deacetylase (HDAC) inhibitor, panobinostat, to upregulate RALDH2 expression and restore the angiogenic potential of MMD ECFCs.
methodsECFCs from healthy normal controls and patients with MMD were isolated and characterized. After panobinostat treatment, western blot, tube formation, and chromatin immunoprecipitation (ChIP) assays were conducted in vitro. A matrigel plug assay was performed in vivo.
resultsPanobinostat increased the levels of Ac-H3 and Ac-H4 in both normal and MMD ECFCs but was much more effective in MMD ECFCs. Increased expression of RALDH2 by panobinostat was observed only in MMD ECFCs. Panobinostat increased the tube formation of both normal and MMD ECFCs in vitro and in vivo, but the effect was greater with MMD ECFCs.
conclusionsWe demonstrated that panobinostat increases the angiogenic ability of MMD ECFCs by regulating RALDH2 acetylation. Our results suggest that panobinostat might be a potent therapeutic option for MMD patients.
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