Panobinostat, a histone deacetylase inhibitor, rescues the angiogenic potential of endothelial colony-forming cells in moyamoya disease
Anshika Jangra, Seung Ah Choi, Eun Jung Koh, Youn Joo Moon, Kyu-Chang Wang, Ji Hoon Phi, Ji Yeoun Lee, Seung-Ki Kim
2019 Volume 35, Issue 5, p823-831
Moyamoya 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.
There are no accessible files associated with this release. You could check other releases for this work for an accessible version.
Know of a fulltext copy of on the public web? Submit a URL and we will archive it
Not in DOAJ
In Keepers Registry
access all versions, variants, and formats of this works (eg, pre-prints)
Crossref Metadata (via API)
SHERPA/RoMEO (journal policies)