ArticlePloS one2011
Effects of the histone deacetylase inhibitor valproic acid on human pericytes in vitro.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Epigenetics in blood-brain barrier disruption.Fluids and barriers of the CNS · 2021Review
- Protein Kinase CK2 Regulates Nerve/Glial Antigen (NG)2-Mediated Angiogenic Activity of Human Pericytes.Cells · 2020Article
- Epigenetic Crosstalk between the Tumor Microenvironment and Ovarian Cancer Cells: A Therapeutic Road Less Traveled.Cancers · 2018Review
- Valproic Acid Induces Endothelial-to-Mesenchymal Transition-Like Phenotypic Switching.Frontiers in pharmacology · 2018Article
- Valproic acid regulates Ang II-induced pericyte-myofibroblastAmerican journal of translational research · 2018Article
- Valproic acid inhibits glioblastoma multiforme cell growth via paraoxonase 2 expression.Oncotarget · 2017Article
- Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound.Advances in wound care · 2016Review
- Pericyte-targeting drug delivery and tissue engineering.International journal of nanomedicine · 2016Review
- Histone deacetylase activity is required for embryonic posterior lateral line development.Cell proliferation · 2014Article
- Histone deacetylase inhibitor treatment increases coronary t-PA release in a porcine ischemia model.PloS one · 2014Article
- Potential roles of HDAC inhibitors in mitigating ischemia-induced brain damage and facilitating endogenous regeneration and recovery.Current pharmaceutical design · 2013Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microvascular pericytes are of key importance in neoformation of blood vessels, in stabilization of newly formed vessels as well as maintenance of angiostasis in resting tissues. Furthermore, pericytes are capable of differentiating into pro-fibrotic collagen type I producing fibroblasts. The present study investigates the effects of the histone deacetylase (HDAC) inhibitor valproic acid (VPA) on pericyte proliferation, cell viability, migration and differentiation. The results show that HDAC inhibition through exposure of pericytes to VPA in vitro causes the inhibition of pericyte proliferation and migration with no effect on cell viability. Pericyte exposure to the potent HDAC inhibitor Trichostatin A caused similar effects on pericyte proliferation, migration and cell viability. HDAC inhibition also inhibited pericyte differentiation into collagen type I producing fibroblasts. Given the importance of pericytes in blood vessel biology a qPCR array focusing on the expression of mRNAs coding for proteins that regulate angiogenesis was performed. The results showed that HDAC inhibition promoted transcription of genes involved in vessel stabilization/maturation in human microvascular pericytes. The present in vitro study demonstrates that VPA influences several aspects of microvascular pericyte biology and suggests an alternative mechanism by which HDAC inhibition affects blood vessels. The results raise the possibility that HDAC inhibition inhibits angiogenesis partly through promoting a pericyte phenotype associated with stabilization/maturation of blood vessels.
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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 OpenQuestion graph.