ArticleArteriosclerosis, thrombosis, and vascular biology2007
Angiotensin II stimulates protein kinase D-dependent histone deacetylase 5 phosphorylation and nuclear export leading to vascular smooth muscle cell hypertrophy.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Targeting epigenetics and non-coding RNAs in atherosclerosis: from mechanisms to therapeutics.Pharmacology & therapeutics · 2019Pooled it
- Phosphorylation of CBX8 by PKD1 suppresses PRC1 activity and promotes cell senescence.Oncogene · 2026Article
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- Epigenetic DNA Methylation and Protein Homocysteinylation: Key Players in Hypertensive Renovascular Damage.International journal of molecular sciences · 2024Review
- HDAC8 regulates protein kinase D phosphorylation in skeletal myoblasts in response to stress signaling.Biochemical and biophysical research communications · 2023Article
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- The microRNA miR-134-5p induces calcium deposition by inhibiting histone deacetylase 5 in vascular smooth muscle cells.Journal of cellular and molecular medicine · 2020Article
- Dysregulations of MicroRNA and Gene Expression in Chronic Venous Disease.Journal of clinical medicine · 2020Article
- Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease.Nature reviews. Cardiology · 2020Review
- Protein kinase D1 phosphorylation of KAT7 enhances its protein stability and promotes replication licensing and cell proliferation.Cell death discovery · 2020Article
- Article
- Epigenetics and vascular diseases.Journal of molecular and cellular cardiology · 2019Review
- Role of p38 MAPK in Atherosclerosis and Aortic Valve Sclerosis.International journal of molecular sciences · 2018Review
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Expression of Class I and Class II a/b Histone Deacetylase is Dysregulated in Hypertensive Animal Models.Korean circulation journal · 2017Article
- A Novel Systems-Biology Algorithm for the Analysis of Coordinated Protein Responses Using Quantitative Proteomics.Molecular & cellular proteomics : MCP · 2016Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression.Circulation research · 2015Article
- A time frame permissive for Protein Kinase D2 activity to direct angiogenesis in mouse embryonic stem cells.Scientific reports · 2015Article
- Post-translational modifications regulate class IIa histone deacetylase (HDAC) function in health and disease.Molecular & cellular proteomics : MCP · 2015Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAngiotensin II (Ang II) induces the phenotypic modulation and hypertrophy of vascular smooth muscle cells (VSMCs), which is implicated in the pathogenesis of hypertension, atherosclerosis, and diabetes. In this study, we tested the hypothesis that histone deacetylases 5 (HDAC5) and its signal pathway play a role in Ang II-induced VSMC hypertrophy. METHODS AND
resultsVSMCs were isolated from the thoracic aortas of male Sprague-Dawley rats and treated with Ang II. We found that Ang II rapidly stimulated phosphorylation of HDAC5 at Serine259/498 residues in a time- and dose- dependent manner. Ang II receptor-1, protein kinase C, and protein kinase D1 (PKD1) mediated HDAC5 phosphorylation. Furthermore, we observed that Ang II stimulated HDAC5 nuclear export, which was dependent on its PKD1-dependent phosphorylation. Consequently, both inhibiting PKD1 and HDAC5 Serine259/498 to Alanine mutant significantly attenuated Ang II-induced myocyte enhancer factor-2 (MEF2) transcriptional activity and protein synthesis in VSMCs.
conclusionThese findings demonstrate for the first time that PKD1-dependent HDAC5 phosphorylation and nuclear export mediates Ang II-induced MEF2 activation and VSMC hypertrophy, and suggest that PKD1 and HDAC5 may emerge as potential targets for the treatment of pathological vascular hypertrophy.
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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 Socratic graph.