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HDAC3 acts as a negative regulator of angiogenesis
Histone deacetylase-3 (HDAC3) is involved in cellular proliferation, apoptosis and transcriptional repression. However, the role of HDAC3 in angiogenesis remains unknown. HDAC3 negatively regulated the expression of angiogenic factors, such as VEGF and plasminogen activator inhibitor-1 (PAI-1). HDAC...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society for Biochemistry and Molecular Biology
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163891/ https://www.ncbi.nlm.nih.gov/pubmed/24286308 http://dx.doi.org/10.5483/BMBRep.2014.47.4.128 |
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author | Park, Deokbum Park, Hyunmi Kim, Youngmi Kim, Hyuna Jeoung, Dooil |
author_facet | Park, Deokbum Park, Hyunmi Kim, Youngmi Kim, Hyuna Jeoung, Dooil |
author_sort | Park, Deokbum |
collection | PubMed |
description | Histone deacetylase-3 (HDAC3) is involved in cellular proliferation, apoptosis and transcriptional repression. However, the role of HDAC3 in angiogenesis remains unknown. HDAC3 negatively regulated the expression of angiogenic factors, such as VEGF and plasminogen activator inhibitor-1 (PAI-1). HDAC3 showed binding to promoter sequences of PAI-1. HDAC3 activity was necessary for the expression regulation of PAI-1 by HDAC3. VEGF decreased the expression of HDAC3, and the down-regulation of HDAC3 enhanced endothelial cell tube formation. HDAC3 negatively regulated tumor-induced angiogenic potential. We show the novel role of HDAC3 as a negative regulator of angiogenesis. [BMB Reports 2014; 47(4): 227-232] |
format | Online Article Text |
id | pubmed-4163891 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Korean Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-41638912014-09-16 HDAC3 acts as a negative regulator of angiogenesis Park, Deokbum Park, Hyunmi Kim, Youngmi Kim, Hyuna Jeoung, Dooil BMB Rep Research Articles Histone deacetylase-3 (HDAC3) is involved in cellular proliferation, apoptosis and transcriptional repression. However, the role of HDAC3 in angiogenesis remains unknown. HDAC3 negatively regulated the expression of angiogenic factors, such as VEGF and plasminogen activator inhibitor-1 (PAI-1). HDAC3 showed binding to promoter sequences of PAI-1. HDAC3 activity was necessary for the expression regulation of PAI-1 by HDAC3. VEGF decreased the expression of HDAC3, and the down-regulation of HDAC3 enhanced endothelial cell tube formation. HDAC3 negatively regulated tumor-induced angiogenic potential. We show the novel role of HDAC3 as a negative regulator of angiogenesis. [BMB Reports 2014; 47(4): 227-232] Korean Society for Biochemistry and Molecular Biology 2014-04 /pmc/articles/PMC4163891/ /pubmed/24286308 http://dx.doi.org/10.5483/BMBRep.2014.47.4.128 Text en Copyright © 2014, Korean Society for Biochemistry and Molecular Biology http://creativecommons.org/licenses/by-nc/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Park, Deokbum Park, Hyunmi Kim, Youngmi Kim, Hyuna Jeoung, Dooil HDAC3 acts as a negative regulator of angiogenesis |
title | HDAC3 acts as a negative regulator of angiogenesis |
title_full | HDAC3 acts as a negative regulator of angiogenesis |
title_fullStr | HDAC3 acts as a negative regulator of angiogenesis |
title_full_unstemmed | HDAC3 acts as a negative regulator of angiogenesis |
title_short | HDAC3 acts as a negative regulator of angiogenesis |
title_sort | hdac3 acts as a negative regulator of angiogenesis |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163891/ https://www.ncbi.nlm.nih.gov/pubmed/24286308 http://dx.doi.org/10.5483/BMBRep.2014.47.4.128 |
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