Histone deacetyltransferase inhibitors Trichostatin A and Mocetinostat differentially regulate MMP9, IL-18 and RECK expression, and attenuate Angiotensin II-induced cardiac fibroblast migration and proliferation
Histone acetylation/deacetylation plays a key role in the epigenetic regulation of multiple pro-fibrotic genes. Here we investigated the effects of histone deacetyltransferase (HDAC) inhibition on angiotensin (Ang)-II-induced pro-fibrotic changes in adult mouse cardiac fibroblasts (CF). CF express c...
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Published in | Hypertension research Vol. 39; no. 10; pp. 709 - 716 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Nature Publishing Group
01.10.2016
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Abstract | Histone acetylation/deacetylation plays a key role in the epigenetic regulation of multiple pro-fibrotic genes. Here we investigated the effects of histone deacetyltransferase (HDAC) inhibition on angiotensin (Ang)-II-induced pro-fibrotic changes in adult mouse cardiac fibroblasts (CF). CF express class I HDACs 1 and 2, and Ang-II induces their activation. Notably, silencing HDAC1 or HDAC2 attenuated Ang-II induced CF proliferation and migration. Under basal conditions, HDAC1 dimerizes with HDAC2 in CF and Ang-II reversed this interaction. Treatment with Trichostatin A (TSA), a broad-spectrum HDAC inhibitor, restored their physical association, and attenuated Ang-II-induced MMP9 expression, IL-18 induction, and extracellular matrix (collagen I, collagen III and fibronectin) production. Further, TSA inhibited Ang-II-induced MMP9 and Il18 transcription by blocking NF-κB and AP-1 binding to their respective promoter regions. By inhibiting Sp1 binding to RECK promoter, TSA reversed Ang-II-induced RECK suppression, collagen and fibronectin expression, and CF migration and proliferation. The class I-specific HDAC inhibitor Mocetinostat (MGCD) recapitulated TSA effects on Ang-II-treated CF. Together, these results demonstrate that targeting HDACs attenuates the pro-inflammatory and pro-fibrotic effects of Ang-II on CF. |
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AbstractList | Histone acetylation/deacetylation plays a key role in the epigenetic regulation of multiple pro-fibrotic genes. Here we investigated the effects of histone deacetyltransferase (HDAC) inhibition on angiotensin (Ang)-II-induced pro-fibrotic changes in adult mouse cardiac fibroblasts (CF). CF express class I HDACs 1 and 2, and Ang-II induces their activation. Notably, silencing HDAC1 or HDAC2 attenuated Ang-II induced CF proliferation and migration. Under basal conditions, HDAC1 dimerizes with HDAC2 in CF and Ang-II reversed this interaction. Treatment with Trichostatin A (TSA), a broad-spectrum HDAC inhibitor, restored their physical association, and attenuated Ang-II-induced MMP9 expression, IL-18 induction, and extracellular matrix (collagen I, collagen III and fibronectin) production. Further, TSA inhibited Ang-II-induced MMP9 and Il18 transcription by blocking NF-κB and AP-1 binding to their respective promoter regions. By inhibiting Sp1 binding to RECK promoter, TSA reversed Ang-II-induced RECK suppression, collagen and fibronectin expression, and CF migration and proliferation. The class I-specific HDAC inhibitor Mocetinostat (MGCD) recapitulated TSA effects on Ang-II-treated CF. Together, these results demonstrate that targeting HDACs attenuates the pro-inflammatory and pro-fibrotic effects of Ang-II on CF. |
Author | Valente, Anthony J Noda, Makoto Somanna, Naveen K Krenz, Maike Higashi, Yusuke Chandrasekar, Bysani McDonald, Kerry S |
Author_xml | – sequence: 1 givenname: Naveen K surname: Somanna fullname: Somanna, Naveen K organization: Department of Microbiology, Tulane University School of Medicine, New Orleans, LA, USA – sequence: 2 givenname: Anthony J surname: Valente fullname: Valente, Anthony J organization: Department of Medicine, University of Texas Health Science Center, San Antonio, TX, USA – sequence: 3 givenname: Maike surname: Krenz fullname: Krenz, Maike organization: Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, USA – sequence: 4 givenname: Kerry S surname: McDonald fullname: McDonald, Kerry S organization: Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, USA – sequence: 5 givenname: Yusuke surname: Higashi fullname: Higashi, Yusuke organization: Medicine/Cardiology, University of Missouri School of Medicine, Columbia, MO, USA – sequence: 6 givenname: Makoto surname: Noda fullname: Noda, Makoto organization: Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan – sequence: 7 givenname: Bysani surname: Chandrasekar fullname: Chandrasekar, Bysani organization: Research Service, Harry S Truman Memorial Veterans Hospital, Columbia, MO, USA |
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SubjectTerms | Angiotensin II - pharmacology Animals Benzamides - pharmacology Cell Death - drug effects Cell Movement - drug effects Cell Proliferation - drug effects Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism GPI-Linked Proteins - metabolism Heart - drug effects Histone Deacetylase Inhibitors - pharmacology Hydroxamic Acids - pharmacology Interleukin-18 - metabolism Matrix Metalloproteinase 9 - metabolism Mice Myocardium - cytology Myocardium - metabolism Pyrimidines - pharmacology |
Title | Histone deacetyltransferase inhibitors Trichostatin A and Mocetinostat differentially regulate MMP9, IL-18 and RECK expression, and attenuate Angiotensin II-induced cardiac fibroblast migration and proliferation |
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