Histone Deacetylase-1 Is Enriched at the Platelet-derived Growth Factor-D Promoter in Response to Interleukin-1β and Forms a Cytokine-inducible Gene-silencing Complex with NF-κB p65 and Interferon Regulatory Factor-1

Liu, Mary Y.; Khachigian, Levon M.

doi:10.1074/jbc.m109.061903

Cited by 8 publications

(1 citation statement)

References 49 publications

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“…The authors also found that the effect of the butyrate was mediated by acetylating H3K and phosphorylating H3-serine10, in addition to dimethylation of H3K9 and H3K4 ( Mathew et al, 2010 ). Besides, HDAC4 and HDAC5 was involved in vascular calcification ( Abend et al, 2017 ; Choe et al, 2020 ) and inflammatory response in VSMCs ( Lee et al, 2008 ), whereas HDAC1 ( Liu and Khachigian, 2009 ) and HDAC5 ( Pietruczuk et al, 2019 ) acted as a proinflammatory molecule in VSMCs. TSA could inhibit VSMC calcification ( Azechi et al, 2013 ).…”

Section: Role Of Hdacs In Atherosclerosismentioning

confidence: 99%

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Chen

et al. 2020

Front. Cell Dev. Biol.

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Atherosclerosis (AS), the most common underlying pathology for coronary artery disease, is a chronic inflammatory, proliferative disease in large- and medium-sized arteries. The vascular endothelium is important for maintaining vascular health. Endothelial dysfunction is a critical early event leading to AS, which is a major risk factor for stroke and myocardial infarction. Accumulating evidence has suggested the critical roles of histone deacetylases (HDACs) in regulating vascular cell homeostasis and AS. The purpose of this review is to present an updated view on the roles of HDACs (Class I, Class II, Class IV) and HDAC inhibitors in vascular dysfunction and AS. We also elaborate on the novel therapeutic targets and agents in atherosclerotic cardiovascular diseases.

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Section: Role Of Hdacs In Atherosclerosismentioning

confidence: 99%

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Chen

et al. 2020

Front. Cell Dev. Biol.

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Cytokines and pregnancy: Potential regulation by histone deacetylases

Munro

Balakrishnan

Lissaman

et al. 2021

Molecular Reproduction Devel

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Cytokines are important regulators of pregnancy and parturition. Aberrant expression of proinflammatory cytokines during pregnancy contributes towards preterm labor, pre‐eclampsia, and gestational diabetes mellitus. The regulation of cytokine expression in human cells is highly complex, involving interactions between environment, transcription factors, and feedback mechanisms. Recent developments in epigenetic research have made tremendous advancements in exploring histone modifications as a key epigenetic regulator of cytokine expression and the effect of their signaling molecules on various organ systems in the human body. Histone acetylation and subsequent deacetylation by histone deacetylases (HDACs) are major epigenetic regulators of protein expression in the human body. The expression of various proinflammatory cytokines, their role in normal and abnormal pregnancy, and their epigenetic regulation via HDACs will be discussed in this review.

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Protective effects of Nebivolol against interleukin-1β (IL-1β)-induced type II collagen destruction mediated by matrix metalloproteinase-13 (MMP-13)

Zhao

Wang

et al. 2017

Cell Stress and Chaperones

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The pathological progression of osteoarthritis (OA) involves degradation of articular cartilage matrix. Type II collagen is the main component of cartilage matrix, which is degraded by pro-inflammatory cytokines such as IL-1β mediated by MMP-13. Nebivolol, a licensed drug used for the treatment of hypertension in clinics, displays its anti-inflammatory capacity in various conditions. However, whether Nebivolol has a protective effect on cartilage matrix degradation has not been reported before. In this study, we investigated the effects of Nebivolol on regulating the expression of MMP-13 and degradation of type II collagen. Our results indicate that Nebivolol alleviated the increase in gene expression, protein expression, and activity of MMP-13 induced by IL-1β. Importantly, IL-1β strikingly reduced the levels of type II collagen in cell culture supernatants, which was reversed by treatment with Nebivolol in a dose-dependent manner. Mechanistically, Nebivolol was found to alleviate the increased levels of phosphorylated IκBα and reduced levels of total IκBα induced by IL-1β, which subsequently mitigated p65 nuclear translocation and the transcriptional activity of NF-κB. Furthermore, our results indicated that IL-1β treatment resulted in a significant increase in expression of the transcriptional factor interferon regulatory factor-1 (IRF-1) at both the mRNA and protein levels, which was significantly ameliorated by treatment with Nebivolol. The combination of these findings suggests that Nebivolol can potentially be applied in human OA treatment.

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Histone Deacetylase-1 Is Enriched at the Platelet-derived Growth Factor-D Promoter in Response to Interleukin-1β and Forms a Cytokine-inducible Gene-silencing Complex with NF-κB p65 and Interferon Regulatory Factor-1

Cited by 8 publications

References 49 publications

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Cytokines and pregnancy: Potential regulation by histone deacetylases

Protective effects of Nebivolol against interleukin-1β (IL-1β)-induced type II collagen destruction mediated by matrix metalloproteinase-13 (MMP-13)

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