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histone deacetylase stenosis

M Rahmatzadeh, H B Liu, S M Krishna, T A Gaspari, I Welungoda, R E Widdop, A E Dear
PURPOSE: Neointimal hyperplasia (NIH), a pathophysiological event identified in bypass graft and stent re-stenosis, is characterised by aberrant vascular smooth muscle cell (VSMC) migration and proliferation. Recent evidence identifies histone deacetylase modulation as a regulator of VSMC proliferation and migration and a potential therapeutic target in the treatment of NIH. The purpose of our study was to determine the in vitro and in vivo potential of a novel agent, MCT-3, to modulate VSMC migration, proliferation and NIH...
October 2014: Cardiovascular Drugs and Therapy
Shouji Matsushima, Junya Kuroda, Tetsuro Ago, Peiyong Zhai, Ji Yeon Park, Lai-Hua Xie, Bin Tian, Junichi Sadoshima
RATIONALE: Oxidation of cysteine residues in class II histone deacetylases (HDACs), including HDAC4, causes nuclear exit, thereby inducing cardiac hypertrophy. The cellular source of reactive oxygen species responsible for oxidation of HDAC4 remains unknown. OBJECTIVE: We investigated whether nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4), a major nicotinamide adenine dinucleotide phosphate oxidase, mediates cysteine oxidation of HDAC4. METHODS AND RESULTS: Phenylephrine (100 μmol/L), an α1 adrenergic agonist, induced upregulation of Nox4 (1...
February 15, 2013: Circulation Research
Simon S Xu, Saydul Alam, Andriana Margariti
Vascular diseases, including atherosclerosis, angioplasty-induced restenosis, vessel graft arteriosclerosis and hypertension-related stenosis, remain the most prevalent cause of death in the developed world. The aetiology of vascular diseases is multifactorial with both genetic and environmental factors. Recently, some of the most promising research identifies the epigenetic modification of the genome to play a major role in the disease development, linking the environmental insults with gene regulation. In this process, modification of DNA by methylation, and histone modification by acetylation, methylation, phosphorylation and/or SUMOylation are reported...
January 2014: Current Vascular Pharmacology
Yi-Te Chen, Jyh-Ding Wei, Jung-Pan Wang, Hsieh-Hsing Lee, En-Rung Chiang, Hung-Chang Lai, Ling-Lan Chen, Yi-Ting Lee, Chih-Chien Tsai, Chien-Lin Liu, Shih-Chieh Hung
STUDY DESIGN: To demonstrate the existence of mesenchymal stem cells (MSCs) in ligamentum flavum (LF) and their pathogenic role in LF hypertrophy. OBJECTIVE: To isolate and characterize LF-derived MSCs and their response to transforming growth factor-beta 1 (TGF-β1) and trichostatin A (TSA), a histone deacetylase inhibitor (HDACi). SUMMARY OF BACKGROUND DATA: LF is a connective tissue, of which hypertrophic changes induce spinal stenosis...
August 15, 2011: Spine
Matthew B Lanktree, Robert A Hegele, Salim Yusuf, Sonia S Anand
BACKGROUND AND PURPOSE: Identification of subclinical atherosclerosis by ultrasonographic measurement of carotid intima-media thickness (IMT) is a validated tool, in conjunction with traditional risk factors, for clinical assessment of cardiovascular disease risk. IMT has also been recognized as a quantitative measure of cardiovascular disease progression in asymptomatic individuals, and many candidate gene association studies have attempted to identify genetic variants associated with interindividual differences in IMT with limited success...
October 2009: Stroke; a Journal of Cerebral Circulation
Mary M Kavurma, Nichola Figg, Martin R Bennett, John Mercer, Levon M Khachigian, Trevor D Littlewood
Apoptosis of VSMCs (vascular smooth-muscle cells) leads to features of atherosclerotic plaque instability. We have demonstrated previously that plaque-derived VSMCs have reduced IGF1 (insulin-like growth factor 1) signalling, resulting from a decrease in the expression of IGF1R (IGF1 receptor) compared with normal aortic VSMCs [Patel, Zhang, Siddle, Soos, Goddard, Weissberg and Bennett (2001) Circ. Res. 88, 895-902]. In the present study, we show that apoptosis induced by oxidative stress is inhibited by ectopic expression of IGF1R...
October 1, 2007: Biochemical Journal
Hae Jin Kee, Il Suk Sohn, Kwang Il Nam, Jong Eun Park, Yong Ri Qian, Zhan Yin, Youngkeun Ahn, Myung Ho Jeong, Yung-Jue Bang, Nacksung Kim, Jong-Keun Kim, Kyung Keun Kim, Jonathan A Epstein, Hyun Kook
BACKGROUND: A number of distinct stress signaling pathways in myocardium cause cardiac hypertrophy and heart failure. Class II histone deacetylases (HDACs) antagonize several stress-induced pathways and hypertrophy. However, cardiac hypertrophy induced by transgenic overexpression of the homeodomain only protein, HOP, can be prevented by the nonspecific HDAC inhibitors trichostatin A and valproic acid, suggesting that alternate targets that oppose class II HDAC function might exist in myocardium...
January 3, 2006: Circulation
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