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https://www.readbyqxmd.com/read/27512969/histone-deacetylase-and-gata-binding-factor-6-regulate-arterial-remodeling-in-angiotensin-ii-induced-hypertension
#1
Gwi Ran Kim, Soo-Na Cho, Hyung-Seok Kim, Seon Young Yu, Sin Young Choi, Yuhee Ryu, Ming Quan Lin, Li Jin, Hae Jin Kee, Myung Ho Jeong
OBJECTIVE: Histone deacetylase (HDAC) inhibitors have been reported to improve essential and secondary hypertension. However, the specific HDAC that might serve as a therapeutic target and the associated upstream and downstream molecules involved in regulating hypertension remain unknown. Our study was aimed at investigating whether a selective inhibitor of class II HDAC (MC1568) modulates hypertension, elucidating the underlying mechanism. METHODS: Hypertension was established by administering angiotensin II (Ang II) to mice before treatment with MC1568...
November 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/22360269/mef2-is-regulated-by-camkii%C3%AE-2-and-a-hdac4-hdac5-heterodimer-in-vascular-smooth-muscle-cells
#2
Roman Ginnan, Li Yan Sun, John J Schwarz, Harold A Singer
VSMCs (vascular smooth muscle cells) dedifferentiate from the contractile to the synthetic phenotype in response to acute vascular diseases such as restenosis and chronic vascular diseases such as atherosclerosis, and contribute to growth of the neointima. We demonstrated previously that balloon catheter injury of rat carotid arteries resulted in increased expression of CaMKII (Ca(2+)/calmodulin-dependent protein kinase) IIδ(2) in the medial wall and the expanding neointima [House and Singer (2008) Arterioscler...
May 15, 2012: Biochemical Journal
https://www.readbyqxmd.com/read/19389706/protein-kinase-a-regulated-assembly-of-a-mef2-middle-dot-hdac4-repressor-complex-controls-c-jun-expression-in-vascular-smooth-muscle-cells
#3
Joseph W Gordon, Christina Pagiatakis, Jahan Salma, Min Du, John J Andreucci, Jianzhong Zhao, Guangpei Hou, Robert L Perry, Qinghong Dan, David Courtman, Michelle P Bendeck, John C McDermott
Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression...
July 10, 2009: Journal of Biological Chemistry
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