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https://www.readbyqxmd.com/read/28504123/erythropoietin-and-small-molecule-agonists-of-the-tissue-protective-erythropoietin-receptor-increase-fxn-expression-in-neuronal-cells-in-vitro-and-in-fxn-deficient-kiko-mice-in-vivo
#1
James L Miller, Myriam Rai, Normand L Frigon, Massimo Pandolfo, Juha Punnonen, Jeffrey R Spencer
Friedreich's ataxia (FRDA) is a progressive neurodegenerative disease caused by reduced levels of the mitochondrial protein frataxin (FXN). Recombinant human erythropoietin (rhEPO) increased FXN protein in vitro and in early clinical studies, while no published reports evaluate rhEPO in animal models of FRDA. STS-E412 and STS-E424 are novel small molecule agonists of the tissue-protective, but not the erythropoietic EPO receptor. We find that rhEPO, STS-E412 and STS-E424 increase FXN expression in vitro and in vivo...
May 11, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28407839/-effect-of-histone-acetylation-deacetylation-imbalances-on-key-gene-of-planar-cell-polarity-pathway
#2
Hong-Yu Duan, Yi Zhang, Kai-Yu Zhou, Chuan Wang, DA-Jian Qiu, Yi-Min Hua
OBJECTIVE: To investigate the effect of histone acetylation/deacetylation imbalances on embryonic hearts of mice and its effect on key genes of planar cell polarity (PCP) pathway-Vangl2, Scrib and Rac1 in H9C2 cells. METHODS: Forty pregnant C57/B6 mice were randomly assigned into three groups: blank group (n=10), vehicle group (n=10), and valproic acid (VPA)-treated group (n=20). In the VPA-treated group, VPA, a histone deacetylase (HDAC) inhibitor, was administered to each individual dam intraperitoneally at a single dose of 700 mg/kg on embryonic day 10...
April 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28394251/eed-orchestration-of-heart-maturation-through-interaction-with-hdacs-is-h3k27me3-independent
#3
Shanshan Ai, Yong Peng, Chen Li, Fei Gu, Xianhong Yu, Yanzhu Yue, Qing Ma, Jinghai Chen, Zhiqiang Lin, Pingzhu Zhou, Huafeng Xie, Terence W Prendiville, Wen Zheng, Yuli Liu, Stuart H Orkin, Da-Zhi Wang, Jia Yu, William T Pu, Aibin He
In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PRC2 writing of H3K27me3 is mechanistically required for gene silencing. Here, we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (embryonic ectoderm development) inactivation in the postnatal heart (Eed(CKO)) caused lethal dilated cardiomyopathy...
April 10, 2017: ELife
https://www.readbyqxmd.com/read/28368536/transcription-factor-crem-mediates-high-glucose-response-in-cardiomyocytes-and-in-a-male-mouse-model-of-prolonged-hyperglycemia
#4
Saviana A Barbati, Claudia Colussi, Lorenza Bacci, Aurora Aiello, Agnese Re, Egidio Stigliano, Andrea M Isidori, Claudio Grassi, Alfredo Pontecorvi, Antonella Farsetti, Carlo Gaetano, Simona Nanni
This study aims at investigating the epigenetic landscape of cardiomyocytes exposed to long elevated glucose levels in vitro and in vivo Exposure of mouse HL-1 and rat differentiated H9C2 cardiomyocyte cell lines to high glucose (30 mM) for 72 hours determined some epigenetic changes including upregulation of class I and III HDAC protein levels and activity, inhibition of histone acetylase p300 activity, increase in histone H3 lysine (K) 27 trimethylation (H3K27me3) and reduction in H3K9 acetylation (H3K9Ac)...
March 22, 2017: Endocrinology
https://www.readbyqxmd.com/read/28315153/effects-of-histone-deacetylase-inhibitory-prodrugs-on-epigenetic-changes-and-dna-damage-response-in-tumor-and-heart-of-glioblastoma-xenograft
#5
Nataly Tarasenko, Abraham Nudelman, Gabriela Rozic, Suzanne M Cutts, Ada Rephaeli
The histone deacetylase (HDAC) inhibitory prodrugs of butyric (AN7) and valproic (AN446) acids, which release the active acids upon metabolic degradation, were studied examining their differential effects on the viability, HDAC inhibitory activity and the DNA damage response (DDR), in glioblastoma cell and normal human astrocytes (NHAs). In xenografts of glioblastoma, AN7 or AN446 given or the combination of each of them with Dox augmented the anticancer activity of Dox and protected the heart from its toxicity...
March 17, 2017: Investigational New Drugs
https://www.readbyqxmd.com/read/28191472/suppression-of-excessive-histone-deacetylases-activity-in-diabetic-hearts-attenuates-myocardial-ischemia-reperfusion-injury-via-mitochondria-apoptosis-pathway
#6
Yang Wu, Yan Leng, Qingtao Meng, Rui Xue, Bo Zhao, Liying Zhan, Zhongyuan Xia
Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion...
2017: Journal of Diabetes Research
https://www.readbyqxmd.com/read/28174211/overlapping-and-divergent-actions-of-structurally-distinct-histone-deacetylase-inhibitors-in-cardiac-fibroblasts
#7
Katherine B Schuetze, Matthew S Stratton, Weston W Blakeslee, Michael F Wempe, Florence F Wagner, Edward B Holson, Yin-Ming Kuo, Andrew J Andrews, Tonya M Gilbert, Jacob M Hooker, Timothy A McKinsey
Inhibitors of zinc-dependent histone deacetylases (HDACs) profoundly affect cellular function by altering gene expression via changes in nucleosomal histone tail acetylation. Historically, investigators have employed pan-HDAC inhibitors, such as the hydroxamate trichostatin A (TSA), which simultaneously targets members of each of the three zinc-dependent HDAC classes (classes I, II, and IV). More recently, class- and isoform-selective HDAC inhibitors have been developed, providing invaluable chemical biology probes for dissecting the roles of distinct HDACs in the control of various physiologic and pathophysiological processes...
April 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28155245/scriptaid-enhances-skeletal-muscle-insulin-action-and-cardiac-function-in-obese-mice
#8
Vidhi Gaur, Timothy Connor, Kylie Venardos, Darren C Henstridge, Sheree D Martin, Courtney Swinton, Shona Morrison, Kathryn Aston-Mourney, Stefan M Gehrig, Roelof van Ewijk, Gordon S Lynch, Mark A Febbraio, Gregory R Steinberg, Mark Hargreaves, Ken R Walder, Sean L McGee
AIM: To determine the effect of Scriptaid, a compound that can replicate aspects of the exercise adaptive response through disruption of the class IIa histone deacetylase (HDAC) corepressor complex, on muscle insulin action in obesity. MATERIALS AND METHODS: Diet-induced obese mice were administered Scriptaid (1 mg/kg) via daily intraperitoneal injection for 4 weeks. Whole-body and skeletal muscle metabolic phenotyping of mice was performed, in addition to echocardiography, to assess cardiac morphology and function...
February 2, 2017: Diabetes, Obesity & Metabolism
https://www.readbyqxmd.com/read/28109123/sodium-butyrate-protects-against-high-fat-diet-induced-cardiac-dysfunction-and-metabolic-disorders-in-type-ii-diabetic-mice
#9
Ling Zhang, Jianfeng Du, Naohiro Yano, Hao Wang, Yu Tina Zhao, Dubielecka-Szczerba Patricia, Shougang Zhuang, Eugene Y Chin, Gangjian Qin, Ting C Zhao
Histone deacetylases are recently identified to act as key regulators for cardiac pathophysiology and metabolic disorders. However, the function of histone deacetylase (HDAC) in controlling cardiac performance in type II diabetes and obesity remains unknown. Here we determine whether HDAC inhibition attenuates high fat diet (HFD)-induced cardiac dysfunction and improves metabolic features. Adult mice were fed with either HFD or standard chow food for 24 weeks. Starting at 12 weeks, mice were divided into four groups randomly, in which sodium butyrate (1%), a potent HDAC inhibitor, was provided to chow and HFD-fed mice in drinking water, respectively...
January 21, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28063219/microrna-1-overexpression-blunts-cardiomyocyte-hypertrophy-elicited-by-thyroid-hormone
#10
Gabriela Placoná Diniz, Caroline Antunes Lino, Camila Rodrigues Moreno, Nathalia Senger, Maria Luiza Morais Barreto-Chaves
It is well-known that increased thyroid hormone (TH) levels induce cardiomyocyte growth. MicroRNAs (miRNAs) have been identified as key players in cardiomyocyte hypertrophy, which is associated with increased risk of heart failure. In this study, we evaluated the miR-1 expression in TH-induced cardiac hypertrophy, as well as the potential involvement of miR-1 in cardiomyocyte hypertrophy elicited by TH in vitro. The possible role of type 1 angiotensin II receptor (AT1R) in the effect promoted by TH in miR-1 expression was also evaluated...
January 7, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27910887/energy-metabolism-regulated-by-hdac-inhibitor-attenuates-cardiac-injury-in-hemorrhagic-rat-model
#11
Qiyuan Kuai, Chunyan Wang, Yanbing Wang, Weijing Li, Gongqing Zhang, Zhixin Qiao, Min He, Xuanlin Wang, Yu Wang, Xingwei Jiang, Lihua Su, Yuezhong He, Suping Ren, Qun Yu
A disturbance of energy metabolism reduces cardiac function in acute severe hemorrhagic patients. Alternatively, adequate energy supply reduces heart failure and increases survival. However, the approach to regulating energy metabolism conductive to vital organs is limited, and the underlying molecular mechanism remains unknown. This study assesses the ability of histone deacetylase inhibitors (HDACIs) to preserve cardiac energy metabolism during lethal hemorrhagic injury. In the lethally hemorrhagic rat and hypoxic myocardial cells, energy metabolism and heart function were well maintained following HDACI treatment, as evident by continuous ATP production with normal cardiac contraction...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27883221/alcohol-exposure-causes-overexpression-of-heart-development-related-genes-by-affecting-the-histone-h3-acetylation-via-bmp-signaling-pathway-in-cardiomyoblast-cells
#12
Jin Shi, Weian Zhao, Bo Pan, Min Zheng, Lina Si, Jing Zhu, Lingjuan Liu, Jie Tian
BACKGROUND: Abusive alcohol utilization of pregnant woman may cause congenital heart disease (CHD) of fetus, where alcohol ignites histone H3 hyperacetylation leading to abnormal development of heart morphogenesis and associated genes. Knowledge about the regularized upstream genes is little, but bone morphogenetic protein (BMP) signaling may actively and prominently take part in alteration in acetylation of histone H3. The supreme objective of this study was to unearth the involvement of BMP signaling pathway in alcohol-driven hyperacetylation of histone H3 in cardiomyoblast cells...
January 2017: Alcoholism, Clinical and Experimental Research
https://www.readbyqxmd.com/read/27673327/roles-of-hdac2-and-hdac8-in-cardiac-remodeling-in-renovascular-hypertensive-rats-and-the-effects-of-valproic-acid-sodium
#13
Rui-Fang Li, Shan-Shan Cao, Wei-Jin Fang, Ying Song, Xue-Ting Luo, Hong-Yun Wang, Jian-Gang Wang
Recent studies indicate that histone deacetylases (HDACs) activity is associated with the development and progression of cardiac hypertrophy. In this study, we investigated the effects of a HDACs inhibitor, valproic acid sodium (VPA), on cardiac remodeling and the differential expression of HDACs in left ventricles (LVs) of renovascular hypertensive rats. Renovascular hypertension was induced in rats by the two-kidney two-clip (2K2C) method. Cardiac remodeling, heart function and the differential expression of HDACs were examined at different weeks after 2K2C operation...
2017: Pharmacology
https://www.readbyqxmd.com/read/27667442/histone-deacetylase-inhibitor-phenylbutyrate-exaggerates-heart-failure-in-pressure-overloaded-mice-independently-of-hdac-inhibition
#14
Jing Ma, Tao Luo, Zhi Zeng, Haiying Fu, Yoshihiro Asano, Yulin Liao, Tetsuo Minamino, Masafumi Kitakaze
4-Sodium phenylbutyrate (PBA) has been reported to inhibit endoplasmic reticulum stress and histone deacetylation (HDAC), both of which are novel therapeutic targets for cardiac hypertrophy and heart failure. However, it is unclear whether PBA can improve heart function. Here, we tested the effects of PBA and some other HDAC inhibitors on cardiac dysfunction induced by pressure overload. Transverse aortic constriction (TAC) was performed on male C57BL/6 mice. PBA treatment (100 mg/kg, 6 weeks) unexpectedly led to a higher mortality, exacerbated cardiac remodelling and dysfunction...
September 26, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27620069/histone-deacetylase-inhibitors-future-therapeutics-for-insulin-resistance-and-type-2-diabetes
#15
Sorabh Sharma, Rajeev Taliyan
Insulin resistance is a common feature of obesity and predisposes the affected individuals to a variety of pathologies, including type 2 diabetes mellitus (T2DM), dyslipidemias, hypertension, cardiovascular disease etc. Insulin resistance is the primary cause of T2DM and it occurs many years before the disease onset. Although Thiazolidinediones (TZDs) such as rosiglitazone and pioglitazone are outstanding insulin sensitizers and are in clinical use since 1990s, however, their serious side effects such as heart attack and bladder cancer have limited their utilization...
September 9, 2016: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
https://www.readbyqxmd.com/read/27610034/histone-deacetylase-inhibitor-cg200745-attenuates-cardiac-hypertrophy-and-fibrosis-in-doca-induced-hypertensive-rats
#16
Eunjo Lee, Min-Ji Song, Hae-Ahm Lee, Seol-Hee Kang, Mina Kim, Eun Kyoung Yang, Do Young Lee, Seonggu Ro, Joong Myung Cho, Inkyeom Kim
CG200745 is a novel inhibitor of histone deacetylases (HDACs), initially developed for treatment of various hematological and solid cancers. Because it is water-soluble, it can be administered orally. We hypothesized that the HDAC inhibitor, CG200745, attenuates cardiac hypertrophy and fibrosis in deoxycorticosterone acetate (DOCA)-induced hypertensive rats. For establishment of hypertension, 40 mg/kg of DOCA was subcutaneously injected four times weekly into Sprague-Dawley rats. All the rats used in this study including those in the sham group had been unilaterally nephrectomized and allowed free access to drinking water containing 1% NaCl...
September 2016: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/27379430/suberoylanilide-hydroxamic-acid-restores-estrogen-reduced-ctni-expression-in-neonatal-hearts-of-mice
#17
Chang Peng, Xiaomei Luo, Qianlu Xing, Huichao Sun, Xupei Huang
Diastolic cardiac dysfunction can be caused by abnormality in cTnI expression during cardiogenesis. In this study, we investigated the effects of estrogen on the abnormal expression of cTnI in the hearts of neonatal mice and its potential epigenetic mechanisms. We then evaluated suberoylanilide hydroxamic acid (SAHA), a HDAC inhibitor, as a new target treatment of diastolic cardiac dysfunction. Postnatal day 0.5 C57BL/6 mice were injected with estrogen for 1 week, then the hearts of 7-day-old neonatal mice were retrieved for examination...
October 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27295551/overexpressed-hdac4-is-associated-with-poor-survival-and-promotes-tumor-progression-in-esophageal-carcinoma
#18
Li-Si Zeng, Xian-Zi Yang, Yue-Feng Wen, Shi-Juan Mail, Meng-He Wang, Mei-Yin Zhang, X F Steven Zheng, Hui-Yun Wang
Histone deacetylases (HDACs) mediate histone deacetylation, leading to transcriptional repression, which is involved in many diseases, including age-related tissue degeneration, heart failure and cancer. In this study, we were aimed to investigate the expression, clinical significance and biological function of HDAC4 in esophageal carcinoma (EC). We found that HDAC4 mRNA and protein are overexpressed in esophageal squamous cell carcinoma (ESCC) tissues and cell lines. HDAC4 overexpression is associated with higher tumor grade, advanced clinical stage and poor survival...
June 2016: Aging
https://www.readbyqxmd.com/read/27255383/histone-deacetylase-inhibitors-prolong-cardiac-repolarization-through-transcriptional-mechanisms
#19
Stan Spence, Mark Deurinck, Haisong Ju, Martin Traebert, LeeAnne McLean, Jennifer Marlowe, Corinne Emotte, Elaine Tritto, Min Tseng, Michael Shultz, Gregory S Friedrichs
Histone deacetylase (HDAC) inhibitors are an emerging class of anticancer agents that modify gene expression by altering the acetylation status of lysine residues of histone proteins, thereby inducing transcription, cell cycle arrest, differentiation, and cell death or apoptosis of cancer cells. In the clinical setting, treatment with HDAC inhibitors has been associated with delayed cardiac repolarization and in rare instances a lethal ventricular tachyarrhythmia known as torsades de pointes. The mechanism(s) of HDAC inhibitor-induced effects on cardiac repolarization is unknown...
September 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/27246208/approaches-for-studying-the-subcellular-localization-interactions-and-regulation-of-histone-deacetylase-5-hdac5
#20
Amanda J Guise, Ileana M Cristea
As a member of the class IIa family of histone deacetylases, the histone deacetylase 5 (HDAC5) is known to undergo nuclear-cytoplasmic shuttling and to be a critical transcriptional regulator. Its misregulation has been linked to prominent human diseases, including cardiac diseases and tumorigenesis. In this chapter, we describe several experimental methods that have proven effective for studying the functions and regulatory features of HDAC5. We present methods for assessing the subcellular localization, protein interactions, posttranslational modifications (PTMs), and activity of HDAC5 from the standpoint of investigating either the endogenous protein or tagged protein forms in human cells...
2016: Methods in Molecular Biology
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