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Epigenetics atherosclerosis

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https://www.readbyqxmd.com/read/28475147/folic-acid-supplementation-delays-atherosclerotic-lesion-development-by-modulating-mcp1-and-vegf-dna-methylation-levels-in-vivo-and-in-vitro
#1
Shanshan Cui, Wen Li, Xin Lv, Pengyan Wang, Yuxia Gao, Guowei Huang
The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic acid may act via an epigenetic gene silencing mechanism to ameliorate atherosclerosis. Here, we investigated the atheroprotective effects of folic acid and the resultant methylation status in high-fat diet-fed ApoE knockout mice and in oxidized low-density lipoprotein-treated human umbilical vein endothelial cells...
May 5, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28460648/endothelial-dysfunction-in-individuals-born-after-fetal-growth-restriction-cardiovascular-and-renal-consequences-and-preventive-approaches
#2
C Yzydorczyk, J B Armengaud, A C Peyter, H Chehade, F Cachat, C Juvet, B Siddeek, S Simoncini, F Sabatier, F Dignat-George, D Mitanchez, U Simeoni
Individuals born after intrauterine growth restriction (IUGR) have an increased risk of perinatal morbidity/mortality, and those who survive face long-term consequences such as cardiovascular-related diseases, including systemic hypertension, atherosclerosis, coronary heart disease and chronic kidney disease. In addition to the demonstrated long-term effects of decreased nephron endowment and hyperactivity of the hypothalamic-pituitary-adrenal axis, individuals born after IUGR also exhibit early alterations in vascular structure and function, which have been identified as key factors of the development of cardiovascular-related diseases...
May 2, 2017: Journal of Developmental Origins of Health and Disease
https://www.readbyqxmd.com/read/28371472/epigenetic-regulation-in-monocyte-macrophage-a-key-player-during-atherosclerosis
#3
Su-Jie Jia, Ke-Qin Gao, Ming Zhao
Atherosclerosis is a chronic inflammatory disease. Recently, a growing body of evidence emphasizes that the monocyte and macrophage differentiation and activation are key processes in the development of atherosclerosis. However, the regulatory mechanism that manipulates the function of monocyte and macrophage is still unclear. Recent years, epigenetic mechanisms have got a widely attention and bring us a new field of vision. More and more evidence shows that epigenetics weigh highly in atherosclerosis by regulating the function and differentiation states of monocyte and macrophage...
April 2, 2017: Cardiovascular Therapeutics
https://www.readbyqxmd.com/read/28351900/long-noncoding-rna-mantis-facilitates-endothelial-angiogenic-function
#4
Matthias S Leisegang, Christian Fork, Ivana Josipovic, Florian Richter, Jens Preussner, Jiong Hu, Matthew J Miller, Jeremy N Epah, Patrick Hofmann, Stefan Günther, Franziska Moll, Chanil Valasarajan, Juliana Heidler, Yuliya Ponomareva, Thomas M Freiman, Lars Maegdefessel, Karl H Plate, Michel Mittelbronn, Shizuka Uchida, Carsten Künne, Konstantinos Stellos, Ralph T Schermuly, Norbert Weissmann, Kavi Devraj, Ilka Wittig, Reinier A Boon, Stefanie Dimmeler, Soni S Pullamsetti, Mario Looso, Francis J Miller, Ralf P Brandes
Background -The angiogenic function of endothelial cells is regulated by numerous mechanisms but the impact of long noncoding RNAs (lncRNAs) has hardly been studied. We set out to identify novel and functionally important endothelial lncRNAs. Methods -Epigenetically controlled lncRNAs in human umbilical vein endothelial cells (HUVEC) were searched by exon-array analysis after knockdown of the histone demethylase JARID1B. Molecular mechanisms were investigated by RNA Pulldown and Immunoprecipitation, Mass spectrometry, Micro-array, several knockdown approaches, CRIPSR-Cas9, Assay for Transposase-Accessible Chromatin-Sequencing and chromatin immunoprecipitation in HUVEC...
March 28, 2017: Circulation
https://www.readbyqxmd.com/read/28332497/epigenetically-driven-anatomical-diversity-of-synovial-fibroblasts-guides-joint-specific-fibroblast-functions
#5
Mojca Frank-Bertoncelj, Michelle Trenkmann, Kerstin Klein, Emmanuel Karouzakis, Hubert Rehrauer, Anna Bratus, Christoph Kolling, Maria Armaka, Andrew Filer, Beat A Michel, Renate E Gay, Christopher D Buckley, George Kollias, Steffen Gay, Caroline Ospelt
A number of human diseases, such as arthritis and atherosclerosis, include characteristic pathology in specific anatomical locations. Here we show transcriptomic differences in synovial fibroblasts from different joint locations and that HOX gene signatures reflect the joint-specific origins of mouse and human synovial fibroblasts and synovial tissues. Alongside DNA methylation and histone modifications, bromodomain and extra-terminal reader proteins regulate joint-specific HOX gene expression. Anatomical transcriptional diversity translates into joint-specific synovial fibroblast phenotypes with distinct adhesive, proliferative, chemotactic and matrix-degrading characteristics and differential responsiveness to TNF, creating a unique microenvironment in each joint...
March 23, 2017: Nature Communications
https://www.readbyqxmd.com/read/28291707/epigenetics-of-atherosclerosis-emerging-mechanisms-and-methods
#6
REVIEW
Nadiya Khyzha, Azad Alizada, Michael D Wilson, Jason E Fish
Atherosclerosis is a vascular pathology characterized by inflammation and plaque build-up within arterial vessel walls. Vessel occlusion, often occurring after plaque rupture, can result in myocardial and cerebral infarction. Epigenetic changes are increasingly being associated with atherosclerosis and are of interest from both therapeutic and biomarker perspectives. Emerging genomic approaches that profile DNA methylation, chromatin accessibility, post-translational histone modifications, transcription factor binding, and RNA expression in low or single cell populations are poised to enhance our spatiotemporal understanding of atherogenesis...
April 2017: Trends in Molecular Medicine
https://www.readbyqxmd.com/read/28289478/cerebral-white-matter-hyperintensities-on-mri-and-acceleration-of-epigenetic-aging-the-atherosclerosis-risk-in-communities-study
#7
Abhay Raina, Xiaoping Zhao, Megan L Grove, Jan Bressler, Rebecca F Gottesman, Weihua Guan, James S Pankow, Eric Boerwinkle, Thomas H Mosley, Myriam Fornage
BACKGROUND: Cerebral white matter hyperintensities (WMH) on magnetic resonance imaging (MRI) are part of the spectrum of brain vascular injury accompanying aging and are associated with a substantial risk of stroke and dementia. We investigated the association of cerebral WMH burden on MRI with a DNA methylation-based biomarker of aging, termed DNA methylation age acceleration, which represents the deviation of the DNA methylation-predicted age from the chronologic age. RESULTS: In this cross-sectional observational study of 713 African-American participants of the Atherosclerosis Risk in Communities study, aged 51-73 years, estimates of predicted age were obtained based on two algorithms (Hannum et al...
2017: Clinical Epigenetics
https://www.readbyqxmd.com/read/28272157/atherosclerosis-cell-biology-and-lipoproteins-focus-on-epigenetic-modification-and-macrophage-biology
#8
Elena Ferrari, Esther Lutgens, Christian Weber, Norbert Gerdes
No abstract text is available yet for this article.
April 2017: Current Opinion in Lipidology
https://www.readbyqxmd.com/read/28239687/protein-phosphatase-5-contributes-to-the-overexpression-of-epigenetically-regulated-t-lymphocyte-genes-in-patients-with-lupus
#9
D Patel, G Gorelik, B Richardson
OBJECTIVE: Lupus develops when genetically predisposed people encounter certain drugs or environmental agents causing oxidative stress such as infections and sun exposure, and then typically follows a chronic relapsing course with flares triggered by the exogenous stressors. Current evidence indicates that these environmental agents can trigger lupus flares by inhibiting the replication of DNA methylation patterns during mitosis in CD4(+) T cells, altering the expression of genes suppressed by this mechanism that convert normal "helper" cells into auto reactive cells which promote lupus flares...
December 2016: Lupus (Los Angeles)
https://www.readbyqxmd.com/read/28193703/methylation-in-the-matrix-metalloproteinase-2-gene-is-associated-with-cerebral-ischemic-stroke
#10
Hsiu-Fen Lin, Edward Hsi, Ling-Chun Huang, Yi-Chu Liao, Suh-Hang H Juo, Ruey-Tay Lin
Matrix metalloproteinase-2 (MMP-2) is involved in the pathophysiology of stroke. Previous studies have shown that MMP-2 activity is increased in stroke; however, evidence of epigenetic regulation of the MMP-2 in stroke is still limited. We examined methylation of the MMP-2 promoter in patients with ischemic stroke. This study included 298 patients with ischemic stroke and 258 age-matched and sex-matched controls. MMP-2 promoter methylation levels were measured by pyrosequencing at eight potential cytosine-guanine (CpG) sites...
February 13, 2017: Journal of Investigative Medicine: the Official Publication of the American Federation for Clinical Research
https://www.readbyqxmd.com/read/28189002/abdominal-aortic-aneurysm-an-independent-disease-to-atherosclerosis
#11
REVIEW
Bradley J Toghill, Athanasios Saratzis, Matthew J Bown
Atherosclerosis and abdominal aortic aneurysms (AAAs) are multifactorial and polygenic diseases with known environmental and genetic risk factors that contribute toward disease development. Atherosclerosis represents an important independent risk factor for AAA, as people with AAA often have atherosclerosis. Studies have shown that comorbidity is usually between ~25% and 55%, but it is still not fully known whether this association is causal or a result of common shared risk profiles. Most recent epidemiological, clinical, and biological evidence suggests that the two pathologies are more distinct than traditionally thought...
March 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
https://www.readbyqxmd.com/read/28188730/involvement-of-histone-methylation-in-macrophage-apoptosis-and-unstable-plaque-formation-in-methionine-induced-hyperhomocysteinemic-apoe-mice
#12
Guangzhi Cong, Ru Yan, Hui Huang, Kai Wang, Ning Yan, Ping Jin, Na Zhang, Jianjun Hou, Dapeng Chen, Shaobin Jia
AIMS: Hyperhomocysteinemia (Hhcy) is an independent risk factor of atherosclerosis and promotes unstable plaque formation. Epigenetic mechanisms play an important role in the pathogenesis of atherosclerosis induced by Hhcy. However, the exact mechanism is still undefined. Lesional apoptotic cells and necrotic core formation contribute greatly to the progression of plaque. The present study sought to determine whether modification of histone methylation is involved in macrophage apoptosis and unstable plaque formation in the condition of Hhcy...
March 15, 2017: Life Sciences
https://www.readbyqxmd.com/read/28183874/novel-insights-into-dna-methylation-and-its-critical-implications-in-diabetic-vascular-complications
#13
REVIEW
Jia Zheng, Jing Cheng, Qian Zhang, Xinhua Xiao
Recent epidemiological and clinical studies have shown that type 2 diabetic patients can develop diabetic vascular complications even after intensive glycaemic control. It has been suggested that this phenomenon could be explained by the hypothesis of 'metabolic memory'. The underlying mechanisms between these enduring effects and the prior hyperglycaemic state are still not well understood. Preliminary studies demonstrate that hyperglycaemia can regulate gene expression by epigenetic modifications, such as DNA methylation, which can persistently exist even after glucose normalization...
April 30, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28125025/inhaled-pollutants-the-molecular-scene-behind-respiratory-and-systemic-diseases-associated-with-ultrafine-particulate-matter
#14
REVIEW
Hussein Traboulsi, Necola Guerrina, Matthew Iu, Dusica Maysinger, Parisa Ariya, Carolyn J Baglole
Air pollution of anthropogenic origin is largely from the combustion of biomass (e.g., wood), fossil fuels (e.g., cars and trucks), incinerators, landfills, agricultural activities and tobacco smoke. Air pollution is a complex mixture that varies in space and time, and contains hundreds of compounds including volatile organic compounds (e.g., benzene), metals, sulphur and nitrogen oxides, ozone and particulate matter (PM). PM0.1 (ultrafine particles (UFP)), those particles with a diameter less than 100 nm (includes nanoparticles (NP)) are considered especially dangerous to human health and may contribute significantly to the development of numerous respiratory and cardiovascular diseases such as chronic obstructive pulmonary disease (COPD) and atherosclerosis...
January 24, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28116311/genetic-and-epigenetic-regulation-of-aortic-aneurysms
#15
REVIEW
Ha Won Kim, Brian K Stansfield
Aneurysms are characterized by structural deterioration of the vascular wall leading to progressive dilatation and, potentially, rupture of the aorta. While aortic aneurysms often remain clinically silent, the morbidity and mortality associated with aneurysm expansion and rupture are considerable. Over 13,000 deaths annually in the United States are attributable to aortic aneurysm rupture with less than 1 in 3 persons with aortic aneurysm rupture surviving to surgical intervention. Environmental and epidemiologic risk factors including smoking, male gender, hypertension, older age, dyslipidemia, atherosclerosis, and family history are highly associated with abdominal aortic aneurysms, while heritable genetic mutations are commonly associated with aneurysms of the thoracic aorta...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28111052/activated-p300-acetyltransferase-activity-modulates-aortic-valvular-calcification-with-osteogenic-transdifferentiation-and-downregulation-of-klotho
#16
Shao-Jung Li, Yu-Hsun Kao, Cheng-Chih Chung, Wei-Yu Chen, Wan-Li Cheng, Yi-Jen Chen
BACKGROUND: The calcific aortic valve (AV) disease is a common disease with the unclear mechanism, and optimal pharmacological treatment remains unavailable. Epigenetic modulation by histone acetyltransferase (HAT) plays a critical role in osteogenic transdifferentiation and atherosclerosis. The purposes of this study were to investigate whether HAT contributes to the pathophysiology of AV calcification and assess the therapeutic potential of HAT inhibition. METHODS: Porcine valvular interstitial cells (VICs) were treated with osteogenic medium (10ng/mL of tumor necrosis factor-α and 4mmol/L of high phosphate) for 7days...
January 5, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28104796/clonal-hematopoiesis-associated-with-tet2-deficiency-accelerates-atherosclerosis-development-in-mice
#17
José J Fuster, Susan MacLauchlan, María A Zuriaga, Maya N Polackal, Allison C Ostriker, Raja Chakraborty, Chia-Ling Wu, Soichi Sano, Sujatha Muralidharan, Cristina Rius, Jacqueline Vuong, Sophia Jacob, Varsha Muralidhar, Avril A B Robertson, Matthew A Cooper, Vicente Andrés, Karen K Hirschi, Kathleen A Martin, Kenneth Walsh
Human aging is associated with an increased frequency of somatic mutations in hematopoietic cells. Several of these recurrent mutations, including those in the gene encoding the epigenetic modifier enzyme TET2, promote expansion of the mutant blood cells. This clonal hematopoiesis correlates with an increased risk of atherosclerotic cardiovascular disease. We studied the effects of the expansion of Tet2-mutant cells in atherosclerosis-prone, low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice. We found that partial bone marrow reconstitution with TET2-deficient cells was sufficient for their clonal expansion and led to a marked increase in atherosclerotic plaque size...
February 24, 2017: Science
https://www.readbyqxmd.com/read/28062506/wnt-signaling-pathway-inhibitor-sclerostin-inhibits-angiotensin-ii-induced-aortic-aneurysm-and-atherosclerosis
#18
Smriti Murali Krishna, Sai-Wang Seto, Roby J Jose, Jiaze Li, Susan K Morton, Erik Biros, Yutang Wang, Vianne Nsengiyumva, Jan H N Lindeman, Gabriela G Loots, Catherine M Rush, Jeffrey M Craig, Jonathan Golledge
OBJECTIVE: Sclerostin (SOST) has been identified as an important regulator of bone formation; however, it has not been previously implicated in arterial disease. The aim of this study was to assess the role of SOST in aortic aneurysm (AA) and atherosclerosis using human samples, a mouse model, and in vitro investigations. APPROACH AND RESULTS: SOST protein was downregulated in human and mouse AA samples compared with controls. Transgenic introduction of human SOST in apolipoprotein E-deficient (ApoE(-/-)) mice (SOST(Tg)...
December 22, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28030845/withdrawn-could-some-epigenetic-modifications-hold-the-key-to-opposing-the-metabolic-syndrome
#19
REVIEW
Giovanni Tarantino, Matteo Nicola Di Minno, Carmine Finelli
Ahead of Print article withdrawn by publisher.
December 21, 2016: Oncotarget
https://www.readbyqxmd.com/read/28029182/nedd4-deficiency-in-vascular-smooth-muscle-promotes-vascular-calcification-by-stabilizing-psmad1
#20
Ji-Hyun Lee, Seon-Ae Jeon, Byung-Gyu Kim, Michiko Takeda, Jae-Jin Cho, Dong-Ik Kim, Hiroshi Kawabe, Je-Yoel Cho
The nonosseous calcification process such as atherosclerosis is one of the major complications in several types of metabolic diseases. In a previous study, we uncovered that aberrant activity of transforming growth factor β (TGF-β) signaling pathway could contribute to the vascular smooth muscle cells' (VSMCs) calcification process. Also, we identified NEDD4 E3 ligase as a key suppressor of bone morphogenetic protein (BMP)/Smad pathway via a polyubiquitination-dependent selective degradation of C-terminal phosphorylated Smad1 (pSmad1) activated by TGF-β...
May 2017: Journal of Bone and Mineral Research: the Official Journal of the American Society for Bone and Mineral Research
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