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https://www.readbyqxmd.com/read/28521864/insulin-induced-inhibition-of-gluconeogenesis-genes-including-glutamic-pyruvic-transaminase-2-is-associated-with-reduced-histone-acetylation-in-a-human-liver-cell-line
#1
Kazue Honma, Michiko Kamikubo, Kazuki Mochizuki, Toshinao Goda
OBJECTIVES: Hepatic glutamic pyruvic transaminase (GPT; also known as alanine aminotransferase) is a gluconeogenesis enzyme that catalyzes conversions between alanine and pyruvic acid. It is also used as a blood biomarker for hepatic damage. In this study, we investigated whether insulin regulates GPT expression, as it does for other gluconeogenesis genes, and if this involves the epigenetic modification of histone acetylation. METHODS: Human liver-derived HepG2 cells were cultured with 0...
June 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28515049/a-generalized-linear-model-for-decomposing-cis-regulatory-parent-of-origin-and-maternal-effects-on-allele-specific-gene-expression
#2
Yasuaki Takada, Ryutaro Miyagi, Aya Takahashi, Toshinori Endo, Naoki Osada
Joint quantification of genetic and epigenetic effects on gene expression is important for understanding the establishment of complex gene regulation systems in living organisms. In particular, genomic imprinting and maternal effects play important roles in the developmental process of mammals and flowering plants. However, the influence of these effects on gene expression are difficult to quantify because they act simultaneously with cis-regulatory mutations. Here we propose a simple method to decompose cis-regulatory (i...
May 17, 2017: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/28514750/epigenome-wide-association-study-in-hepatocellular-carcinoma-identification-of-stochastic-epigenetic-mutations-through-an-innovative-statistical-approach
#3
REVIEW
Davide Gentilini, Stefania Scala, Germano Gaudenzi, Paolo Garagnani, Miriam Capri, Matteo Cescon, Gian Luca Grazi, Maria Giulia Bacalini, Serena Pisoni, Alessandra Dicitore, Luisa Circelli, Sara Santagata, Francesco Izzo, Anna Maria Di Blasio, Luca Persani, Claudio Franceschi, Giovanni Vitale
Hepatocellular carcinoma (HCC) results from accumulation of both genetic and epigenetic alterations. We investigated the genome-wide DNA methylation profile in 69 pairs of HCC and adjacent non-cancerous liver tissues using the Infinium HumanMethylation 450K BeadChip array. An innovative analytical approach has been adopted to identify Stochastic Epigenetic Mutations (SEMs) in HCC.HCC and peritumoral tissues showed a different epigenetic profile, mainly characterized by loss of DNA methylation in HCC. Total number of SEMs was significantly higher in HCC tumor (median: 77,370) than in peritumoral (median: 5,656) tissues and correlated with tumor grade...
April 27, 2017: Oncotarget
https://www.readbyqxmd.com/read/28509806/advances-in-management-of-hepatocellular-carcinoma
#4
Manon Allaire, Jean-Charles Nault
PURPOSE OF REVIEW: Hepatocellular carcinoma (HCC) is one of the leading causes of death by cancer worldwide due to a dismal prognosis. The aim of this review is to summarize the main advances in the pathophysiology and management of HCC. RECENT FINDINGS: Genomic analysis has recently delineated the key signaling pathways aberrantly deregulated in HCC (telomere maintenance, cell cycle gene, Wnt/β-catenin, epigenetic modifier, oxidative stress etc.). Major advances in the clinical care of patients with HCC are helping to refine the diagnosis algorithm and tumor staging...
May 15, 2017: Current Opinion in Oncology
https://www.readbyqxmd.com/read/28506744/hepatic-stellate-cells-as-key-target-in-liver-fibrosis
#5
Takaaki Higashi, Scott L Friedman, Yujin Hoshida
Progressive liver fibrosis, induced by chronic viral and metabolic disorders, leads to more than one million deaths annually via development of cirrhosis, although no antifibrotic therapy has been approved to date. Transdifferentiation (or "activation") of hepatic stellate cells is the major cellular source of matrix protein-secreting myofibroblasts, the major driver of liver fibrogenesis. Paracrine signals from injured epithelial cells, fibrotic tissue microenvironment, immune and systemic metabolic dysregulation, enteric dysbiosis, and hepatitis viral products can directly or indirectly induce stellate cell activation...
May 12, 2017: Advanced Drug Delivery Reviews
https://www.readbyqxmd.com/read/28502747/chicken-egg-fetal-liver-dna-and-histopathologic-effects-of-structurally-diverse-carcinogens-and-non-carcinogens
#6
M J Iatropoulos, T Kobets, J-D Duan, K D Brunnemann, E Vock, U Deschl, G M Williams
Chicken egg fetal livers were evaluated for histopathological changes produced by four genotoxic hepatocarcinogens: 2-acetylaminofluorene (AAF), aflatoxin B1 (AFB1), benzo[a]pyrene (BaP), diethylnitrosamine (DEN); four structurally related non- or weakly- carcinogenic comparators: fluorene (FLU), aflatoxin B2 (AFB2), benzo[e]pyrene (BeP), N-nitrosodiethanolamine (NDELA); two epigenetic hepatocarcinogens: clofibric acid (CFA), phenobarbital (PB); and the non-carcinogen, D-mannitol (MAN). CFA, PB and MAN were also assessed for formation of DNA adducts using the (32)P nucleotide postlabeling (NPL) assay and for DNA breaks using the comet assay...
May 11, 2017: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
https://www.readbyqxmd.com/read/28500476/update-on-apoa5-genetics-toward-a-better-understanding-of-its-physiological-impact
#7
REVIEW
Montse Guardiola, Josep Ribalta
PURPOSE OF REVIEW: This review is intended to summarize the genetic studies published during the last 3 years that help us understand the physiology of apoAV and its clinical implications. RECENT FINDINGS: APOA5 is probably the gene with the strongest effect on triglyceride (TG) metabolism. APOA5 is almost exclusively expressed in the liver, and its product apoAV has a very low circulating concentration. New physiological roles of apoAV have been recently elucidated, such as control of chylomicron production in the intestine and TG accumulation in adipose tissue...
July 2017: Current Atherosclerosis Reports
https://www.readbyqxmd.com/read/28495587/dose-response-analysis-of-epigenetic-metabolic-and-apical-endpoints-after-short-term-exposure-to-experimental-hepatotoxicants
#8
Isabelle R Miousse, Lynea A Murphy, Haixia Lin, Melissa R Schisler, Jinchun Sun, Marie-Cecile G Chalbot, Radhakrishna Sura, Kamin Johnson, Matthew J LeBaron, Ilias G Kavouras, Laura K Schnackenberg, Richard D Beger, Reza J Rasoulpour, Igor Koturbash
Identification of sensitive and novel biomarkers or endpoints associated with toxicity and carcinogenesis is of a high priority. There is increasing interest in the incorporation of epigenetic and metabolic biomarkers to complement apical data; however, a number of questions, including the tissue specificity, dose-response patterns, early detection of those endpoints, and the added value need to be addressed. In this study, we investigated the dose-response relationship between apical, epigenetic, and metabolomics endpoints following short-term exposure to experimental hepatotoxicants, clofibrate (CF) and phenobarbital (PB)...
May 8, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/28487545/mechanisms-of-hepatic-stellate-cell-activation
#9
REVIEW
Takuma Tsuchida, Scott L Friedman
Hepatic fibrosis is a dynamic process characterized by the net accumulation of extracellular matrix resulting from chronic liver injury of any aetiology, including viral infection, alcoholic liver disease and NASH. Activation of hepatic stellate cells (HSCs) - transdifferentiation of quiescent, vitamin-A-storing cells into proliferative, fibrogenic myofibroblasts - is now well established as a central driver of fibrosis in experimental and human liver injury. Yet, the continued discovery of novel pathways and mediators, including autophagy, endoplasmic reticulum stress, oxidative stress, retinol and cholesterol metabolism, epigenetics and receptor-mediated signals, reveals the complexity of HSC activation...
May 10, 2017: Nature Reviews. Gastroenterology & Hepatology
https://www.readbyqxmd.com/read/28470093/genetic-and-epigenetic-mechanisms-underlying-arsenic-associated-diabetes-mellitus-a-perspective-of-the-current-evidence
#10
Elizabeth M Martin, Miroslav Stýblo, Rebecca C Fry
Chronic exposure to arsenic has been associated with the development of diabetes mellitus (DM), a disease characterized by hyperglycemia resulting from dysregulation of glucose homeostasis. This review summarizes four major mechanisms by which arsenic induces diabetes, namely inhibition of insulin-dependent glucose uptake, pancreatic β-cell damage, pancreatic β-cell dysfunction and stimulation of liver gluconeogenesis that are supported by both in vivo and in vitro studies. Additionally, the role of polymorphic variants associated with arsenic toxicity and disease susceptibility, as well as epigenetic modifications associated with arsenic exposure, are considered in the context of arsenic-associated DM...
May 4, 2017: Epigenomics
https://www.readbyqxmd.com/read/28468239/choline-other-methyl-donors-and-epigenetics
#11
Steven Zeisel
Choline dietary intake varies such that many people do not achieve adequate intakes. Diet intake of choline can modulate methylation because, via betaine homocysteine methyltransferase (BHMT), this nutrient (and its metabolite, betaine) regulate the concentrations of S-adenosylhomocysteine and S-adenosylmethionine. Some of the epigenetic mechanisms that modify gene expression without modifying the genetic code depend on the methylation of DNA or of histones; and diet availability of choline and other methyl-group donors influences both of these methylations...
April 29, 2017: Nutrients
https://www.readbyqxmd.com/read/28467776/histoneh3-demethylase-jmjd2a-promotes-growth-of-liver-cancer-cells-through-up-regulating-mir372
#12
Jiahui An, Jie Xu, Jiao Li, Song Jia, Xiaonan Li, Yanan Lu, Yuxin Yang, Zhuojia Lin, Xiaoru Xin, Mengying Wu, Qidi Zheng, Hu Pu, Xin Gui, Tianming Li, Dongdong Lu
Changes in histone lysine methylation status have been observed during cancer formation. JMJD2A protein is a demethylase that is overexpressed in several tumors. Herein, our results demonstrate that JMJD2A accelerates malignant progression of liver cancer cells in vitro and in vivo. Mechanistically, JMJD2A promoted the expression and mature of pre-miR372 epigenetically. Notably, miR372 blocks the editing of 13th exon-introns-14th exon and forms a novel transcript( JMJD2AΔ) of JMJD2A. In particular, JMJD2A inhibited P21(WAF1/Cip1) expression by decreasing H3K9me3 dependent on JMJD2AΔ...
April 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28467484/chromatin-modifying-agents-convert-fibroblasts-to-oct4-and-vegfr-2-capillary-tube-forming-cells
#13
Anita Wary, Neil Wary, Jugajyoti Baruah, Victoria Mastej, Kishore K Wary
RATIONALE: The human epigenome is plastic. The goal of this study was to address if fibroblast cells can be epigenetically modified to promote neovessel formation. METHODS AND RESULTS: Here, we used highly abundant human adult dermal fibroblast cells (hADFCs) that were treated with the chromatin-modifying agents 5-aza-2'-deoxycytidine and trichostatin A, and subsequently subjected to differentiation by activating Wnt signaling. Our results show that these epigenetically modified hADFCs increasingly expressed β-catenin, pluripotency factor octamer-binding transcription factor-4 (OCT4, also known as POU5F1), and endothelial cell (EC) marker called vascular endothelial growth factor receptor-2 (VEGFR-2, also known as Fetal Liver Kinase-1)...
2017: PloS One
https://www.readbyqxmd.com/read/28466692/dna-methylation-changes-in-tbx3-in-a-mouse-model-exposed-to-polybrominated-diphenyl-ethers
#14
Takashi Shimbo, June K Dunnick, Amy Brix, Deepak Mav, Ruchir Shah, John D Roberts, Paul A Wade
DE-71, a commercial mixture of polybrominated diphenyl ethers widely used in flame retardants, is a pervasive environmental contaminant due to its continuing release from waste material and its long half-life in humans. Although the genotoxic potential of DE-71 appears to be low based on bacterial mutagenicity, it remains a public health concern due to its reported involvement in tumor development. Molecular mechanisms by which DE-71 influences tumor incidence or progression remain understudied. We used liver carcinoma tissue from mice exposed to DE-71 to test the hypothesis that epigenetic alterations consistent with tumor development, specifically DNA methylation, result from long-term DE-71 exposure...
January 1, 2017: International Journal of Toxicology
https://www.readbyqxmd.com/read/28465351/an-hnf4%C3%AE-microrna-194-192-signaling-axis-maintains-hepatic-cell-function
#15
Aoi Morimoto, Mana Kannari, Yuichi Tsuchida, Shota Sasaki, Chinatsu Saito, Tsuyoshi Matsuta, Tsukasa Maeda, Megumi Akiyama, Takahiro Nakamura, Masakiyo Sakaguchi, Nobukazu Nameki, Frank J Gonzalez, Yusuke Inoue
HNF4α controls the expression of liver-specific protein-coding genes. However, some microRNAs (miRNAs) are also modulated by HNF4α, and it is not known whether they are direct targets of HNF4α, and whether they influence the hepatic function. In this study, we found that HNF4α regulates miRNAs, indicated by marked down-regulation of miR-194 and miR-192 (miR-194/192) in liver-specific Hnf4a-null (Hnf4a(ΔH)) mice. Transactivation of the shared miR-194/192 promoter was dependent on HNF4α expression, indicating that miR194/192 is a target gene of HNF4α...
May 2, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28456008/donor-dependent-and-other-nondefined-factors-have-greater-influence-on-the-hepatic-phenotype-than-the-starting-cell-type-in-induced-pluripotent-stem-cell-derived-hepatocyte-like-cells
#16
James A Heslop, Richard Kia, Christopher S Pridgeon, Rowena L Sison-Young, Triantafillos Liloglou, Mohamed Elmasry, Stephen W Fenwick, John S Mills, Neil R Kitteringham, Chris E Goldring, Bong K Park
Drug-induced liver injury is the greatest cause of post-marketing drug withdrawal; therefore, substantial resources are directed toward triaging potentially dangerous new compounds at all stages of drug development. One of the major factors preventing effective screening of new compounds is the lack of a predictive in vitro model of hepatotoxicity. Primary human hepatocytes offer a metabolically relevant model for which the molecular initiating events of hepatotoxicity can be examined; however, these cells vary greatly between donors and dedifferentiate rapidly in culture...
May 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28453285/pharmacological-reprogramming-of-somatic-cells-for-regenerative-medicine
#17
Min Xie, Shibing Tang, Ke Li, Sheng Ding
Lost or damaged cells in tissues and organs can be replaced by transplanting therapeutically competent cells. This approach requires methods that effectively manipulate cellular identities and properties to generate sufficient numbers of desired cell types for transplantation. These cells can be generated by reprogramming readily available somatic cells, such as fibroblasts, into induced pluripotent stem cells (iPSCs), which can replicate indefinitely and give rise to any somatic cell type. This reprogramming can be achieved with genetic methods, such as forced expression of pluripotency-inducing transcription factors (TFs), which can be further improved, or even avoided, with pharmacological agents...
April 28, 2017: Accounts of Chemical Research
https://www.readbyqxmd.com/read/28450421/the-landscape-of-histone-modifications-in-a-high-fat-diet-induced-obese-dio-mouse-model
#18
Litong Nie, Lin Shuai, Mingrui Zhu, Ping Liu, Zhi-Fu Xie, Shangwen Jiang, Hao-Wen Jiang, Jia Li, Yingming Zhao, Jing-Ya Li, Minjia Tan
Type 2 diabetes (T2D) is a major chronic healthcare concern worldwide. Emerging evidence suggests that a histone-modification-mediated epigenetic mechanism underlies T2D. Nevertheless, the dynamics of histone marks in T2D have not yet been carefully analyzed. Using a mass spectrometry-based label-free and chemical stable isotope labeling quantitative proteomic approach, we systematically profiled liver histone post-translational modifications (PTMs) in a prediabetic high-fat-diet-induced obese (DIO) mouse model...
April 27, 2017: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/28442573/cell-cycle-dependent-degradation-of-the-methyltransferase-setd3-attenuates-cell-proliferation-and-liver-tumorigenesis
#19
Xiaoqing Cheng, Yuan Hao, Wenjie Shu, Mengjie Zhao, Chen Zhao, Yuan Wu, Xiaodan Peng, Pinfang Yao, Daibiao Xiao, Guoliang Qing, Zhengying Pan, Lei Yin, Desheng Hu, Hai-Ning Du
Histone modifications, including lysine methylation, are epigenetic marks that influence many biological pathways. Accordingly, many methyltransferases have critical roles in various biological processes, and their dysregulation is often associated with cancer. However, the biological functions and regulation of many methyltransferases are unclear. Here, we report that a human homolog of the methyltransferase SET domain containing 3 (SETD3) is cell cycle regulated: SETD3 protein levels peaked in S phase and were lowest in M phase...
April 25, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28433418/binge-alcohol-alters-pnpla3-levels-in-liver-through-epigenetic-mechanism-involving-histone-h3-acetylation
#20
REVIEW
Ricardo J Restrepo, Robert W Lim, Ronald J Korthuis, Shivendra D Shukla
The human PNPLA3 (patatin-like phospholipase domain-containing 3) gene codes for a protein which is highly expressed in adipose tissue and liver, and is implicated in lipid homeostasis. While PNPLA3 protein contains regions homologous to functional lipolytic proteins, the regulation of its tissue expression is reflective of lipogenic genes. A naturally occurring genetic variant of PNPLA3 in humans has been linked to increased susceptibility to alcoholic liver disease. We have examined the modulatory effect of alcohol on PNPLA3 protein and mRNA expression as well as the association of its gene promoter with acetylated histone H3K9 by chromatin immunoprecipitation (ChIP) assay in rat hepatocytes in vitro, and in vivo in mouse and rat models of acute binge, chronic, and chronic followed by acute binge ethanol administration...
May 2017: Alcohol
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