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https://www.readbyqxmd.com/read/29733819/mitochondrial-proteome-disruption-in-the-diabetic-heart-through-targeted-epigenetic-regulation-at-the-mitochondrial-heat-shock-protein-70-mthsp70-nuclear-locus
#1
Danielle L Shepherd, Quincy A Hathaway, Cody E Nichols, Andrya J Durr, Mark V Pinti, Kristen M Hughes, Amina Kunovac, Seth M Stine, John M Hollander
>99% of the mitochondrial proteome is nuclear-encoded. The mitochondrion relies on a coordinated multi-complex process for nuclear genome-encoded mitochondrial protein import. Mitochondrial heat shock protein 70 (mtHsp70) is a key component of this process and a central constituent of the protein import motor. Type 2 diabetes mellitus (T2DM) disrupts mitochondrial proteomic signature which is associated with decreased protein import efficiency. The goal of this study was to manipulate the mitochondrial protein import process through targeted restoration of mtHsp70, in an effort to restore proteomic signature and mitochondrial function in the T2DM heart...
May 4, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29719834/genomic-instabilities-cellular-senescence-and-aging-in-vitro-in-vivo-and-aging-like-human-syndromes
#2
REVIEW
Gabriel Lidzbarsky, Danielle Gutman, Huda Adwan Shekhidem, Lital Sharvit, Gil Atzmon
As average life span and elderly people prevalence in the western world population is gradually increasing, the incidence of age-related diseases such as cancer, heart diseases, diabetes, and dementia is increasing, bearing social and economic consequences worldwide. Understanding the molecular basis of aging-related processes can help extend the organism's health span, i.e., the life period in which the organism is free of chronic diseases or decrease in basic body functions. During the last few decades, immense progress was made in the understanding of major components of aging and healthy aging biology, including genomic instability, telomere attrition, epigenetic changes, proteostasis, nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and intracellular communications...
2018: Frontiers in Medicine
https://www.readbyqxmd.com/read/29705945/could-alzheimer-s-disease-originate-in-the-periphery-and-if-so-how-so
#3
REVIEW
Gerwyn Morris, Michael Berk, Michael Maes, Basant K Puri
The classical amyloid cascade model for Alzheimer's disease (AD) has been challenged by several findings. Here, an alternative molecular neurobiological model is proposed. It is shown that the presence of the APOE ε4 allele, altered miRNA expression and epigenetic dysregulation in the promoter region and exon 1 of TREM2, as well as ANK1 hypermethylation and altered levels of histone post-translational methylation leading to increased transcription of TNFA, could variously explain increased levels of peripheral and central inflammation found in AD...
April 29, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29695452/ppar%C3%AE-agonist-pioglitazone-reverses-pulmonary-hypertension-and-prevents-right-heart-failure-via-fatty-acid-oxidation
#4
Ekaterina Legchenko, Philippe Chouvarine, Paul Borchert, Angeles Fernandez-Gonzalez, Erin Snay, Martin Meier, Lavinia Maegel, S Alex Mitsialis, Eva A Rog-Zielinska, Stella Kourembanas, Danny Jonigk, Georg Hansmann
Right ventricular (RV) heart failure is the leading cause of death in pulmonary arterial hypertension (PAH). Peroxisome proliferator-activated receptor γ (PPARγ) acts as a vasoprotective metabolic regulator in smooth muscle and endothelial cells; however, its role in the heart is unclear. We report that deletion of PPARγ in cardiomyocytes leads to biventricular systolic dysfunction and intramyocellular lipid accumulation in mice. In the SU5416/hypoxia (SuHx) rat model, oral treatment with the PPARγ agonist pioglitazone completely reverses severe PAH and vascular remodeling and prevents RV failure...
April 25, 2018: Science Translational Medicine
https://www.readbyqxmd.com/read/29668680/mitochondrial-nicotinamide-adenine-dinucleotide-reduced-nadh-oxidation-links-the-tricarboxylic-acid-tca-cycle-with-methionine-metabolism-and-nuclear-dna-methylation
#5
Oswaldo A Lozoya, Inmaculada Martinez-Reyes, Tianyuan Wang, Dagoberto Grenet, Pierre Bushel, Jianying Li, Navdeep Chandel, Richard P Woychik, Janine H Santos
Mitochondrial function affects many aspects of cellular physiology, and, most recently, its role in epigenetics has been reported. Mechanistically, how mitochondrial function alters DNA methylation patterns in the nucleus remains ill defined. Using a cell culture model of induced mitochondrial DNA (mtDNA) depletion, in this study we show that progressive mitochondrial dysfunction leads to an early transcriptional and metabolic program centered on the metabolism of various amino acids, including those involved in the methionine cycle...
April 18, 2018: PLoS Biology
https://www.readbyqxmd.com/read/29576612/protein-kinase-a-mediated-phosphorylation-regulates-stat3-activation-and-oncogenic-ezh2-activity
#6
Ali R Özeş, Nick Pulliam, Mustafa G Ertosun, Özlem Yılmaz, Jessica Tang, Ece Çopuroğlu, Daniela Matei, Osman N Özeş, Kenneth P Nephew
Polycomb repressive complex 2 (PRC2) member enhancer of zeste homolog 2 (EZH2) trimethylates histone H3 lysine 27 (H3K27me3), alters chromatin structure and contributes to epigenetic regulation of gene expression in normal and disease processes. Phosphorylation of EZH2 augmented EZH2 oncogenic activity in cancer but observations have been limited to threonine 350 (T350) and serine 21 (S21) residues by cyclin-dependent kinase 1 and protein kinase B, respectively. In addition, phosphorylation of the evolutionarily conserved T372 motif of EZH2 by p38 resulted in EZH2 interaction with Ying Yang 1 and promoted muscle stem cell differentiation...
March 26, 2018: Oncogene
https://www.readbyqxmd.com/read/29512466/mitochondria-a-connecting-link-in-the-major-depressive-disorder-jigsaw
#7
Shilpa Sharma, Ravi Shankar Akundi
BACKGROUND: Depression is a widespread phenomenon with varying degrees of pathology in different patients. Various hypotheses have been proposed for the cause and continuance of depression. Some of these include, but not limited to, the monoamine hypothesis, the neuroendocrine hypothesis, and the more recent epigenetic and inflammatory hypotheses. OBJECTIVE: In this article, we review all the above hypotheses with a focus on the role of mitochondria as the connecting link...
March 2, 2018: Current Neuropharmacology
https://www.readbyqxmd.com/read/29501571/integrated-omics-analysis-reveals-new-drug-induced-mitochondrial-perturbations-in-human-hepatocytes
#8
Jarno E J Wolters, Simone G J van Breda, Jonas Grossmann, Claudia Fortes, Florian Caiment, Jos C S Kleinjans
We performed a multiple 'omics study by integrating data on epigenomic, transcriptomic, and proteomic perturbations associated with mitochondrial dysfunction in primary human hepatocytes caused by the liver toxicant valproic acid (VPA), to deeper understand downstream events following epigenetic alterations in the mitochondrial genome. Furthermore, we investigated persistence of cross-omics changes after terminating drug treatment. Upon transient methylation changes of mitochondrial genes during VPA-treatment, increasing complexities of gene-interaction networks across time were demonstrated, which normalized during washout...
June 1, 2018: Toxicology Letters
https://www.readbyqxmd.com/read/29436254/therapeutic-targets-for-altering-mitochondrial-dysfunction-associated-with-diabetic-retinopathy
#9
Renu A Kowluru, Manish Mishra
Retinopathy remains as one of the most feared blinding complications of diabetes, and with the prevalence of this life-long disease escalating at an alarming rate, the incidence of retinopathy is also climbing. Although the cutting edge research has identified many molecular mechanisms associated with its development, the exact mechanism how diabetes damages the retina remains obscure, limiting therapeutic options for this devastating disease. Areas covered: This review focuses on the central role of mitochondrial dysfunction/damage in the pathogenesis of diabetic retinopathy, and how damaged mitochondria initiates a self-perpetuating vicious cycles of free radicals...
March 2018: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/29389735/psychological-stress-and-mitochondria-a-conceptual-framework
#10
Martin Picard, Bruce S McEwen
BACKGROUND: The integration of biological, psychological, and social factors in medicine has benefited from increasingly precise stress response biomarkers. Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states...
February 2018: Psychosomatic Medicine
https://www.readbyqxmd.com/read/29284398/mechanisms-of-radiation-bystander-and-non-targeted-effects-implications-to-radiation-carcinogenesis-and-radiotherapy
#11
Rasoul Yahyapour, Elahe Motevaseli, Abolhasan Rezaeyan, Hamid Abdollahi, Bagher Farhood, Mohsen Cheki, Masoud Najafi, Vilmar Villa
Knowledge of radiobiology is of paramount importance to be able to grasp and have an in-depth understanding of the consequences of ionizing radiation. One of the most important effects of this physical stressor's interaction to targeted and non-targeted cells, tissues and organs is on the late effects on the development of primary and secondary cancers. Thus, an in-depth understanding of the mechanisms of radiation carcinogenesis remain to be elucidated, and some studies have demonstrated or proposed a role of non-targeted effect in excess risk of cancer incidence...
December 29, 2017: Current Radiopharmaceuticals
https://www.readbyqxmd.com/read/29241213/antibiotics-induced-obesity-a-mitochondrial-perspective
#12
Melisa J Andrade, Chinchu Jayaprakash, Smitha Bhat, Nikolaos Evangelatos, Angela Brand, Kapaettu Satyamoorthy
Antibiotics are the first line of treatment against infections and have contributed immensely to reduce the morbidity and mortality rates. Recently, extensive use of antibiotics has led to alterations of the gut microbiome, predisposition to various diseases and most importantly, increase in the emergence of antibiotic-resistant bacteria, which poses a major threat to global public health. Another major issue faced worldwide due to unregulated use of antibiotics in children as well as in adults is the influence of metabolism and body weight homeostasis, leading to obesity...
December 15, 2017: Public Health Genomics
https://www.readbyqxmd.com/read/29221988/modulations-of-keap1-nrf2-signaling-axis-by-tiia-ameliorated-the-oxidative-stress-induced-myocardial-apoptosis
#13
Shi-Hai Yan, Ning-Wei Zhao, Zhi-Rong Geng, Jia-Yin Shen, Fu-Ming Liu, Dong Yan, Jie Zhou, Chao Nie, Cheng-Cai Huang, Zhu-Yuan Fang
Mounting evidence has strongly implicated oxidative stress in the development of cardiac dysfunction, and myocardial apoptosis contributes to the pathogenesis of heart failure. Quantitative cardiac proteomics data revealed that pressure load by TAC resulted in a significant decline in mitochondrial metabolic activity, where TIIA (Tanshinone IIA sulfonate) treatment reversed it in vivo, which might be mediated by Nrf2. In NRVMs, TIIA treatment ameliorated H2 O2 -induced caspase-3/9 activations through the suppression of p38 and mTOR signaling pathways, where caspase-mediated cleavage of YY1 and PARP resulted in the defects in mitochondrial biogenesis and DNA repair, and this event finally led to cardiomyocyte apoptosis...
February 1, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29161229/sex-and-dose-specific-effects-of-maternal-bisphenol-a-exposure-on-pancreatic-islets-of-first-and-second-generation-adult-mice-offspring
#14
Amita Bansal, Cetewayo Rashid, Frances Xin, Changhong Li, Erzsebet Polyak, Anna Duemler, Tom van der Meer, Martha Stefaniak, Sana Wajid, Nicolai Doliba, Marisa S Bartolomei, Rebecca A Simmons
BACKGROUND: Exposure to the environmental endocrine disruptor bisphenol A (BPA) is ubiquitous and associated with the increased risk of diabetes and obesity. However, the underlying mechanisms remain unknown. We recently demonstrated that perinatal BPA exposure is associated with higher body fat, impaired glucose tolerance, and reduced insulin secretion in first- (F1) and second-generation (F2) C57BL/6J male mice offspring. OBJECTIVE: We sought to determine the multigenerational effects of maternal bisphenol A exposure on mouse pancreatic islets...
September 27, 2017: Environmental Health Perspectives
https://www.readbyqxmd.com/read/29118760/septic-shock-and-the-aging-process-a-molecular-comparison
#15
Fabiano Pinheiro da Silva, Marcel Cerqueira César Machado
Aging is a continuous process promoted by both intrinsic and extrinsic factors that each trigger a multitude of molecular events. Increasing evidence supports a central role for inflammation in this progression. Here, we discuss how the low-grade chronic inflammation that characterizes aging is tightly interconnected with other important aspects of this process, such as DNA damage, mitochondrial dysfunction, and epigenetic changes. Similarly, inflammation also plays a critical role in many morbid conditions that affect patients who are admitted to Intensive Care...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29110598/sirt1-as-a-therapeutic-target-in-diabetic-complications
#16
Justyna Strycharz, Żaneta Rygielska, Ewa Świderska, Józef Drzewoski, Janusz Szemraj, Leszek Szmigiero, Agnieszka Śliwińska
Background SIRT1 is an epigenetic enzyme involved in histone and non-histone protein deacetylation. It acts primarily as a metabolic sensor, which responses to changing energy status by deacetylating crucial transcription factors and cofactors. In this way, SIRT1 regulates mitochondrial function and biogenesis, oxidative stress, inflammation, apoptosis and cellular senescence. Disturbance of all of these phenomena promotes the pathogenesis of diabetic complications. These disorders are inseparably connected with chronic hyperglycemia, which possesses a strong epigenetic determinant...
November 6, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/29073779/mitochondrial-nad-nadh-redox-state-and-diabetic-cardiomyopathy
#17
Jessica M Berthiaume, Jacob G Kurdys, Danina M Muntean, Mariana G Rosca
SIGNIFICANCE: Diabetic cardiomyopathy (DCM) is a frequent complication occurring even in well-controlled asymptomatic diabetic patients, and it may advance to heart failure (HF). Recent Advances: The diabetic heart is characterized by a state of "metabolic rigidity" involving enhanced rates of fatty acid uptake and mitochondrial oxidation as the predominant energy source, and it exhibits mitochondrial electron transport chain defects. These alterations promote redox state changes evidenced by a decreased NAD+ /NADH ratio associated with an increase in acetyl-CoA/CoA ratio...
December 11, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/29059699/identification-of-the-genomic-region-under-epigenetic-regulation-during-non-alcoholic-fatty-liver-disease-progression
#18
Kikuko Hotta, Takuya Kitamoto, Aya Kitamoto, Yuji Ogawa, Yasushi Honda, Takaomi Kessoku, Masato Yoneda, Kento Imajo, Wataru Tomeno, Satoru Saito, Atsushi Nakajima
AIM: The progression of non-alcoholic fatty liver disease (NAFLD) is affected by epigenetics. We undertook co-methylation and differentially methylated region (DMR) analyses to identify the genomic region that is under epigenetic regulation during NAFLD progression. METHODS: We collected liver biopsy specimens from 60 Japanese patients with NAFLD and classified these into mild (fibrosis stages 0-2) or advanced (fibrosis stages 3-4) NAFLD. We carried out a genome-wide DNA methylation analysis and identified the differentially methylated CpGs between mild and advanced NAFLD...
February 2018: Hepatology Research: the Official Journal of the Japan Society of Hepatology
https://www.readbyqxmd.com/read/29043077/recent-advances-in-understanding-werner-syndrome
#19
REVIEW
Raghavendra A Shamanna, Deborah L Croteau, Jong-Hyuk Lee, Vilhelm A Bohr
Aging, the universal phenomenon, affects human health and is the primary risk factor for major disease pathologies. Progeroid diseases, which mimic aging at an accelerated rate, have provided cues in understanding the hallmarks of aging. Mutations in DNA repair genes as well as in telomerase subunits are known to cause progeroid syndromes. Werner syndrome (WS), which is characterized by accelerated aging, is an autosomal-recessive genetic disorder. Hallmarks that define the aging process include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulation of nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication...
2017: F1000Research
https://www.readbyqxmd.com/read/29027980/the-plasticizer-bisphenol-a-perturbs-the-hepatic-epigenome-a-systems-level-analysis-of-the-mirnome
#20
Ludivine Renaud, Willian A da Silveira, E Starr Hazard, Jonathan Simpson, Silvia Falcinelli, Dongjun Chung, Oliana Carnevali, Gary Hardiman
Ubiquitous exposure to bisphenol A (BPA), an endocrine disruptor (ED), has raised concerns for both human and ecosystem health. Epigenetic factors, including microRNAs (miRNAs), are key regulators of gene expression during cancer. The effect of BPA exposure on the zebrafish epigenome remains poorly characterized. Zebrafish represents an excellent model to study cancer as the organism develops a disease that resembles human cancer. Using zebrafish as a systems toxicology model, we hypothesized that chronic BPA-exposure impacts the miRNome in adult zebrafish and establishes an epigenome more susceptible to cancer development...
October 13, 2017: Genes
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