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https://www.readbyqxmd.com/read/27925196/sirt1-sirt3-axis-regulates-cellular-response-to-oxidative-stress-and-etoposide
#1
Ilaria Carnevale, Laura Pellegrini, Patrizia D'Aquila, Serena Saladini, Emanuela Lococo, Lucia Polletta, Enza Vernucci, Eleonora Foglio, Stefano Coppola, Luigi Sansone, Giuseppe Passarino, Dina Bellizzi, Matteo A Russo, Massimo Fini, Marco Tafani
Sirtuins are conserved NAD+-dependent deacylases. SIRT1 is a nuclear and cytoplasmic sirtuin involved in the control of histones a transcription factors function. SIRT3 is a mitochondrial protein, which regulates mitochondrial function. Although both SIRT1 and SIRT3 have been implicated in resistance to cellular stress, the link between these two sirtuins has not been studied so far. Here we aimed to unravel: i) the role of SIRT1-SIRT3 axis for cellular response to oxidative stress and DNA damage; ii) how mammalian cells modulate such SIRT1-SIRT3 axis and which mechanisms are involved...
December 7, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27923775/the-plasticizer-bbp-selectively-inhibits-epigenetic-regulator-sirtuin-during-differentiation-of-c3h10t1-2-stem-cell-line
#2
Jian Zhang, Mahua Choudhury
Exposure to environmental chemicals can perturb an individual's metabolic set point, especially during critical periods of development, and as a result increase his or her propensity towards obesity that is manifested later in life and possibly in successive generations. We hypothesized that benzyl butyl phthalate (BBP), a widespread endocrine disruptor, may impair one important epigenetic regulator, sirtuin, in mesenchymal stem cells and induce adipogenesis. Our results showed that gene expression of two well-known adipogenic markers, aP2 and PPARγ, were significantly increased from day 2 to day 8 under 50μM BBP exposure when compared to control in C3H10T1/2 stem cells (p<0...
December 3, 2016: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/27890624/mitochondrial-camp-prevents-apoptosis-modulating-sirt3-protein-level-and-opa1-processing-in-cardiac-myoblast-cells
#3
Anna Signorile, Arcangela Santeramo, Grazia Tamma, Tommaso Pellegrino, Susanna D'Oria, Paolo Lattanzio, Domenico De Rasmo
Mitochondria, responding to a wide variety of signals, including oxidative stress, are critical in regulating apoptosis that plays a key role in the pathogenesis of a variety of cardiovascular diseases. A number of mitochondrial proteins and pathways have been found to be involved in the mitochondrial dependent apoptosis mechanism, such as optic atrophy 1 (OPA1), sirtuin 3 (Sirt3), deacetylase enzyme and cAMP signal. In the present work we report a network among OPA1, Sirt3 and cAMP in ROS-dependent apoptosis...
November 24, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27888691/redox-imbalance-and-mitochondrial-abnormalities-in-the-diabetic-lung
#4
Jinzi Wu, Zhen Jin, Liang-Jun Yan
Although the lung is one of the least studied organs in diabetes, increasing evidence indicates that it is an inevitable target of diabetic complications. Nevertheless, the underlying biochemical mechanisms of lung injury in diabetes remain largely unexplored. Given that redox imbalance, oxidative stress, and mitochondrial dysfunction have been implicated in diabetic tissue injury, we set out to investigate mechanisms of lung injury in diabetes. The objective of this study was to evaluate NADH/NAD(+) redox status, oxidative stress, and mitochondrial abnormalities in the diabetic lung...
November 17, 2016: Redox Biology
https://www.readbyqxmd.com/read/27882448/sirtuins-and-their-roles-in-brain-aging-and-neurodegenerative-disorders
#5
Henryk Jęśko, Przemysław Wencel, Robert P Strosznajder, Joanna B Strosznajder
Sirtuins (SIRT1-SIRT7) are unique histone deacetylases (HDACs) whose activity depends on NAD(+) levels and thus on the cellular metabolic status. SIRTs regulate energy metabolism and mitochondrial function. They orchestrate the stress response and damage repair. Through these functions sirtuins modulate the course of aging and affect neurodegenerative diseases. SIRTSs interact with multiple signaling proteins, transcription factors (TFs) and poly(ADP-ribose) polymerases (PARPs) another class of NAD(+)-dependent post-translational protein modifiers...
November 24, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/27881304/mitochondrial-sirtuin-network-reveals-dynamic-sirt3-dependent-deacetylation-in-response-to-membrane-depolarization
#6
Wen Yang, Koji Nagasawa, Christian Münch, Yingjie Xu, Kyle Satterstrom, Seungmin Jeong, Sebastian D Hayes, Mark P Jedrychowski, F Sejal Vyas, Elma Zaganjor, Virginia Guarani, Alison E Ringel, Steven P Gygi, J Wade Harper, Marcia C Haigis
Mitochondrial sirtuins, SIRT3-5, are NAD(+)-dependent deacylases and ADP-ribosyltransferases that are critical for stress responses. However, a comprehensive understanding of sirtuin targets, regulation of sirtuin activity, and the relationships between sirtuins remains a key challenge in mitochondrial physiology. Here, we employ systematic interaction proteomics to elucidate the mitochondrial sirtuin protein interaction landscape. This work reveals sirtuin interactions with numerous functional modules within mitochondria, identifies candidate sirtuin substrates, and uncovers a fundamental role for sequestration of SIRT3 by ATP synthase in mitochondrial homeostasis...
November 3, 2016: Cell
https://www.readbyqxmd.com/read/27880725/mouse-sirt3-promotes-autophagy-in-angii-induced-myocardial-hypertrophy-through-the-deacetylation-of-foxo1
#7
Jingyuan Li, Tongshuai Chen, Ming Xiao, Na Li, Shujian Wang, Hongyan Su, Xiaobin Guo, Hui Liu, Fangying Yan, Yi Yang, Yun Zhang, Peili Bu
Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family. The processed short form of Sirt3 has been demonstrated to target many mediators of energy metabolism and mitochondrial stress adaptive program. Autophagy serves as a dynamic recycling mechanism and provides energy or metabolic substrates. Among the mechanisms triggered by cardiac stress, opinions vary as to whether autophagy is a protective or detrimental response. Here, by inducing the Sirt3-knockout mice to myocardial hypertrophy with chronic angiotensin II infusion for four weeks, we determined the role of Sirt3 in myocardial hypertrophy and autophagy...
November 17, 2016: Oncotarget
https://www.readbyqxmd.com/read/27856259/potential-suppression-of-the-high-glucose-and-insulin-induced-retinal-neovascularization-by-sirtuin-3-in-the-human-retinal-endothelial-cells
#8
Xin-Bang Mao, Zhi-Peng You, Chen Wu, Jun Huang
Retinal neovascularization generally play roles in the formation of various severe eye diseases, such as age-related macular degeneration and diabetic retinopathy. The regulation of neovascularization-related pathways by Sirtuin 3 (Sirt3), a major mitochondrial NAD(+)-dependent deacetylase, give us a cue that Sirt3 may participate in the retinal neovascularization. However, the mechanism remains unclear. Here, we established a retinal neovascularization model by using human retinal endothelial cells (HRECs) under the induction of high glucose and insulin (HGI)...
November 14, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27856258/aspirin-increases-mitochondrial-fatty-acid-oxidation
#9
Radha Uppala, Brianne Dudiak, Megan E Beck, Sivakama S Bharathi, Yuxun Zhang, Donna B Stolz, Eric S Goetzman
The metabolic effects of salicylates are poorly understood. This study investigated the effects of aspirin on fatty acid oxidation. Aspirin increased mitochondrial long-chain fatty acid oxidation, but inhibited peroxisomal fatty acid oxidation, in two different cell lines. Aspirin increased mitochondrial protein acetylation and was found to be a stronger acetylating agent in vitro than acetyl-CoA. However, aspirin-induced acetylation did not alter the activity of fatty acid oxidation proteins, and knocking out the mitochondrial deacetylase SIRT3 did not affect the induction of long-chain fatty acid oxidation by aspirin...
November 14, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27823629/javamide-i-o-methyl-ester-increases-p53-acetylation-and-induces-cell-death-via-activating-caspase-3-7-in-monocytic-thp-1-cells
#10
Jae B Park
BACKGROUND: Javamide-I and-II are phenolic amide compounds found in Coffea sp. Previous study suggested that javamide-II may be a potent compound with Sirt1/2 inhibition activity. PURPOSE: However, the effects of javamide-I and the its O-methyl ester on Sirt inhibition, p53 acetylation and cell death have not been investigated. METHODS: The isolation and synthesis of javamide-I and its O-methyl ester analogue were confirmed by NMR. Their potential effects on Sirt1/2/3, p53 acetylation and cell death were examined using sirt assay, silico analysis, Western blot, caspase 3/7 and apoptotic assay methods...
December 1, 2016: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/27819129/roles-of-sirt3-in-heart-failure-from-bench-to-bedside
#11
De-Xing Hu, Xian-Bao Liu, Wen-Chao Song, Jian-An Wang
Heart failure (HF) represents the most common endpoint of most cardiovascular diseases (CVDs) which are the leading causes of death around the world. Despite the advances in treating CVDs, the prevalence of HF continues to increase. It is believed that better results of prognosis are obtained from prevention rather than additional treatment for HF. Therefore, it is reasonable to prevent the development of CVDs or other complications to HF. Most types of HF are attributed to contractile dysfunction, cardiac hypertrophy or remodeling, and ischemic injuries...
2016: Journal of Zhejiang University. Science. B
https://www.readbyqxmd.com/read/27815257/sirt3-blocks-myofibroblast-differentiation-and-pulmonary-fibrosis-by-preventing-mitochondrial-dna-damage
#12
Samik Bindu, Vinodkumar B Pillai, Abhinav Kanwal, Sadhana Samant, Gokhan Mutlu, Eric Verdin, Nickolai O Dulin, Mahesh P Gupta
Myofibroblast differentiation is a key process in the pathogenesis of fibrotic diseases. Transforming growth factor-β1 (TGFβ1) is a powerful inducer of myofibroblast differentiation and is implicated in pathogenensis of tissue fibrosis. This study was undertaken to determine the role of mitochondrial deacetylase, SIRT3 in TGF-β1-induced myofibroblast differentiqtion in vitro and lung fibrosis in vivo. Treatment of human lung fibroblasts with TGFβ1 resulted in increased expression of fibrosis markers, smooth muscle alpha-actin (α-SMA), collagen-1 and fibronectin...
November 4, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/27794418/sirt3-deficiency-exacerbates-diabetic-cardiac-dysfunction-role-of-foxo3a-parkin-mediated-mitophagy
#13
REVIEW
Wenjun Yu, Beilei Gao, Na Li, Jiaxing Wang, Cuiting Qiu, Guoyong Zhang, Min Liu, Rongqing Zhang, Congye Li, Gang Ji, Yingmei Zhang
Diabetic cardiomyopathy (DCM) is often associated with suppressed cardiac autophagy, mitochondrial structural and functional impairment. Sirtuin-3 (Sirt3) has been reported to play a crucial role in mitochondrial homeostasis and confers a protective role against the onset and development of DCM although the precise mechanism(s) remains elusive. Here we hypothesized that Sirt3 exerts cardioprotection against DCM by activating Parkin-mediated mitophagy, en route to preserved mitochondrial homeostasis and suppressed cardiomyocyte apoptosis...
October 26, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27791271/sirt3-and-p53-deacetylation-in-aging-and-cancer
#14
REVIEW
Jijun Chen, Aiqin Wang, Qingqi Chen
The mammalian Sirtuins are a family of highly conserved nicotinamide adenine dinucleotide (NAD +)-dependent histone deacetylase. The mammalian Sirtuins family has identified seven different types of sirtuin. Sirtuins 3(SirT3) is localized to mitochondria, and is a multiple functional protein deacylase through deacetylating a variety of substrates. Cellular senescence represents a permanent withdraw from cell cycle in response to diverse stress; it is controlled by the p53 and retinoblastoma protein (RB) tumor suppressors, and constitutes a potent anticancer mechanisms...
October 28, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27790619/sirt3-in-cardiac-physiology-and-disease
#15
REVIEW
Christoph Koentges, Christoph Bode, Heiko Bugger
Functional defects in mitochondrial biology causally contribute to various human diseases, including cardiovascular disease. Impairment in oxidative phosphorylation, mitochondrial oxidative stress, and increased opening of the mitochondrial permeability transition pore add to the underlying mechanisms of heart failure or myocardial ischemia-reperfusion (IR) injury. Recent evidence demonstrated that the mitochondrial NAD(+)-dependent deacetylase sirtuin 3 (SIRT3) may regulate these mitochondrial functions by reversible protein lysine deacetylation...
2016: Frontiers in Cardiovascular Medicine
https://www.readbyqxmd.com/read/27773814/role-of-sirtuin3-in-high-glucose-induced-apoptosis-in-renal-tubular-epithelial-cells
#16
Xiaocui Jiao, Ying Li, Tao Zhang, Maodong Liu, Yanqing Chi
The apoptosis of renal tubular epithelial cells contributes to the pathogenesis of diabetic nephropathy. High glucose-induced mitochondrial oxidative stress is considered to be an important mediator for renal tubular cell apoptosis. Sirtuin3(Sirt3), a kind of mitochondria-localized nicotinamide adenine dinucleotide(NAD(+))-dependent protein deacetylase, has been reported to regulate the generation of ROS in mitochondria through regulating acetylation level and activity of several key mitochondrial enzymes. In this study, we investigated the role of Sirt3 on high glucose-induced apoptosis in HK-2 cells...
October 20, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27732568/sirt3-is-attenuated-in-systemic-sclerosis-skin-and-lungs-and-its-pharmacologic-activation-mitigates-organ-fibrosis
#17
Kaname Akamata, Jun Wei, Mitra Bhattacharyya, Paul Cheresh, Michael Y Bonner, Jack L Arbiser, Kirtee Raparia, Mahesh P Gupta, David W Kamp, John Varga
Constitutive fibroblast activation is responsible for organ fibrosis in fibrotic disorders including systemic sclerosis (SSc), but the underlying mechanisms are not fully understood, and effective therapies are lacking. We investigated the expression of the mitochondrial deacetylase sirtuin 3 (SIRT3) and its modulation by hexafluoro, a novel fluorinated synthetic honokiol analogue, in the context of fibrosis. We find that augmenting cellular SIRT3 by forced expression in normal lung and skin fibroblasts, or by hexafluoro treatment, blocked intracellular TGF-ß signaling and fibrotic responses, and mitigated the activated phenotype of SSc fibroblasts...
October 6, 2016: Oncotarget
https://www.readbyqxmd.com/read/27731402/melatonin-improves-age-induced-fertility-decline-and-attenuates-ovarian-mitochondrial-oxidative-stress-in-mice
#18
Chao Song, Wei Peng, Songna Yin, Jiamin Zhao, Beibei Fu, Jingcheng Zhang, Tingchao Mao, Haibo Wu, Yong Zhang
Increasing evidence shows that melatonin protected against age-related mitochondrial oxidative damage. However, the protective effects of melatonin against ovarian aging has not been explored. Young Kunming females (aged 2-3 months) were fed with melatonin added to drinking water for 6 or 12 months (mo). We found that long-term (12 mo) melatonin treatment significantly reduced ovarian aging, as indicated by substantial increases in litter size, pool of follicles, and telomere length as well as oocyte quantity and quality...
October 12, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27725455/identification-of-a-selective-sirt2-inhibitor-and-its-anti-breast-cancer-activity
#19
Asad Ali Shah, Akihiro Ito, Akiko Nakata, Minoru Yoshida
SIRT2 is a member of the human sirtuin family of proteins and possesses nicotinamide adenine dinucleotide (NAD)-dependent lysine deacetylase activity. SIRT2 has been involved in various cellular processes including gene transcription, genome constancy, and the cell cycle. In addition, SIRT2 is deeply implicated in diverse diseases including cancer. In this study, we identified a small molecule inhibitor of SIRT2 with a structure different from known SIRT2 inhibitors by screening from a chemical library. The hit compound showed a high selectivity toward SIRT2 as it only inhibited SIRT2, and not other sirtuins including SIRT1 and SIRT3 or zinc-dependent histone deacetylases (HDACs) including HDAC1 and HDAC6, in vitro...
2016: Biological & Pharmaceutical Bulletin
https://www.readbyqxmd.com/read/27722009/poly-adp-ribose-polymerase-1-contributes-to-oxidative-stress-through-downregulation-of-sirtuin-3-during-cisplatin-nephrotoxicity
#20
Sang Pil Yoon, Jinu Kim
Enhanced oxidative stress is a hallmark of cisplatin nephrotoxicity, and inhibition of poly(ADP-ribose) polymerase 1 (PARP1) attenuates oxidative stress during cisplatin nephrotoxicity; however, the precise mechanisms behind its action remain elusive. Here, using an in vitro model of cisplatin-induced injury to human kidney proximal tubular cells, we demonstrated that the protective effect of PARP1 inhibition on oxidative stress is associated with sirtuin 3 (SIRT3) activation. Exposure to 400 µM cisplatin for 8 hours in cells decreased activity and expression of manganese superoxide dismutase (MnSOD), catalase, glutathione peroxidase (GPX), and SIRT3, while it increased their lysine acetylation...
September 2016: Anatomy & Cell Biology
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