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https://www.readbyqxmd.com/read/27916422/pgc-1-alpha-interacts-with-microrna-217-to-functionally-regulate-breast-cancer-cell-proliferation
#1
Shaohui Zhang, Xinguo Liu, Jianming Liu, Heng Guo, Hongfeng Xu, Geng Zhang
BACKGROUND: In this study, we explored the functional mechanism of PPARg co-activator 1-alpha (PGC-1α) in regulating miR-217-mediated breast cancer development in vitro. METHODS: Dual-luciferase activity assay was applied to examine the binding of miR-217 on PGC-1α gene. Breast cancer cell lines, MCF-7 and MDA-MB-231 were infected by lentivirus to constitutively downregulate miR-217. Its regulation on PGC-1α expression was investigated by qRT-PCR and western blot...
December 1, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/27913603/the-tumor-suppressor-flcn-mediates-an-alternate-mtor-pathway-to-regulate-browning-of-adipose-tissue
#2
Shogo Wada, Michael Neinast, Cholsoon Jang, Yasir H Ibrahim, Gina Lee, Apoorva Babu, Jian Li, Atsushi Hoshino, Glenn C Rowe, James Rhee, José A Martina, Rosa Puertollano, John Blenis, Michael Morley, Joseph A Baur, Patrick Seale, Zoltan Arany
Noncanonical mechanistic target of rapamycin (mTOR) pathways remain poorly understood. Mutations in the tumor suppressor folliculin (FLCN) cause Birt-Hogg-Dubé syndrome, a hamartomatous disease marked by mitochondria-rich kidney tumors. FLCN functionally interacts with mTOR and is expressed in most tissues, but its role in fat has not been explored. We show here that FLCN regulates adipose tissue browning via mTOR and the transcription factor TFE3. Adipose-specific deletion of FLCN relieves mTOR-dependent cytoplasmic retention of TFE3, leading to direct induction of the PGC-1 transcriptional coactivators, drivers of mitochondrial biogenesis and the browning program...
December 2, 2016: Genes & Development
https://www.readbyqxmd.com/read/27904582/the-role-of-peroxisome-proliferator-activated-receptor-coactivator-1-gene-in-skin-aging
#3
REVIEW
Shahrzad Aghaei, Mohammad Ali Nilforoushzadeh, Maryam Aghaei
Skin aging is a continuous process that exhibits fine and deep wrinkles, thin and transparent skin, loss of underlying fat, dry skin and itch, following decreased collagen and elastin synthesis. Both extrinsic and intrinsic agents are considered in the pathogenesis on skin aging. Extrinsic factors such as sun exposure, windy and dry weather, nutrition, and lifestyle may induce premature aging, toxic-free radicals, and reactive oxygen species due to decreasing normal function of mitochondria which play the major intrinsic factors in premature skin aging...
2016: Journal of Research in Medical Sciences: the Official Journal of Isfahan University of Medical Sciences
https://www.readbyqxmd.com/read/27789709/concerted-action-of-pgc-1-related-coactivator-prc-and-c-myc-in-the-stress-response-to-mitochondrial-dysfunction
#4
Natalie Gleyzer, Richard C Scarpulla
PGC-1-related coactivator (PRC) has a dual function in growth-regulated mitochondrial biogenesis and as a sensor of metabolic stress. PRC induction by mitochondrial inhibitors, intracellular ROS, or topoisomerase I inhibition orchestrates an inflammatory program associated with the adaptation to cellular stress. Activation of this program is accompanied by the coordinate expression of c-MYC, which is linked kinetically to that of PRC in response to multiple stress inducers. Here, we show that the c-MYC inhibitor 10058-F4 blocks the induction of c-MYC, PRC, and representative PRC-dependent stress genes by the respiratory chain uncoupler, carbonyl cyanide m-chlorophenyl hydrazine (CCCP)...
December 2, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27780821/adult-expression-of-pgc-1%C3%AE-and-1%C3%AE-in-skeletal-muscle-is-not-required-for-endurance-exercise-induced-enhancement-of-exercise-capacity
#5
Christopher Ballmann, Yawen Tang, Zachary Bush, Glenn C Rowe
Exercise has been shown to be the best intervention in the treatment of many diseases. Many of the benefits of exercise are mediated by adaptions induced in skeletal muscle. The peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family of transcriptional coactivators has emerged as being key mediators of the exercise response and is considered to be essential for many of the adaptions seen in skeletal muscle. However, the contribution of the PGC-1s in skeletal muscle has been evaluated by the use of either whole body or congenital skeletal muscle-specific deletion...
December 1, 2016: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/27699582/peroxisome-proliferator-activated-receptor-gamma-co-activator-1-gene-gly482ser-polymorphism-is-associated-with-the-response-of-low-density-lipoprotein-cholesterol-concentrations-to-exercise-training-in-elderly-japanese
#6
Takuro Tobina, Yukari Mori, Yukiko Doi, Fuki Nakayama, Akira Kiyonaga, Hiroaki Tanaka
Muscle peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1)α gene expression is influenced by the Gly482Ser gene polymorphism, which is a candidate genetic risk factor for diabetes mellitus and obesity. This study investigated the effects of PGC-1 gene Gly482Ser polymorphisms on alterations in glucose and lipid metabolism induced by exercise training. A 12-week intervention study was performed for 119 participants who were more than 65 years of age and completed exercise training at lactate threshold intensity...
October 3, 2016: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/27638713/gene-therapy-targeting-mitochondrial-pathway-in-parkinson-s-disease
#7
Chi-Jing Choong, Hideki Mochizuki
Parkinson's disease (PD) presents a relative selective localization of pathology to substantia nigra and well-defined motor symptoms caused by dopaminergic degeneration that makes it an ideal target for gene therapy. Parallel progress in viral vector systems enables the delivery of therapeutic genes directly into brain with reasonable safety along with sustained transgene expression. To date, gene therapy for PD that has reached clinical trial evaluation is mainly based on symptomatic approach that involves enzyme replacement strategy and restorative approach that depends on the addition of neurotrophic factors...
September 16, 2016: Journal of Neural Transmission
https://www.readbyqxmd.com/read/27576732/pre-b-cell-colony-enhancing-factor-protects-against-apoptotic-neuronal-death-and-mitochondrial-damage-in-ischemia
#8
Xiaowan Wang, Hailong Li, Shinghua Ding
We previously demonstrated that Pre-B-cell colony-enhancing factor (PBEF), also known as nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in mammalian NAD(+) biosynthesis pathway, plays a brain and neuronal protective role in ischemic stroke. In this study, we further investigated the mechanism of its neuroprotective effect after ischemia in the primary cultured mouse cortical neurons. Using apoptotic cell death assay, fluorescent imaging, molecular biology, mitochondrial biogenesis measurements and Western blotting analysis, our results show that the overexpression of PBEF in neurons can significantly promote neuronal survival, reduce the translocation of apoptosis inducing factor (AIF) from mitochondria to nuclei and inhibit the activation of capase-3 after glutamate-induced excitotoxicity...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27543774/effects-of-diclofenac-sodium-on-the-hippocampus-of-rats-with-acute-subdural-hematoma-histological-stereological-and-molecular-approach
#9
A P Türkmen, S Kaplan, A Aksoy, Bz Altunkaynak, Kk Yurt, E Elibol, C Çokluk, Me Onger
This study was aimed at evaluating the potential effects of acute subdural hematoma (ASDH) and diclofenac sodium (DS) therapy following ASDH on the rat hippocampus. Twenty-four male Sprague Dawley rats were used and divided into four groups. 0.1 ml of non-heparinized autologous blood from the tail vein of the animals in the non-treatment group (NTG) and treatment group (TG) was injected into the subdural space. The TG received intramuscular diclofenac sodium at a 15 mg/kg dose daily from the postoperative second hour to the seventh day after the operation...
2016: Folia Neuropathologica
https://www.readbyqxmd.com/read/27461561/lipolysis-and-thermogenesis-in-adipose-tissues-as-new-potential-mechanisms-for-metabolic-benefits-of-dietary-fiber
#10
Shu-Fen Han, Jun Jiao, Wei Zhang, Jia-Ying Xu, Weiguo Zhang, Chun-Ling Fu, Li-Qiang Qin
OBJECTIVE: Dietary fiber consumption is associated with reduced risk for the development of noncommunicable diseases. The aim of the present study was to evaluate the effects of cereal dietary fiber on the levels of proteins involved in lipolysis and thermogenesis in white adipose tissue (WAT) and brown adipose tissue (BAT) of C57 BL/6 J mice fed a high-fat diet (HFD). METHODS: Male C57BL/6 J mice were fed normal chow diet (Chow), HFD, HFD plus oat fiber (H-oat), or HFD plus wheat bran fiber (H-wheat) for 24 wk...
January 2017: Nutrition
https://www.readbyqxmd.com/read/27444220/features-of-an-altered-ampk-metabolic-pathway-in-gilbert-s-syndrome-and-its-role-in-metabolic-health
#11
Christine Mölzer, Marlies Wallner, Carina Kern, Anela Tosevska, Ursula Schwarz, Rene Zadnikar, Daniel Doberer, Rodrig Marculescu, Karl-Heinz Wagner
Energy metabolism, involving the ATP-dependent AMPK-PgC-Ppar pathway impacts metabolic health immensely, in that its impairment can lead to obesity, giving rise to disease. Based on observations that individuals with Gilbert's syndrome (GS; UGT1A1(*)28 promoter mutation) are generally lighter, leaner and healthier than controls, specific inter-group differences in the AMPK pathway regulation were explored. Therefore, a case-control study involving 120 fasted, healthy, age- and gender matched subjects with/without GS, was conducted...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27418542/pgc-1-alpha-regulates-ho-1-expression-mitochondrial-dynamics-and-biogenesis-role-of-epoxyeicosatrienoic-acid
#12
Shailendra P Singh, Joseph Schragenheim, Jian Cao, John R Falck, Nader G Abraham, Lars Bellner
BACKGROUND/OBJECTIVES: Obesity is a risk factor in the development of type 2 diabetes mellitus (DM2), which is associated with increased morbidity and mortality, predominantly as a result of cardiovascular complications. Increased adiposity is a systemic condition characterized by increased oxidative stress (ROS), increased inflammation, inhibition of anti-oxidant genes such as HO-1 and increased degradation of epoxyeicosatrienoic acids (EETs). We previously demonstrated that EETs attenuate mitochondrial ROS...
September 2016: Prostaglandins & Other Lipid Mediators
https://www.readbyqxmd.com/read/27335690/increased-expression-of-estrogen-related-receptor-%C3%AE-during-adaptation-of-adult-cardiomyocytes-to-sustained-hypoxia
#13
Kathryn F Cunningham, Gyda C Beeson, Craig C Beeson, Paul J McDermott
UNLABELLED: Estrogen-related Receptors (ERR) are members of the steroid hormone receptor superfamily of transcription factors that regulate expression of genes required for energy metabolism including mitochondrial biogenesis, fatty acid oxidation and oxidative phosphorylation. While ERRα and EPPγ isoforms are known to share a wide array of target genes in the adult myocardium, the function of ERRβ has not been characterized in cardiomyocytes. The purpose of this study was to determine the role of ERRβ in regulating energy metabolism in adult cardiomyocytes in primary culture...
2016: American Journal of Cardiovascular Disease
https://www.readbyqxmd.com/read/27236077/the-role-of-pgc-1%C3%AE-and-mrp1-in-lead-induced-mitochondrial-toxicity-in-testicular-sertoli-cells
#14
Zhen Li, Xi Liu, Lu Wang, Yan Wang, Chuang Du, Siyuan Xu, Yucheng Zhang, Chunhong Wang, Chengfeng Yang
The lead-induced toxic effect on mitochondria in Sertoli cells is not well studied and the underlying mechanism is poorly understood. Here we reported the potential role of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and multidrug resistance protein 1 (MRP1) in lead acetate-induced mitochondrial toxicity in mouse testicular Sertoli cells TM4 line. We found that lead acetate treatment significantly reduced the expression level of PGC-1α, but increased the level of MRP1 in mitochondria of TM4 cells...
April 29, 2016: Toxicology
https://www.readbyqxmd.com/read/27235860/pgc-1%C3%AE-ameliorates-angiotensinii-induced-enos-dysfunction-in-human-aortic-endothelial-cells
#15
Jie Li, Xiao-Yong Geng, Xiao-Liang Cong
Increasing evidences support that PGC-1α participates in regulating endothelial homeostasis, in part by mediating endothelial nitric oxide (NO) synthase (eNOS) activity and NO production. However, the molecular mechanisms by which PGC-1α regulates eNOS activity are not completely understood. In the present study, we investigated the effects of PGC-1α on eNOS dysfunction and further explore the underlying mechanisms. The results showed that PGC-1α expression was downregulated after AngiotensinII (AngII) treatment and paralleled with the decreased NO generation in human aortic endothelial cells...
August 2016: Vascular Pharmacology
https://www.readbyqxmd.com/read/27230643/molecular-and-cellular-mechanisms-of-cardiovascular-disorders-in-diabetes
#16
Manasi S Shah, Michael Brownlee
The clinical correlations linking diabetes mellitus with accelerated atherosclerosis, cardiomyopathy, and increased post-myocardial infarction fatality rates are increasingly understood in mechanistic terms. The multiple mechanisms discussed in this review seem to share a common element: prolonged increases in reactive oxygen species (ROS) production in diabetic cardiovascular cells. Intracellular hyperglycemia causes excessive ROS production. This activates nuclear poly(ADP-ribose) polymerase, which inhibits GAPDH, shunting early glycolytic intermediates into pathogenic signaling pathways...
May 27, 2016: Circulation Research
https://www.readbyqxmd.com/read/27228549/long-term-exercise-training-prevents-mammary-tumorigenesis-induced-muscle-wasting-in-rats-through-the-regulation-of-tweak-signalling
#17
Ana Isabel Padrão, Ana Cristina Corrêa Figueira, Ana Rocha-Faustino, Adelina Gama, Maria Margarida Loureiro, Maria João Neuparth, Daniel Moreira-Gonçalves, Rui Vitorino, Francisco Amado, Lúcio Lara Santos, Paula A Oliveira, José Alberto Duarte, Rita Ferreira
AIM: Exercise training has been suggested as a non-pharmacological approach to prevent skeletal muscle wasting and improve muscle function in cancer cachexia. However, little is known about the molecular mechanisms underlying such beneficial effect. In the present study we aimed to, firstly, examine the contribution of TWEAK signalling to cancer-induced skeletal muscle wasting and, secondly, evaluate whether long-term exercise alters TWEAK signalling and prevents muscle wasting. METHODS: Female Sprague-Dawley rats were randomly assigned to control and exercise groups...
May 26, 2016: Acta Physiologica
https://www.readbyqxmd.com/read/27225627/fuel-for-the-work-required-a-practical-approach-to-amalgamating-train-low-paradigms-for-endurance-athletes
#18
Samuel G Impey, Kelly M Hammond, Sam O Shepherd, Adam P Sharples, Claire Stewart, Marie Limb, Kenneth Smith, Andrew Philp, Stewart Jeromson, D Lee Hamilton, Graeme L Close, James P Morton
Using an amalgamation of previously studied "train-low" paradigms, we tested the effects of reduced carbohydrate (CHO) but high leucine availability on cell-signaling responses associated with exercise-induced regulation of mitochondrial biogenesis and muscle protein synthesis (MPS). In a repeated-measures crossover design, 11 males completed an exhaustive cycling protocol with high CHO availability before, during, and after exercise (HIGH) or alternatively, low CHO but high protein (leucine enriched) availability (LOW + LEU)...
May 2016: Physiological Reports
https://www.readbyqxmd.com/read/27224420/epoxyeicosatrienoic-acids-regulate-adipocyte-differentiation-of-mouse-3t3-cells-via-pgc-1%C3%AE-activation-which-is-required-for-ho-1-expression-and-increased-mitochondrial-function
#19
Maayan Waldman, Lars Bellner, Luca Vanella, Joseph Schragenheim, Komal Sodhi, Shailendra P Singh, Daohong Lin, Anand Lakhkar, Jiangwei Li, Edith Hochhauser, Michael Arad, Zbigniew Darzynkiewicz, Atallah Kappas, Nader G Abraham
Epoxyeicosatrienoic acid (EET) contributes to browning of white adipose stem cells to ameliorate obesity/diabetes and insulin resistance. In the current study, we show that EET altered preadipocyte function, enhanced peroxisome proliferation-activated receptor γ coactivator α (PGC-1α) expression, and increased mitochondrial function in the 3T3-L1 preadipocyte subjected to adipogenesis. Cells treated with EET resulted in an increase, P < 0.05, in PGC-1α and a decrease in mitochondria-derived ROS (MitoSox), P < 0...
July 15, 2016: Stem Cells and Development
https://www.readbyqxmd.com/read/27221886/telomere-mitochondrion-links-contribute-to-induction-of-senescence-in-mcf-7-cells-after-carbon-ion-irradiation
#20
Guo-Ying Miao, Xin Zhou, Xin Zhang, Yi Xie, Chao Sun, Yang Liu, Lu Gan, Hong Zhang
The effects of carbon-ion irradiation on cancer cell telomere function have not been comprehensively studied. In our previous report cancer cells with telomere dysfunction were more sensitive to carbon-ion irradiation, but the underlying mechanisms remained unclear. Here we found that telomerase activity was suppressed by carbon-ion irradiation via hTERT down-regulation. Inhibition of telomere activity by MST-312 further increased cancer cell radiosensitivity to carbon-ion radiation. hTERT suppression caused by either carbon-ion irradiation or MST-312 impaired mitochondrial function, as indicated by decreased membrane potential, mtDNA copy number, mitochondrial mass, total ATP levels and elevated reactive oxygen species (ROS)...
2016: Asian Pacific Journal of Cancer Prevention: APJCP
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