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https://www.readbyqxmd.com/read/28899858/redd1-induction-regulates-the-skeletal-muscle-gene-expression-signature-following-acute-aerobic-exercise
#1
Bradley S Gordon, Jennifer L Steiner, Michael L Rossetti, Shuxi Qiao, Leif W Ellisen, Subramaniam S Govindarajan, Alexey M Eroshkin, Dave L Williamson, Paul M Coen
The metabolic stress placed on skeletal muscle by aerobic exercise promotes acute and long-term health benefits in part through changes in gene expression. However, the transducers that mediate altered gene expression signatures have not been completely elucidated. Regulated in Development and DNA Damage 1 (REDD1) is a stress-induced protein whose expression is transiently increased in skeletal muscle following acute aerobic exercise. However, the role of this induction remains unclear. Because REDD1 altered gene expression in other model systems, we sought to determine whether REDD1 induction following acute exercise altered the gene expression signature in muscle...
September 12, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28767526/exercise-protects-skeletal-muscle-during-chronic-doxorubicin-administration
#2
Jared M Dickinson, Andrew C D'Lugos, Tara N Mahmood, Jordan C Ormsby, Lara Salvo, W Logan Dedmon, Shivam H Patel, Mark S Katsma, Farouk Mookadam, Rayna J Gonzales, Taben M Hale, Chad C Carroll, Siddhartha S Angadi
PURPOSE: To assess the ability for exercise training performed before and during bi-weekly doxorubicin (DOX) administration to attenuate adverse effects of DOX on skeletal muscle. We hypothesized that DOX treatment would increase REDD1, impair mammalian target of rapamycin (mTOR) signaling, and reduce muscle fiber size, and that exercise training would attenuate these responses. METHODS: Eight-week old ovariectomized female Sprague-Dawley rats were randomized to one of four treatments: Exercise+DOX (Ex-Dox); Ex+Vehicle (Ex-Veh), Sedentary+DOX (Sed-Dox); and Sed+Veh (Sed-Veh)...
July 31, 2017: Medicine and Science in Sports and Exercise
https://www.readbyqxmd.com/read/28765650/implication-of-redd1-in-the-activation-of-inflammatory-pathways
#3
Faustine Pastor, Karine Dumas, Marie-Astrid Barthélémy, Claire Regazzetti, Noémie Druelle, Pascal Peraldi, Mireille Cormont, Jean-François Tanti, Sophie Giorgetti-Peraldi
In response to endotoxemia, the organism triggers an inflammatory response, and the visceral adipose tissue represents a major source of proinflammatory cytokines. The regulation of inflammation response in the adipose tissue is thus of crucial importance. We demonstrated that Regulated in development and DNA damage response-1 (REDD1) is involved in inflammation. REDD1 expression was increased in response to lipopolysaccharide (LPS) in bone marrow derived macrophages (BMDM) and in epidydimal adipose tissue...
August 1, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28666461/glyceollins-trigger-anti-proliferative-effects-through-estradiol-dependent-and-independent-pathways-in-breast-cancer-cells
#4
Sylvain Lecomte, Frederic Chalmel, François Ferriere, Frederic Percevault, Nicolas Plu, Christian Saligaut, Claire Surel, Marie Lelong, Theo Efstathiou, Farzad Pakdel
BACKGROUND: Estrogen receptors (ER) α and β are found in both women and men in many tissues, where they have different functions, including having roles in cell proliferation and differentiation of the reproductive tract. In addition to estradiol (E2), a natural hormone, numerous compounds are able to bind ERs and modulate their activities. Among these compounds, phytoestrogens such as isoflavones, which are found in plants, are promising therapeutics for several pathologies. Glyceollins are second metabolites of isoflavones that are mainly produced in soybean in response to an elicitor...
June 30, 2017: Cell Communication and Signaling: CCS
https://www.readbyqxmd.com/read/28620021/correction-for-wolff-et-al-cell-type-dependent-regulation-of-mtorc1-by-redd1-and-the-tumor-suppressors-tsc1-tsc2-and-lkb1-in-response-to-hypoxia
#5
Nicholas C Wolff, Silvia Vega-Rubin-de-Celis, Xian-Jin Xie, Diego H Castrillon, Wareef Kabbani, James Brugarolas
No abstract text is available yet for this article.
July 1, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28503190/essential-amino-acid-ingestion-alters-expression-of-genes-associated-with-amino-acid-sensing-transport-and-mtorc1-regulation-in-human-skeletal-muscle
#6
Ted G Graber, Michael S Borack, Paul T Reidy, Elena Volpi, Blake B Rasmussen
BACKGROUND: Amino acid availability stimulates protein synthesis via the mTORC1 (mechanistic target of rapamycin complex 1) signaling pathway. In response to an increase in cellular amino acid availability, translocation of cytosolic mTORC1 to the lysosomal surface is required to stimulate mTORC1 kinase activity. However, research elucidating the amino acid responsive mechanisms have thus far only been conducted in in vitro models. Our primary objective was to determine whether an increase in amino acid availability within human skeletal muscle in vivo would alter the expression of genes associated with amino acid sensing, transport and mTORC1 regulation...
2017: Nutrition & Metabolism
https://www.readbyqxmd.com/read/28367506/regulation-of-protein-and-mrna-expression-of-the-mtorc1-repressor-redd1-in-response-to-leucine-and-serum
#7
Adam J Black, Bradley S Gordon, Michael D Dennis, Leonard S Jefferson, Scot R Kimball
Expression of the mTORC1 repressor, Regulated in DNA Damage and Development 1 (REDD1), is elevated in skeletal muscle during various catabolic conditions including fasting, hindlimb immobilization, and sepsis. Conversely, REDD1 expression is suppressed by anabolic stimuli such as resistance exercise or nutrient consumption following a fast. Though it is known that nutrient consumption reduces REDD1 expression, it is largely unknown how nutrients and hormones individually contribute to the reduction in REDD1 expression...
December 2016: Biochemistry and Biophysics Reports
https://www.readbyqxmd.com/read/28342915/regulated-in-development-and-dna-damage-responses-1-redd1-links-stress-with-il-1%C3%AE-mediated-familial-mediterranean-fever-attack-through-autophagy-driven-neutrophil-extracellular-traps
#8
Panagiotis Skendros, Akrivi Chrysanthopoulou, François Rousset, Konstantinos Kambas, Athanasios Arampatzioglou, Alexandros Mitsios, Veronique Bocly, Theocharis Konstantinidis, Philippe Pellet, Iliana Angelidou, Eirini Apostolidou, Dimitrios Ritis, Victoria Tsironidou, Sotiris Galtsidis, Charalampos Papagoras, Dimitrios Stakos, Georgios Kouklakis, Vasiliki Dalla, Maria Koffa, Ioannis Mitroulis, Ioannis Theodorou, Konstantinos Ritis
BACKGROUND: Familial Mediterranean fever (FMF) is an IL-1β-dependent autoinflammatory disease caused by mutations of Mediterranean fever (MEFV) encoding pyrin and characterized by inflammatory attacks induced by physical or psychological stress. OBJECTIVE: We investigated the underlying mechanism that links stress-induced inflammatory attacks with neutrophil activation and release of IL-1β-bearing neutrophil extracellular traps (NETs) in patients with FMF. METHODS: RNA sequencing was performed in peripheral neutrophils from 3 patients with FMF isolated both during attacks and remission, 8 patients in remission, and 8 healthy subjects...
March 23, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28334504/regulated-in-development-and-dna-damage-response-1-deficiency-impairs-autophagy-and-mitochondrial-biogenesis-in-articular-cartilage-and-increases-the-severity-of-experimental-osteoarthritis
#9
Oscar Alvarez-Garcia, Tokio Matsuzaki, Merissa Olmer, Lars Plate, Jeffery W Kelly, Martin K Lotz
OBJECTIVE: Regulated in development and DNA damage response 1 (REDD1) is an endogenous inhibitor of mechanistic target of rapamycin (mTOR) that regulates cellular stress responses. REDD1 expression is decreased in aged and osteoarthritic (OA) cartilage, and it regulates mTOR signaling and autophagy in articular chondrocytes in vitro. This study was undertaken to investigate the effects of REDD1 deletion in vivo using a mouse model of experimental OA. METHODS: OA severity was histologically assessed in 4-month-old wild-type and REDD1(-/-) mice subjected to surgical destabilization of the medial meniscus (DMM)...
July 2017: Arthritis & Rheumatology
https://www.readbyqxmd.com/read/28332630/pml-nuclear-bodies-contribute-to-the-basal-expression-of-the-mtor-inhibitor-ddit4
#10
Jayme Salsman, Alex Stathakis, Ellen Parker, Dudley Chung, Livia E Anthes, Kara L Koskowich, Sara Lahsaee, Daniel Gaston, Kimberly R Kukurba, Kevin S Smith, Ian C Chute, Daniel Léger, Laura D Frost, Stephen B Montgomery, Stephen M Lewis, Christopher Eskiw, Graham Dellaire
The promyelocytic leukemia (PML) protein is an essential component of PML nuclear bodies (PML NBs) frequently lost in cancer. PML NBs coordinate chromosomal regions via modification of nuclear proteins that in turn may regulate genes in the vicinity of these bodies. However, few PML NB-associated genes have been identified. PML and PML NBs can also regulate mTOR and cell fate decisions in response to cellular stresses. We now demonstrate that PML depletion in U2OS cells or TERT-immortalized normal human diploid fibroblasts results in decreased expression of the mTOR inhibitor DDIT4 (REDD1)...
March 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28324785/-ub006-a-new-fatty-acid-synthase-inhibitor-and-cytotoxic-agent-without-anorexic-side-effects
#11
Kamil Makowski, Joan Francesc Mir, Paula Mera, Xavier Ariza, Guillermina Asins, Fausto G Hegardt, Laura Herrero, Jordi García, Dolors Serra
C75 is a synthetic anticancer drug that inhibits fatty acid synthase (FAS) and shows a potent anorexigenic side effect. In order to find new cytotoxic compounds that do not impact food intake, we synthesized a new family of C75 derivatives. The most promising anticancer compound among them was UB006 ((4SR,5SR)-4-(hydroxymethyl)-3-methylene-5-octyldihydrofuran-2(3H)-one). The effects of this compound on cytotoxicity, food intake and body weight were studied in UB006 racemic mixture and in both its enantiomers separately...
May 5, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28199842/the-mtor-and-pp2a-pathways-regulate-phd2-phosphorylation-to-fine-tune-hif1%C3%AE-levels-and-colorectal-cancer-cell-survival-under-hypoxia
#12
Giusy Di Conza, Sarah Trusso Cafarello, Stefan Loroch, Daniela Mennerich, Sofie Deschoemaeker, Mario Di Matteo, Manuel Ehling, Kris Gevaert, Hans Prenen, Rene Peiman Zahedi, Albert Sickmann, Thomas Kietzmann, Fabiola Moretti, Massimiliano Mazzone
Oxygen-dependent HIF1α hydroxylation and degradation are strictly controlled by PHD2. In hypoxia, HIF1α partly escapes degradation because of low oxygen availability. Here, we show that PHD2 is phosphorylated on serine 125 (S125) by the mechanistic target of rapamycin (mTOR) downstream kinase P70S6K and that this phosphorylation increases its ability to degrade HIF1α. mTOR blockade in hypoxia by REDD1 restrains P70S6K and unleashes PP2A phosphatase activity. Through its regulatory subunit B55α, PP2A directly dephosphorylates PHD2 on S125, resulting in a further reduction of PHD2 activity that ultimately boosts HIF1α accumulation...
February 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28115701/induction-of-dormancy-in-hypoxic-human-papillomavirus-positive-cancer-cells
#13
Karin Hoppe-Seyler, Felicitas Bossler, Claudia Lohrey, Julia Bulkescher, Frank Rösl, Lars Jansen, Arnulf Mayer, Peter Vaupel, Matthias Dürst, Felix Hoppe-Seyler
Oncogenic human papillomaviruses (HPVs) are closely linked to major human malignancies, including cervical and head and neck cancers. It is widely assumed that HPV-positive cancer cells are under selection pressure to continuously express the viral E6/E7 oncogenes, that their intracellular p53 levels are reconstituted on E6/E7 repression, and that E6/E7 inhibition phenotypically results in cellular senescence. Here we show that hypoxic conditions, as are often found in subregions of cervical and head and neck cancers, enable HPV-positive cancer cells to escape from these regulatory principles: E6/E7 is efficiently repressed, yet, p53 levels do not increase...
February 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27982685/responses-of-skeletal-muscle-hypertrophy-in-wistar-rats-to-different-resistance-exercise-models
#14
T F Luciano, S O Marques, B L Pieri, D R de Souza, L V Araújo, R T Nesi, D L Scheffer, V H Comin, R A Pinho, A P Muller, C T de Souza
This study aimed to compare the effects of three different resistance exercise models on the quadriceps muscle cross-sectional area, as well as on mTOR phosphorylation and other pivotal molecules involved in the upstream regulation of mTOR. Twenty-four male Wistar rats were divided into untrained (control), endurance resistance training, strength resistance training, and hypertrophy resistance training (HRT) groups (n=6). After 12 weeks of training, the red portion of the quadriceps was removed for histological and Western blot analyses...
May 4, 2017: Physiological Research
https://www.readbyqxmd.com/read/27922594/cacna1c-in-the-prefrontal-cortex-regulates-depression-related-behaviors-via-redd1
#15
Zeeba D Kabir, Anni S Lee, Caitlin E Burgdorf, Delaney K Fischer, Aditi M Rajadhyaksha, Ethan Mok, Bryant Rizzo, Richard C Rice, Kamalpreet Singh, Kristie T Ota, Danielle M Gerhard, Kathryn C Schierberl, Michael J Glass, Ronald S Duman, Anjali M Rajadhyaksha
The CACNA1C gene that encodes the L-type Ca(2+) channel (LTCC) Cav1.2 subunit has emerged as a candidate risk gene for multiple neuropsychiatric disorders including bipolar disorder, major depressive disorder, and schizophrenia, all marked with depression-related symptoms. Although cacna1c heterozygous (HET) mice have been previously reported to exhibit an antidepressant-like phenotype, the molecular and circuit-level dysfunction remains unknown. Here we report that viral vector-mediated deletion of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna1c HET mice using the sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST)...
September 2017: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
https://www.readbyqxmd.com/read/27913296/regulation-of-skeletal-muscle-insulin-stimulated-signaling-through-the-mek-redd1-mtor-axis
#16
Cory M Dungan, David L Williamson
Recent findings in adipocytes suggest that mitogen-activated protein kinase (MAPK)/extracellular-regulated signaling kinase (ERK) kinase 1/2 (MEK1/2) signaling regulates regulated in development and DNA damage 1 (REDD1) protein expression. Similarly, our previous work show that a lack of REDD1 protein expression, and associated hyperactive basal mechanistic target of rapamycin (mTOR) signaling, limits skeletal muscle's response to insulin. Therefore, we sought to determine: 1) if MEK1/2 inhibition is sufficient to reduce REDD1 protein expression and subsequently insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation via negative feedback of hyperactive mTOR in REDD1 wild-type (WT) mice and 2) if rapamycin-mediated mTOR inhibition is sufficient to improve IRS-1 tyrosine phosphorylation in REDD1 knockout (KO) mice...
January 22, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27909227/castration-alters-protein-balance-after-high-frequency-muscle-contraction
#17
Jennifer L Steiner, David H Fukuda, Michael L Rossetti, Jay R Hoffman, Bradley S Gordon
Resistance exercise increases muscle mass by shifting protein balance in favor of protein accretion. Androgens independently alter protein balance, but it is unknown whether androgens alter this measure after resistance exercise. To answer this, male mice were subjected to sham or castration surgery 7-8 wk before undergoing a bout of unilateral, high-frequency, electrically induced muscle contractions in the fasted or refed state. Puromycin was injected 30 min before euthanasia to measure protein synthesis...
February 1, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/27829135/macrophage-metabolism-shapes-angiogenesis-in-tumors
#18
COMMENT
Alberto Mantovani, Massimo Locati
In this issue, Wenes et al. (2016) show that REDD1, an mTOR inhibitor induced by hypoxia, enhances glycolysis in tumor-associated macrophages (TAMs). Metabolic competition for glucose between TAMs and endothelial cells leads to an abnormal, leaky vascular network. Targeting REDD1 normalizes glycolysis in TAMs, stabilizes the vascular network, and inhibits metastasis.
November 8, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27787518/glioblastoma-hypoxia-and-autophagy-a-survival-prone-m%C3%A3-nage-%C3%A3-trois
#19
REVIEW
Soha Jawhari, Marie-Hélène Ratinaud, Mireille Verdier
Glioblastoma multiforme is the most common and the most aggressive primary brain tumor. It is characterized by a high degree of hypoxia and also by a remarkable resistance to therapy because of its adaptation capabilities that include autophagy. This degradation process allows the recycling of cellular components, leading to the formation of metabolic precursors and production of adenosine triphosphate. Hypoxia can induce autophagy through the activation of several autophagy-related proteins such as BNIP3, AMPK, REDD1, PML, and the unfolded protein response-related transcription factors ATF4 and CHOP...
October 27, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27773694/macrophage-metabolism-controls-tumor-blood-vessel-morphogenesis-and-metastasis
#20
Mathias Wenes, Min Shang, Mario Di Matteo, Jermaine Goveia, Rosa Martín-Pérez, Jens Serneels, Hans Prenen, Bart Ghesquière, Peter Carmeliet, Massimiliano Mazzone
Hypoxic tumor-associated macrophages (TAMs) acquire angiogenic and immunosuppressive properties. Yet it remains unknown if metabolic changes influence these functions. Here, we argue that hypoxic TAMs strongly upregulate the expression of REDD1, a negative regulator of mTOR. REDD1-mediated mTOR inhibition hinders glycolysis in TAMs and curtails their excessive angiogenic response, with consequent formation of abnormal blood vessels. Accordingly, REDD1 deficiency in TAMs leads to the formation of smoothly aligned, pericyte-covered, functional vessels, which prevents vessel leakiness, hypoxia, and metastases...
November 8, 2016: Cell Metabolism
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