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https://www.readbyqxmd.com/read/29712770/redd1-autophagy-pathway-is-associated-with-neutrophil-driven-il-1%C3%AE-inflammatory-response-in-active-ulcerative-colitis
#1
Iliana Angelidou, Akrivi Chrysanthopoulou, Alexandros Mitsios, Stella Arelaki, Athanasios Arampatzioglou, Konstantinos Kambas, Dimitrios Ritis, Victoria Tsironidou, Ioannis Moschos, Vasiliki Dalla, Dimitrios Stakos, Georgios Kouklakis, Ioannis Mitroulis, Konstantinos Ritis, Panagiotis Skendros
Infiltration of neutrophils into colonic mucosa has been associated with the severity of ulcerative colitis (UC). We investigated the effect of disease microenvironment on the release of neutrophil extracellular traps (NETs) as well as the involved mechanisms in NETosis and whether certain NET proteins are correlated with disease phenotype. Peripheral blood neutrophils, sera, and colonic tissue were collected from treatment-naive and mesalazine-treated patients with active UC, treatment-naive patients with active Crohn's disease, patients suffering from infectious colitis, or healthy individuals (controls)...
April 30, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29596905/rapamycin-modulates-glucocorticoid-receptor-function-blocks-atrophogene-redd1-and-protects-skin-from-steroid-atrophy
#2
Ekaterina Lesovaya, Shivani Agarwal, Ben Readhead, Elena Vinokour, Gleb Baida, Pankaj Bhalla, Kirill Kirsanov, Marianna Yakubovskaya, Leonidas C Platanias, Joel T Dudley, Irina Budunova
Glucocorticoids have excellent therapeutic properties; however, they cause significant adverse atrophogenic effects. mTOR complex 1 (mTORC1) inhibitor, REDD1 (regulated in development and DNA damage 1), has been recently identified as a key mediator of glucocorticoid-induced atrophy. We performed computational screening of connectivity map database (CMAP) to identify putative REDD1 inhibitors. The top selected candidates included Rapamycin, which was unexpected because it inhibits pro-proliferative mTOR signaling...
March 26, 2018: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29483210/egf-receptor-and-mtorc1-are-novel-therapeutic-targets-in-nonseminomatous-germ-cell-tumors
#3
Kenneth S Chen, Nicholas J Fustino, Abhay A Shukla, Emily K Stroup, Albert Budhipramono, Christina Ateek, Sarai H Stuart, Kiyoshi Yamaguchi, Payal Kapur, A Lindsay Frazier, Lawrence Lum, Leendert H J Looijenga, Theodore W Laetsch, Dinesh Rakheja, James F Amatruda
Germ cell tumors (GCT) are malignant tumors that arise from pluripotent embryonic germ cells and occur in children and young adults. GCTs are treated with cisplatin-based regimens which, while overall effective, fail to cure all patients and cause significant adverse late effects. The seminoma and nonseminoma forms of GCT exhibit distinct differentiation states, clinical behavior, and response to treatment; however, the molecular mechanisms of GCT differentiation are not fully understood. We tested whether the activity of the mTORC1 and MAPK pathways were differentially active in the two classes of GCT...
May 2018: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/29386513/hexokinase-2-depletion-inhibits-glycolysis-and-induces-oxidative-phosphorylation-in-hepatocellular-carcinoma-and-sensitizes-to-metformin
#4
Dannielle DeWaal, Veronique Nogueira, Alexander R Terry, Krushna C Patra, Sang-Min Jeon, Grace Guzman, Jennifer Au, Christopher P Long, Maciek R Antoniewicz, Nissim Hay
Hepatocellular carcinoma (HCC) cells are metabolically distinct from normal hepatocytes by expressing the high-affinity hexokinase (HK2) and suppressing glucokinase (GCK). This is exploited to selectively target HCC. Hepatic HK2 deletion inhibits tumor incidence in a mouse model of hepatocarcinogenesis. Silencing HK2 in human HCC cells inhibits tumorigenesis and increases cell death, which cannot be restored by GCK or mitochondrial binding deficient HK2. Upon HK2 silencing, glucose flux to pyruvate and lactate is inhibited, but TCA fluxes are maintained...
January 31, 2018: Nature Communications
https://www.readbyqxmd.com/read/29322792/krasg12d-loh-promotes-malignant-biological-behavior-and-energy-metabolism-of-pancreatic-ductal-adenocarcinoma-cells-through-the-mtor-signaling-pathway
#5
X Shen, L G Chang, M Y Hu, D Yan, L N Zhou, Y Ma, S K Ling, Y Q Fu, S Y Zhang, B Kong, P L Huang
Oncogenic Kras with loss of heterozygosity (LOH) is frequently detected in various tumours. However, the exact function and mechanism by which KrasG12D-LOH operates remain unclear. Therefore, the current study investigated the effect of KrasG12D-LOH on the malignant phenotype of pancreatic ductal adenocarcinoma (PDAC) cells. Our investigation revealed that KrasG12D-LOH is associated with increased proliferation, invasion and reduced apoptosis in PDAC cells. The results also exhibited enhanced glycolytic phenotype of KrasG12D-LOH PDAC cells...
2018: Neoplasma
https://www.readbyqxmd.com/read/29230965/prevention-of-chemotherapy-induced-cachexia-by-acvr2b-ligand-blocking-has-different-effects-on-heart-and-skeletal-muscle
#6
Juha J Hulmi, Tuuli A Nissinen, Markus Räsänen, Joni Degerman, Juulia H Lautaoja, Karthik Amudhala Hemanthakumar, Janne T Backman, Olli Ritvos, Mika Silvennoinen, Riikka Kivelä
BACKGROUND: Toxicity of chemotherapy on skeletal muscles and the heart may significantly contribute to cancer cachexia, mortality, and decreased quality of life. Doxorubicin (DOX) is an effective cytostatic agent, which unfortunately has toxic effects on many healthy tissues. Blocking of activin receptor type IIB (ACVR2B) ligands is an often used strategy to prevent skeletal muscle loss, but its effects on the heart are relatively unknown. METHODS: The effects of DOX treatment with or without pre-treatment with soluble ACVR2B-Fc (sACVR2B-Fc) were investigated...
December 11, 2017: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/29208245/mammalian-target-of-rapamycin-signaling-is-a-mechanistic-link-between-increased-endoplasmic-reticulum-stress-and-autophagy-in-the-placentas-of-pregnancies-complicated-by-growth-restriction
#7
Tai-Ho Hung, T'sang-T'ang Hsieh, Chung-Pu Wu, Meng-Jen Li, Yi-Lin Yeh, Szu-Fu Chen
INTRODUCTION: Increased endoplasmic reticulum (ER) stress and autophagy have been noted in the placentas of pregnancies complicated by idiopathic intrauterine growth restriction (IUGR); however, the cause of these phenomena remains unclear. We surmised that oxygen-glucose deprivation (OGD) may increase ER stress and autophagy and that mammalian target of rapamycin (mTOR) signaling is involved in regulating placental ER stress and autophagy in pregnancies complicated by IUGR. METHODS: We obtained placentas from women with normal term pregnancies and pregnancies complicated by IUGR to compare ER stress, mTOR signaling, and levels of autophagy-related proteins between the two groups and used primary cytotrophoblast cells treated with or without salubrinal (an ER stress inhibitor), MHY1485 (an mTOR activator), or rapamycin (an mTOR inhibitor) to investigate the effects of OGD on ER stress, mTOR activity, and autophagy levels in vitro...
December 2017: Placenta
https://www.readbyqxmd.com/read/29074598/deletion-of-the-akt-mtorc1-repressor-redd1-prevents-visual-dysfunction-in-a-rodent-model-of-type-1-diabetes
#8
William P Miller, Chen Yang, Maria L Mihailescu, Joshua A Moore, Weiwei Dai, Alistair J Barber, Michael D Dennis
Diabetes-induced visual dysfunction is associated with significant neuroretinal cell death. The current study was designed to investigate the role of the Protein Regulated in Development and DNA Damage Response 1 (REDD1) in diabetes-induced retinal cell death and visual dysfunction. We recently demonstrated that REDD1 protein expression was elevated in response to hyperglycemia in the retina of diabetic rodents. REDD1 is an important regulator of Akt and mammalian target of rapamycin and as such plays a key role in neuronal function and survival...
January 2018: Diabetes
https://www.readbyqxmd.com/read/28978511/chronic-stress-inhibits-growth-and-induces-proteolytic-mechanisms-through-two-different-nonoverlapping-pathways-in-the-skeletal-muscle-of-a-teleost-fish
#9
Cristián A Valenzuela, Rodrigo Zuloaga, Luis Mercado, Ingibjörg Eir Einarsdottir, Björn Thrandur Björnsson, Juan Antonio Valdés, Alfredo Molina
Chronic stress detrimentally affects animal health and homeostasis, with somatic growth, and thus skeletal muscle, being particularly affected. A detailed understanding of the underlying endocrine and molecular mechanisms of how chronic stress affects skeletal muscle growth remains lacking. To address this issue, the present study assessed primary (plasma cortisol), secondary (key components of the GH/IGF system, muscular proteolytic pathways, and apoptosis), and tertiary (growth performance) stress responses in fine flounder ( Paralichthys adspersus) exposed to crowding chronic stress...
January 1, 2018: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28968688/mir-181a-participates-in-contextual-fear-memory-formation-via-activating-mtor-signaling-pathway
#10
Xu-Feng Xu, Xu Jing, Hui-Xian Ma, Rong-Rong Yuan, Qing Dong, Jun-Lu Dong, Xiao-Fei Han, Zhe-Yu Chen, Xiang-Zhi Li, Yue Wang
Long-term memory formation has been proven to require gene expression and new protein synthesis. MicroRNAs (miRNAs), as an endogenous small non-coding RNAs, inhibit the expression of their mRNA targets, through which involve in new memory formation. In this study, elevated miR-181a levels were found to be responsible for hippocampal contextual fear memory consolidation. Using a luciferase reporter assay, we indicated that miR-181a targets 2 upstream molecules of mTOR pathway, namely, PRKAA1 and REDD1. Upregulated miR-181a can downregulate the PRKAA1 and REDD1 protein levels and promote mTOR activity to facilitate hippocampal fear memory consolidation...
August 22, 2017: Cerebral Cortex
https://www.readbyqxmd.com/read/28953980/influenza-virus-differentially-activates-mtorc1-and-mtorc2-signaling-to-maximize-late-stage-replication
#11
Sharon K Kuss-Duerkop, Juan Wang, Ignacio Mena, Kris White, Giorgi Metreveli, Ramanavelan Sakthivel, Miguel A Mata, Raquel Muñoz-Moreno, Xiang Chen, Florian Krammer, Michael S Diamond, Zhijian J Chen, Adolfo García-Sastre, Beatriz M A Fontoura
Influenza A virus usurps host signaling factors to regulate its replication. One example is mTOR, a cellular regulator of protein synthesis, growth and motility. While the role of mTORC1 in viral infection has been studied, the mechanisms that induce mTORC1 activation and the substrates regulated by mTORC1 during influenza virus infection have not been established. In addition, the role of mTORC2 during influenza virus infection remains unknown. Here we show that mTORC2 and PDPK1 differentially phosphorylate AKT upon influenza virus infection...
September 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28899858/redd1-induction-regulates-the-skeletal-muscle-gene-expression-signature-following-acute-aerobic-exercise
#12
Bradley S Gordon, Jennifer L Steiner, Michael L Rossetti, Shuxi Qiao, Leif W Ellisen, Subramaniam S Govindarajan, Alexey M Eroshkin, David 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...
December 1, 2017: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/28767526/exercise-protects-skeletal-muscle-during-chronic-doxorubicin-administration
#13
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: This study aimed to assess the ability for exercise training performed before and during biweekly 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)...
December 2017: Medicine and Science in Sports and Exercise
https://www.readbyqxmd.com/read/28765650/implication-of-redd1-in-the-activation-of-inflammatory-pathways
#14
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
#15
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
#16
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
#17
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
#18
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
#19
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...
November 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
#20
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
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