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endoplasmic reticulum stress

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https://www.readbyqxmd.com/read/28934387/mutations-in-tgm6-induce-the-unfolded-protein-response-in-sca35
#1
Debasmita Tripathy, Beatrice Vignoli, Nandini Ramesh, Maria Jose Polanco, Marie Coutelier, Christopher D Stephen, Marco Canossa, Marie-Lorraine Monin, Pascale Aeschlimann, Shannon Turberville, Daniel Aeschlimann, Jeremy D Schmahmann, Marios Hadjivassiliou, Alexandra Durr, Udai B Pandey, Maria Pennuto, Manuela Basso
Spinocerebellar ataxia type 35 (SCA35) is a rare autosomal-dominant neurodegenerative disease caused by mutations in the TGM6 gene, which codes for transglutaminase 6 (TG6). Mutations in TG6 induce cerebellar degeneration by an unknown mechanism. We identified seven patients bearing new mutations in TGM6. To gain insights into the molecular basis of mutant TG6-induced neurotoxicity, we analyzed all the seven new TG6 mutants and the five TG6 mutants previously linked to SCA35. We found that the wild-type (TG6-WT) protein mainly localized to the nucleus and perinuclear area, whereas five TG6 mutations showed nuclear depletion, increased accumulation in the perinuclear area, insolubility and loss of enzymatic function...
October 1, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28933787/blocking-autophagy-enhances-the-apoptotic-effect-of-18%C3%AE-glycyrrhetinic-acid-on-human-sarcoma-cells-via-endoplasmic-reticulum-stress-and-jnk-activation
#2
Shuying Shen, Menglu Zhou, Kangmao Huang, Yizheng Wu, Yan Ma, Jiying Wang, Jianjun Ma, Shunwu Fan
Sarcoma, a rare form of cancer, is unlike the much more common carcinomas as it occurs in a distinct type of tissue. The potent antitumor effects of 18β-glycyrrhetinic acid (GA), a novel naturally derived agent, have been demonstrated in various cancers. However, the effect of GA on human sarcoma, and the underlying mechanisms, remain to be elucidated. In the current study, we show that GA inhibits sarcoma cell proliferation by inducing G0/G1-phase arrest. Exposure to GA resulted in the activation of caspase-3, -8, and -9, indicating that GA induced apoptosis through both extrinsic and intrinsic pathways...
September 21, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28933598/autophagy-gene-atg7-regulates-ultraviolet-radiation-induced-inflammation-and-skin-tumorigenesis
#3
Lei Qiang, Ashley Sample, Christopher R Shea, Keyoumars Soltani, Kay F Macleod, Yu-Ying He
Macroautophagy (hereafter autophagy) is a cellular "self-eating" process that is implicated in many human cancers, where it can act to either promote or suppress tumorigenesis. However, the role of autophagy in regulation of inflammation during tumorigenesis remains unclear. Here we show that autophagy is induced in the epidermis by ultraviolet (UV) irradiation and autophagy gene Atg7 promoted UV-induced inflammation and skin tumorigenesis. Atg7 regulated UV-induced cytokine expression and secretion, and promoted Ptgs2/Cox-2 expression through both a CREB1/CREB-dependent cell autonomous mechanism and an IL1B/IL1β-dependent non-cell autonomous mechanism...
September 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28933591/suppression-of-chrn-endocytosis-by-carbonic-anhydrase-car3-in-the-pathogenesis-of-myasthenia-gravis
#4
Ailian Du, Shiqian Huang, Xiaonan Zhao, Kuan Feng, Shuangyan Zhang, Jiefang Huang, Xiang Miao, Fulvio Baggi, Rennolds S Ostrom, Yanyun Zhang, Xiangjun Chen, Congfeng Xu
Myasthenia gravis is an autoimmune disorder of the neuromuscular junction manifested as fatigable muscle weakness, which is typically caused by pathogenic autoantibodies against postsynaptic CHRN/AChR (cholinergic receptor nicotinic) in the endplate of skeletal muscle. Our previous studies have identified CA3 (carbonic anhydrase 3) as a specific protein insufficient in skeletal muscle from myasthenia gravis patients. In this study, we investigated the underlying mechanism of how CA3 insufficiency might contribute to myasthenia gravis...
September 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28933220/elucidation-of-gene-expression-patterns-in-the-brain-after-spinal-cord-injury
#5
Ahreum Baek, Sung-Rae Cho, Sung Hoon Kim
Spinal cord injury (SCI) is a devastating neurological disease. The pathophysiological mechanisms of SCI have been reported to be relevant to central nervous system injury such as brain injury. In this study, gene expression of the brain after SCI was elucidated using transcriptome analysis to characterize the temporal changes in global gene expression patterns in a SCI mouse model. Subjects were randomly classified into 3 groups: sham control, acute (3 h post-injury), and subacute (2 wk post-injury) groups...
July 2017: Cell Transplantation
https://www.readbyqxmd.com/read/28932945/necrostatin-1-mitigates-endoplasmic-reticulum-stress-after-spinal-cord-injury
#6
Shuang Wang, Jin Wu, Yu-Zhe Zeng, Song-Song Wu, Guo-Rong Deng, Zhi-Da Chen, Bin Lin
Necrostatin-1 (Nec-1) has been shown to inhibit necroptosis and convey a significant protective effect after spinal cord injury (SCI). This small molecule inhibitor may reduce tissue damage and restore neurological function by lessening mitochondrial injury after SCI and preserving energy homeostasis. However, the effects of Nec-1 on endoplasmic reticulum stress (ERS)-an important pathological consequence of SCI-are still not clear. The present study investigates the relationship between necroptosis and ERS in a rat model of SCI...
September 20, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28932194/h2s-induced-sulfhydration-biological-function-and-detection-methodology
#7
REVIEW
Da Zhang, Junbao Du, Chaoshu Tang, Yaqian Huang, Hongfang Jin
At appropriate concentrations, hydrogen sulfide, a well-known gasotransmitter, plays important roles in both physiology and pathophysiology. Increasing evidence suggests that modifying thiol groups of specific cysteines in target proteins via sulfhydration or persulfidation is one of the important mechanisms responsible for the biological functions of hydrogen sulfide. A variety of key proteins of different cellular pathways in mammals have been reported to be sulfhydrated by hydrogen sulfide to participate and regulate the processes of cell survival/death, cell differentiation, cell proliferation/hypertrophy, cellular metabolism, mitochondrial bioenergetics/biogenesis, endoplasmic reticulum stress, vasorelaxtion, inflammation, oxidative stress, etc...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28931802/hepatitis-c-virus-infection-increases-c-jun-n-terminal-kinase-jnk-phosphorylation-and-accentuates-hepatocyte-lipoapoptosis
#8
Hiroko Takaki, Yuko Akazawa, Youko Kido, Mami Morishita, Takuya Honda, Hidetaka Shibata, Satoshi Miuma, Hisamitsu Miyaaki, Naota Taura, Hisayoshi Kondo, Kazuhiko Nakao
BACKGROUND Hepatitis C virus (HCV) infection and metabolic diseases including nonalcoholic steatohepatitis (NASH) exhibit a complex interplay. Although free fatty acid-mediated apoptosis is a prominent feature of NASH, the impact of HCV infection on hepatocyte lipotoxicity has remained largely unexplored. The study aimed at identifying whether infection by HCV affected the apoptotic pathway in hepatocytes during fatty acid assault. MATERIAL AND METHODS OR6 cells, which are derived from human hepatocellular carcinoma Huh-7 cells and harbor a full-length HCV RNA genome replication system, were treated with palmitate...
September 21, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28931068/erk1-2-signalling-protects-against-apoptosis-following-endoplasmic-reticulum-stress-but-cannot-provide-long-term-protection-against-bax-bak-independent-cell-death
#9
Nicola J Darling, Kathryn Balmanno, Simon J Cook
Disruption of protein folding in the endoplasmic reticulum (ER) causes ER stress. Activation of the unfolded protein response (UPR) acts to restore protein homeostasis or, if ER stress is severe or persistent, drive apoptosis, which is thought to proceed through the cell intrinsic, mitochondrial pathway. Indeed, cells that lack the key executioner proteins BAX and BAK are protected from ER stress-induced apoptosis. Here we show that chronic ER stress causes the progressive inhibition of the extracellular signal-regulated kinase (ERK1/2) signalling pathway...
2017: PloS One
https://www.readbyqxmd.com/read/28930750/tauroursodeoxycholic-acid-reduces-arterial-stiffness-and-improves-endothelial-dysfunction-in-type-2-diabetic-mice
#10
Micah L Battson, Dustin M Lee, Dillon K Jarrell, Shoufei Hou, Kayl E Ecton, Anna B Phan, Christopher L Gentile
BACKGROUND/AIMS: Endoplasmic reticulum (ER) stress has emerged as a potential mechanism contributing to diabetes and its comorbidities. However, the importance of ER stress in diabetic vascular dysfunction is unclear. The purpose of this study was to examine the effects of the ER stress inhibitor, tauroursodeoxycholic acid (TUDCA), on arterial stiffness and endothelial dysfunction in type 2 diabetic mice. METHODS: Carotid and mesenteric artery endothelial function were assessed via ex vivo pressure myography, and arterial stiffness was measured by aortic pulse wave velocity...
September 21, 2017: Journal of Vascular Research
https://www.readbyqxmd.com/read/28930172/rhein-induces-oxidative-stress-and-apoptosis-in-mouse-blastocysts-and-has-immunotoxic-effects-during-embryonic-development
#11
Chien-Hsun Huang, Wen-Hsiung Chan
Rhein, a glucoside chemical compound found in a traditional Chinese medicine derived from the roots of rhubarb, induces cell apoptosis and is considered to have high potential as an antitumor drug. Several previous studies showed that rhein can inhibit cell proliferation and trigger mitochondria-related or endoplasmic reticulum (ER) stress-dependent apoptotic processes. However, the side effects of rhein on pre- and post-implantation embryonic development remain unclear. Here, we show that rhein has cytotoxic effects on blastocyst-stage mouse embryos and induces oxidative stress and immunotoxicity in mouse fetuses...
September 20, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28929569/evaluation-of-chemical-chaperones-based-on-the-monitoring-of-bip-promoter-activity-and-visualization-of-extracellular-vesicles-by-real-time-bioluminescence-imaging
#12
Tomohisa Horibe, Nanako Okushima, Aya Torisawa, Ryutaro Akiyoshi, Yoko Hatta-Ohashi, Hirobumi Suzuki, Koji Kawakami
It is known that endoplasmic reticulum (ER) stress in cells and extracellular vesicles (EVs) plays a significant role in cancer cells, therefore the evaluation of compounds that can regulate ER stress and EV secretion would be a suitable system for further screening and development of new drugs. In this study, we evaluated chemical chaperones derived from natural products based on monitoring Bip/GRP78 promoter activity during cancer cell growth, at the level of the single cell, by a bioluminescence microscopy system that had several advantages compared with fluorescence imaging...
September 20, 2017: Luminescence: the Journal of Biological and Chemical Luminescence
https://www.readbyqxmd.com/read/28929337/escherichia-coli-aggravates-endoplasmic-reticulum-stress-and-triggers-chop-dependent-apoptosis-in-weaned-pigs
#13
Qian Jiang, Shuai Chen, Wenkai Ren, Gang Liu, Kang Yao, Guoyao Wu, Yulong Yin
Intestinal cells can sense the presence of pathogens and trigger many important signaling pathways to maintain tissue homeostasis and normal function. Escherichia coli and lipopolysaccharides (LPS) are the main pathogenic factors of intestinal disease in pigs. However, the roles of endoplasmic reticulum stress (ERS) and its mediated apoptosis in intestinal malfunction induced by E. coli or LPS remain unclear. In the present study, we aimed to evaluate whether ERS could be activated by E. coli fed to piglets and whether the underlying mechanisms of this disease process could be exploited...
September 19, 2017: Amino Acids
https://www.readbyqxmd.com/read/28929194/adapting-secretory-proteostasis-and-function-through-the-unfolded-protein-response
#14
Madeline Y Wong, Andrew S DiChiara, Patreece H Suen, Kenny Chen, Ngoc-Duc Doan, Matthew D Shoulders
Cells address challenges to protein folding in the secretory pathway by engaging endoplasmic reticulum (ER)-localized protective mechanisms that are collectively termed the unfolded protein response (UPR). By the action of the transmembrane signal transducers IRE1, PERK, and ATF6, the UPR induces networks of genes whose products alleviate the burden of protein misfolding. The UPR also plays instructive roles in cell differentiation and development, aids in the response to pathogens, and coordinates the output of professional secretory cells...
September 20, 2017: Current Topics in Microbiology and Immunology
https://www.readbyqxmd.com/read/28928733/crosstalk-between-signaling-pathways-in-pemphigus-a-role-for-endoplasmic-reticulum-stress-in-p38-mitogen-activated-protein-kinase-activation
#15
Gabriel A Cipolla, Jong Kook Park, Robert M Lavker, Maria Luiza Petzl-Erler
Pemphigus consists of a group of chronic blistering skin diseases mediated by autoantibodies (autoAbs). The dogma that pemphigus is caused by keratinocyte dissociation (acantholysis) as a distinctive and direct consequence of the presence of autoAb targeting two main proteins of the desmosome-desmoglein (DSG) 1 and/or DSG3-has been put to the test. Several outside-in signaling events elicited by pemphigus autoAb in keratinocytes have been described, among which stands out p38 mitogen-activated protein kinase (p38 MAPK) engagement and its apoptotic effect on keratinocytes...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28928238/talk-1-channels-control-%C3%AE-cell-endoplasmic-reticulum-ca-2-homeostasis
#16
Nicholas C Vierra, Prasanna K Dadi, Sarah C Milian, Matthew T Dickerson, Kelli L Jordan, Patrick Gilon, David A Jacobson
Ca(2+) handling by the endoplasmic reticulum (ER) serves critical roles in controlling pancreatic β cell function and becomes perturbed during the pathogenesis of diabetes. ER Ca(2+) homeostasis is determined by ion movements across the ER membrane, including K(+) flux through K(+) channels. We demonstrated that K(+) flux through ER-localized TALK-1 channels facilitated Ca(2+) release from the ER in mouse and human β cells. We found that β cells from mice lacking TALK-1 exhibited reduced basal cytosolic Ca(2+) and increased ER Ca(2+) concentrations, suggesting reduced ER Ca(2+) leak...
September 19, 2017: Science Signaling
https://www.readbyqxmd.com/read/28928140/selenoprotein-t-is-a-novel-ost-subunit-that-regulates-upr-signaling-and-hormone-secretion
#17
Abdallah Hamieh, Dorthe Cartier, Houssni Abid, André Calas, Carole Burel, Christine Bucharles, Cedric Jehan, Luca Grumolato, Marc Landry, Patrice Lerouge, Youssef Anouar, Isabelle Lihrmann
Selenoprotein T (SelT) is a recently characterized thioredoxin-like protein whose expression is very high during development, but is confined to endocrine tissues in adulthood where its function is unknown. We report here that SelT is required for adaptation to the stressful conditions of high hormone level production in endocrine cells. Using immunofluorescence and TEM immunogold approaches, we find that SelT is expressed at the endoplasmic reticulum membrane in all hormone-producing pituitary cell types. SelT knockdown in corticotrope cells promotes unfolded protein response (UPR) and ER stress and lowers endoplasmic reticulum-associated protein degradation (ERAD) and hormone production...
September 19, 2017: EMBO Reports
https://www.readbyqxmd.com/read/28927431/role-of-the-sigma-1-receptor-chaperone-in-rod-and-cone-photoreceptor-degenerations-in-a-mouse-model-of-retinitis-pigmentosa
#18
Huan Yang, Yingmei Fu, Xinying Liu, Pawan K Shahi, Timur A Mavlyutov, Jun Li, Annie Yao, Steven Z-W Guo, Bikash R Pattnaik, Lian-Wang Guo
BACKGROUND: Retinitis pigmentosa (RP) is the most common inherited retinal degenerative disease yet with no effective treatment available. The sigma-1 receptor (S1R), a ligand-regulated chaperone, emerges as a potential retina-protective therapeutic target. In particular, pharmacological activation of S1R was recently shown to rescue cones in the rd10 mouse, a rod Pde6b mutant that recapitulates the RP pathology of autonomous rod degeneration followed by secondary death of cones. The mechanisms underlying the S1R protection for cones are not understood in detail...
September 19, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28923079/endoplasmic-reticulum-stress-cooperates-with-toll-like-receptor-ligation-in-driving-activation-of-rheumatoid-arthritis-fibroblast-like-synoviocytes
#19
Pawel A Kabala, Chiara Angiolilli, Nataliya Yeremenko, Aleksander M Grabiec, Barbara Giovannone, Desiree Pots, Timothy R Radstake, Dominique Baeten, Kris A Reedquist
BACKGROUND: Endoplasmic reticulum (ER) stress has proinflammatory properties, and transgenic animal studies of rheumatoid arthritis (RA) indicate its relevance in the process of joint destruction. Because currently available studies are focused primarily on myeloid cells, we assessed how ER stress might affect the inflammatory responses of stromal cells in RA. METHODS: ER stress was induced in RA fibroblast-like synoviocytes (FLS), dermal fibroblasts, and macrophages with thapsigargin or tunicamycin alone or in combination with Toll-like receptor (TLR) ligands, and gene expression and messenger RNA (mRNA) stability was measured by quantitative polymerase chain reaction...
September 18, 2017: Arthritis Research & Therapy
https://www.readbyqxmd.com/read/28922472/mirna-506-promotes-primary-biliary-cholangitis-like-features-in-cholangiocytes-and-immune-activation
#20
Oihane Erice, Patricia Munoz-Garrido, Javier Vaquero, Maria J Perugorria, Maite G Fernandez-Barrena, Elena Saez, Alvaro Santos-Laso, Ander Arbelaiz, Raul Jimenez-Agüero, Joaquin Fernandez-Irigoyen, Enrique Santamaria, Verónica Torrano, Arkaitz Carracedo, Meenakshisundaram Ananthanarayanan, Marco Marzioni, Jesus Prieto, Ulrich Beuers, Ronald P Oude Elferink, Nicholas F LaRusso, Luis Bujanda, Jose J G Marin, Jesus M Banales
Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease associated with autoimmune phenomena targeting intrahepatic bile duct cells (cholangiocytes). Although PBC etiopathogenesis still remains obscure, development of anti-mitochondrial auto-antibodies against pyruvate dehydrogenase complex-E2 (PDC-E2) is a common feature. MicroRNA (miR) dysregulation occurs in liver and immune cells of PBC patients, but their functional relevance is largely unknown. We previously reported that miR-506 is overexpressed in PBC cholangiocytes and directly targets both Cl(-) /HCO3(-) anion exchanger 2 (AE2) and type III inositol 1,4,5-trisphosphate receptor (InsP3R3), leading to cholestasis...
September 18, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
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