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https://www.readbyqxmd.com/read/27915415/exendin-4-protects-huvecs-from-tunicamycin-induced-apoptosis-via-inhibiting-the-ire1a-jnk-caspase-3-pathway
#1
Li Wu, XiaoYing Liu, LinXi Wang, YanPing Wang, LiJing Wang, BinBin Guan, Zhou Chen, LiBin Liu
PURPOSE: The abnormal increase of apoptosis of endothelial cells induced by endoplasmic reticulum stress is a significant factor for vascular disease, especially for atherosclerosis. Protecting endothelial cells from endoplasmic reticulum stress is a crucial strategies to combate these diseases. The goal of this study was to explore the effect of Exendin-4, a glucagon-like peptide-1 receptor agonist, on tunicamycin-induced apoptosis in human umbilical vein endothelial cells. METHODS: All studies were performed in primary human umbilical vein endothelial cells treated with tunicamycin with or without Exendin-4 pretreatment...
December 3, 2016: Endocrine
https://www.readbyqxmd.com/read/27909053/endoplasmic-reticulum-stress-and-ca2-depletion-differentially-modulate-the-sterol-regulatory-protein-pcsk9-to-control-lipid-metabolism
#2
Paul Lebeau, Ali Al-Hashimi, Sudesh Sood, Sarka Lhotak, Pei Yu, Gabriel Gyulay, Guillaume Pare, S R Wayne Chen, Bernardo Trigatti, Annik Prat, Nabil Seidah, Richard C Austin
Accumulating evidence implicates endoplasmic reticulum (ER) stress as a mediator of impaired lipid metabolism, thereby contributing to fatty liver disease and atherosclerosis. Previous studies demonstrated that ER stress can activate the sterol regulatory element-binding protein-2 (SREBP2), an ER localized transcription factor that directly upregulates sterol-regulatory genes, including PCSK9. Given that PCSK9 contributes to atherosclerosis by targeting low-density lipoprotein (LDL) receptor (LDLR) degradation, our present study investigates a novel mechanism by which ER stress plays a role in lipid metabolism by examining its ability to modulate PCSK9 expression...
December 1, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27895089/oxidized-high-density-lipoprotein-induces-macrophage-apoptosis-via-toll-like-receptor-4-dependent-chop-pathway
#3
Shutong Yao, Hua Tian, Li Zhao, Jinguo Li, Libo Yang, Feng Yue, Yanyan Li, Peng Jiao, Nana Yang, Yiwei Wang, Xiangjian Zhang, Shucun Qin
Oxidized high-density lipoprotein (ox-HDL), unlike native HDL that exerts antiatherogenic effects, plays a proatherogenic role. However, the underlying mechanisms are not completely understood. This study was designed to explore the inductive effect of ox-HDL on endoplasmic reticulum (ER) stress-C/EBP homologous protein (CHOP)-mediated macrophage apoptosis and its upstream mechanisms. Our results showed that ox-HDL could be ingested by macrophages, causing intracellular lipid accumulation. Like tunicamycin (an ER stress inducer), ox-HDL induced macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase and eukaryotic translation initiation factor 2α, and upregulation of glucose regulated protein 78 and CHOP, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and CHOP gene silencing...
November 28, 2016: Journal of Lipid Research
https://www.readbyqxmd.com/read/27894854/decreased-level-of-endogenous-ghrelin-is-involved-in-the-progression-of-lung-injury-induced-by-oleic-acid
#4
Zhijun Liu, Ting Yu, Haitao Yang, Xiuli Tian, Linlin Feng
AIMS: Acute lung injury (ALI) is associated with excessive mortality and lacks appropriate therapy. Ghrelin is a novel peptide that protects the lung against ALI. This study aimed to investigate the role of endogenous ghrelin in the pathogenesis of ALI. MAIN METHODS: We used a rat oleic acid (OA)-induced ALI model. Pulmonary impairment was detected by hematoxylin and eosin (HE) staining, lung mechanics, wet/dry weight ratio, and arterial blood gas analysis. Plasma and lung content of ghrelin was examined by ELISA, and mRNA expression of ghrelin was measured by quantitative real-time PCR...
November 25, 2016: Life Sciences
https://www.readbyqxmd.com/read/27886513/a-potential-role-for-endoplasmic-reticulum-stress-in-progesterone-deficiency-in-obese-women
#5
Nozomi Takahashi, Miyuki Harada, Yasushi Hirota, Lin Zhao, Jerilee Mk Azhary, Osamu Yoshino, Gentaro Izumi, Tetsuya Hirata, Kaori Koga, Osamu Wada-Hiraike, Tomoyuki Fujii, Yutaka Osuga
Obesity in reproductive-aged women is associated with shorter luteal phase and lower progesterone levels. Lipid accumulation in follicles of obese women compromises endoplasmic reticulum (ER) function, activating ER stress in granulosa cells. We hypothesized that ER stress activation in granulosa-lutein cells (GLCs) would modulate progesterone production and contribute to obesity-associated progesterone deficiency. Pretreatment with an ER stress inducer, tunicamycin or thapsigargin, inhibited human chorionic gonadotropin (hCG)-stimulated progesterone production in cultured human GLCs...
November 25, 2016: Endocrinology
https://www.readbyqxmd.com/read/27885588/a-mouse-model-reveals-that-mfsd2a-is-critical-for-unfolded-protein-response-upon-exposure-to-tunicamycin
#6
Hiroshi Moritake, Megumi Obara, Yusuke Saito, Ayako Kashimada, Masatoshi Takagi, Megumi Funakoshi-Tago, Tomofusa Fukuyama, Mikio Yoshioka, Akira Inoue, Hiroyuki Komatsu, Hideki Nishitoh, Hiroaki Kataoka, Hiroyuki Nunoi
Major facilitator superfamily domain containing 2a (Mfsd2a) is a member of the major facilitator superfamily. Mfsd2a functions as a transporter for docosahexaenoic acid and also plays a role in the unfolded protein response (UPR) upon tunicamycin (TM) exposure. UPR is involved in the pathogenesis of various human diseases. TM and thapsigargin are representative experimental reagents that induce UPR. To elucidate the detailed function of Mfsd2a in UPR in vivo, we generated Mfsd2a-deficient mice and investigated the role of Mfsd2a during UPR induced by TM or thapsigargin...
November 24, 2016: Human Cell
https://www.readbyqxmd.com/read/27882945/adiponectin-reduces-er-stress-induced-apoptosis-through-ppar%C3%AE-transcriptional-regulation-of-atf2-in-mouse-adipose
#7
Zhenjiang Liu, Lu Gan, Tianjiao Wu, Fei Feng, Dan Luo, Huihui Gu, Shimin Liu, Chao Sun
Adiponectin is a cytokine produced predominantly by adipose tissue and correlates with glucose and lipid homeostasis. However, the effects of adiponectin on endoplasmic reticulum (ER) stress and apoptosis of adipose tissue remain elusive. In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Moreover, ER stress-triggered adipocyte apoptosis by increasing cellular FFA level and Ca(2+) level...
November 24, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27870947/subcellular-localization-of-the-flt3-itd-oncogene-plays-a-significant-role-in-the-production-of-nox-and-p22-phox-derived-reactive-oxygen-species-in-acute-myeloid-leukemia
#8
Jennifer N Moloney, Joanna Stanicka, Thomas G Cotter
Internal tandem duplication of the juxtamembrane domain of FMS-like tyrosine kinase 3 (FLT3-ITD) receptor is the most prevalent FLT3 mutation accounting for 20% of acute myeloid leukemia (AML) patients. FLT3-ITD mutation results in ligand-independent constitutive activation of the receptor at the plasma membrane and 'impaired trafficking' of the receptor in compartments of the endomembrane system, such as the endoplasmic reticulum (ER). FLT3-ITD expressing cells have been shown to generate increased levels of reactive oxygen species (ROS), in particular NADPH oxidase (NOX)-generated ROS which act as pro-survival signals...
November 11, 2016: Leukemia Research
https://www.readbyqxmd.com/read/27862269/arp2-3-complex-and-mps3-are-required-for-regulation-of-ribosome-biosynthesis-in-the-secretory-stress-response
#9
Yukari Yabuki, Masako Katayama, Yushi Kodama, Akiko Sakamoto, Ayumi Yatsuhashi, Kouichi Funato, Keiko Mizuta
Secretory defects cause transcriptional repression of ribosome biogenesis in Saccharomyces cerevisiae. However, the molecular mechanism underlying secretory defect-induced transcriptional repression of ribosome biogenesis remains to be fully elucidated. In this study, we demonstrated that the Arp2/3 complex was required for reduction of ribosome protein gene expression in response to defective secretion by addition of tunicamycin. Two cmd1 mutants, cmd1-228 and cmd1-239 that cause mislocalization of calmodulin and defective mitotic spindle formation, respectively, fail to interact with Arc35, a component of the Arp2/3 complex...
November 10, 2016: Yeast
https://www.readbyqxmd.com/read/27856453/rasgrf-couples-nox4-dependent-endoplasmic-reticulum-signaling-to-ras
#10
Ru Feng Wu, Chengxu Liao, Hadi Hatoum, Guosheng Fu, Christhiaan D Ochoa, Lance S Terada
OBJECTIVES: In response to endoplasmic reticulum (ER) stress, endothelial cells initiate corrective pathways such as the unfolded protein response. Recent studies suggest that reactive oxygen species produced on the ER may participate in homeostatic signaling through Ras in response to ER stress. We sought to identify mechanisms responsible for this focal signaling pathway. APPROACH AND RESULTS: In endothelial cells, we found that ER stress induced by tunicamycin activates the NADPH oxidase Nox4 focally on the ER surface but not on the plasma membrane...
November 17, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/27815077/quantitation-of-wall-teichoic-acid-in-staphylococcus-aureus-by-direct-measurement-of-monomeric-units-using-lc-ms-ms
#11
Olga Berejnaia, Hao Wang, Marc Labroli, Christine Yang, Charles Gill, Jianying Xiao, David Hesk, Reynalda DeJesus, Jing Su, Christopher M Tan, Payal R Sheth, Michael Kavana, David G McLaren
The emergence of methicillin-resistant Staphylococcus aureus (MRSA) has created an urgent need for new therapeutic agents capable of combating this threat. We have previously reported on the discovery of novel inhibitors targeting enzymes involved in the biosynthesis of wall teichoic acid (WTA) and demonstrated that these agents can restore β-lactam efficacy against MRSA. In those previous reports pathway engagement of inhibitors was demonstrated by reduction in WTA levels measured by polyacrylamide gel electrophoresis...
November 2, 2016: Analytical Biochemistry
https://www.readbyqxmd.com/read/27813270/endoplasmic-reticulum-stress-contributes-to-ferritin-molecules-mediated-macrophage-migration-via-p-selectin-glycoprotein-ligand-1
#12
Chi-Mei Wang, Yue-Hwa Chen, Yu-Chieh Lee, Jung-Su Chang
SCOPE: Obesity is associated with elevated serum ferritin and increased macrophage activation and infiltration; however, the causal mechanisms underlying this relationship remain undefined. METHODS AND RESULTS: Serum ferritin and soluble P-selectin glycoprotein ligand (sPSGL)-1 level were higher in obese adolescents and patients with moderate nonalcoholic fatty liver disease (NAFLD) compared with controls (all p < 0.05). Multivariate linear regression revealed that serum ferritin was independently associated with sPSGL-1 (B = 0...
November 4, 2016: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/27813192/naltrexone-changes-the-expression-of-lipid-metabolism-related-proteins-in-the-endoplasmic-reticulum-er-stress-induced-hepatic-steatosis-in-mice
#13
Azam Moslehi, Fatemeh Nabavizadeh, Ali Zekri, Fatemeh Amiri
Endoplasmic reticulum (ER) stress is closely associated with several chronic diseases such as obesity, atherosclerosis, type 2 diabetes, and hepatic steatosis. Steatosis in hepatocytes may also lead to disorders such as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), fibrosis, and possibly cirrhosis. Opioid peptides are involved in triglyceride and cholesterol dysregulation. Naltrexone also attenuates ER stress induced hepatic steatosis in mice. In this study, we evaluated the effects of naltrexone on the expression of lipid metabolism-related nuclear factors and enzymes in the ER stress induced hepatic steatosis...
November 4, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27811171/fibroblast-growth-factor-21-reverses-suppression-of-adiponectin-expression-via-inhibiting-endoplasmic-reticulum-stress-in-adipose-tissue-of-obese-mice
#14
Qinyue Guo, Lin Xu, Jiali Liu, Huixia Li, Hongzhi Sun, Shufang Wu, Bo Zhou
Fibroblast growth factor 21 (FGF21) has recently emerged as a novel endocrine hormone involved in the regulation of glucose and lipid metabolism. However, the exact mechanisms whereby FGF21 mediates insulin sensitivity remain not fully understood. In the present study, FGF21was administrated in high-fat diet-induced obese mice and tunicamycin-induced 3T3-L1 adipocytes, and metabolic parameters, endoplasmic reticulum (ER) stress indicators, and insulin signaling molecular were assessed by Western blotting. The administration of FGF21 in obese mice reduced body weight, blood glucose and serum insulin, and increased insulin sensitivity, resulting in alleviation of insulin resistance...
November 3, 2016: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27808250/mtorc1-inhibitor-rapamycin-and-er-stressor-tunicamycin-induce-differential-patterns-of-er-mitochondria-coupling
#15
Roberto Bravo-Sagua, Camila López-Crisosto, Valentina Parra, Marcelo Rodriguez-Peña, Beverly A Rothermel, Andrew F G Quest, Sergio Lavandero
Efficient mitochondrial Ca(2+) uptake takes place at contact points between the ER and mitochondria, and represents a key regulator of many cell functions. In a previous study with HeLa cells, we showed that ER-to-mitochondria Ca(2+) transfer increases during the early phase of ER stress induced by tunicamycin as an adaptive response to stimulate mitochondrial bioenergetics. It remains unknown whether other types of stress signals trigger similar responses. Here we observed that rapamycin, which inhibits the nutrient-sensing complex mTORC1, increased ER-mitochondria coupling in HeLa cells to a similar extent as did tunicamycin...
November 3, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27803246/the-rim101-pathway-contributes-to-er-stress-adaptation-through-sensing-the-state-of-plasma-membrane
#16
Keisuke Obara, Akio Kihara
Yeast cells sense alterations in the plasma membrane (PM) lipid asymmetry and external alkalization by the sensor protein Rim21, which functions in the Rim101 pathway. Rim101 signaling is initiated at the PM by the recruitment of the Rim101 signaling complex. The PM physically associates with the cortical endoplasmic reticulum (ER) to form ER-PM contact sites, where several signaling events, lipid exchange, and ion transport take place. In the present study, we investigated the spatial relationship between ER-PM contact sites and the sites of Rim101 signaling...
November 1, 2016: Biochemical Journal
https://www.readbyqxmd.com/read/27796797/sublethal-endoplasmic-reticulum-stress-caused-by-the-mutation-of-immunoglobulin-heavy-chain-binding-protein-induces%C3%A2-the-synthesis-of-a-mitochondrial-protein-pyrroline-5-carboxylate-reductase-1
#17
Hisayo Jin, Mari Komita, Haruhiko Koseki, Tomohiko Aoe
Most human neurodegenerative diseases are sporadic and appear later in life. Aging and neurodegeneration are closely associated, and recent investigations reveal that endoplasmic reticulum (ER) stress is involved in the progression of these features. Immunoglobulin heavy chain-binding protein (BiP) is an ER chaperone that is central to ER functions. We produced knock-in mice expressing a mutant BiP that lacked the retrieval sequence to elucidate the effect of a functional defect in an ER chaperone in multicellular organisms...
October 28, 2016: Cell Stress & Chaperones
https://www.readbyqxmd.com/read/27783653/humanin-protects-rpe-cells-from-endoplasmic-reticulum-stress-induced-apoptosis-by-upregulation-of-mitochondrial-glutathione
#18
Douglas Matsunaga, Parameswaran G Sreekumar, Keijiro Ishikawa, Hiroto Terasaki, Ernesto Barron, Pinchas Cohen, Ram Kannan, David R Hinton
Humanin (HN) is a small mitochondrial-encoded peptide with neuroprotective properties. We have recently shown protection of retinal pigmented epithelium (RPE) cells by HN in oxidative stress; however, the effect of HN on endoplasmic reticulum (ER) stress has not been evaluated in any cell type. Our aim here was to study the effect of HN on ER stress-induced apoptosis in RPE cells with a specific focus on ER-mitochondrial cross-talk. Dose dependent effects of ER stressors (tunicamycin (TM), brefeldin A, and thapsigargin) were studied after 12 hr of treatment in confluent primary human RPE cells with or without 12 hr of HN pretreatment (1-20 μg/mL)...
2016: PloS One
https://www.readbyqxmd.com/read/27780373/p62-sqstm1-is-required-for-the-protection-against-endoplasmic-reticulum-stress-induced-apoptotic-cell-death
#19
Jeong Su Park, Sue Young Oh, Da Hyun Lee, Yu Seol Lee, Su Haeng Sung, Hye Won Ji, Moon Joo Lee, Yong-Ho Lee, Sue Goo Rhee, Soo Han Bae
Endoplasmic reticulum (ER) stress is triggered by various cellular stresses that disturb protein folding or calcium homeostasis in the ER. To cope with these stresses, ER stress activates the unfolded protein response (UPR) pathway, but unresolved ER stress induces reactive oxygen species (ROS) accumulation leading to apoptotic cell death. However, the mechanisms that underlie protection from ER stress-induced cell death are not clearly defined. The nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) pathway plays a crucial role in the protection of cells against ROS-mediated oxidative damage...
October 26, 2016: Free Radical Research
https://www.readbyqxmd.com/read/27779479/pronociceptive-effects-induced-by-cutaneous-application-of-a-transient-receptor-potential-ankyrin-1-trpa1-channel-agonist-methylglyoxal-in-diabetic-animals-comparison-with-tunicamycin-induced-endoplastic-reticulum-stress
#20
H Viisanen, H Chapman, H Wei, M Lasierra Losada, A Koivisto, K E Akerman, A Pertovaara
Methylglyoxal (MG) is a reactive carbonyl compound generated in diabetes mellitus. MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity. Here we studied whether exposure to diabetes and thereby to elevated endogenous MG modulates hypersensitivity induced by intradermal MG. Moreover, since diabetes induces endoplasmic reticulum (ER) stress, we compared the role of TRPA1 in diabetes and ER stress by assessing whether tunicamycin-induced ER stress, without diabetes, produces TRPA1-mediated pain hypersensitivity and by assessing whether ER stress and diabetes have similar modulatory effects on MG-induced hypersensitivity...
August 2016: Journal of Physiology and Pharmacology: An Official Journal of the Polish Physiological Society
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