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ischemia and endoplasmic reticulum

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https://www.readbyqxmd.com/read/27910195/mulberrofuran-g-protects-ischemic-injury-induced-cell-death-via-inhibition-of-nox4-mediated-ros-generation-and-er-stress
#1
Sungeun Hong, Jaeyoung Kwon, Dong-Woo Kim, Hak Ju Lee, Dongho Lee, Woongchon Mar
The aim of this study was to investigate the neuroprotective effect of mulberrofuran G (MG) in in vitro and in vivo models of cerebral ischemia. MG was isolated from the root bark of Morus bombycis. MG inhibited nicotinamide adenine dinucleotide phosphate oxidase (NOX) enzyme activity and oxygen-glucose deprivation/reoxygenation (OGD/R)-induced NOX4 protein expression in SH-SY5Y cells. MG inhibited the expression of activated caspase-3 and caspase-9 and cleaved poly adenine dinucleotide phosphate-ribose polymerase in OGD/R-induced SH-SY5Y cells...
December 2, 2016: Phytotherapy Research: PTR
https://www.readbyqxmd.com/read/27904664/tauroursodeoxycholic-acid-inhibits-endoplasmic-reticulum-stress-blocks-mitochondrial-permeability-transition-pore-opening-and-suppresses-reperfusion-injury-through-gsk-3%C3%A3-in-cardiac-h9c2-cells
#2
Yuxi Xie, Yonggui He, Zhiliang Cai, Jianhang Cai, Mengyao Xi, Yidong Zhang, Jinkun Xi
This study investigates whether inhibition of endoplasmic reticulum (ER) stress prevents opening of the mitochondrial permeability transition pore (mPTP) and evaluates the corresponding signaling pathways involved in this process. Exposure of cardiac H9c2 cells to 800 µM H2O2 for 20 min opened mPTP in response to oxidative stress, as demonstrated by quenching of tetramethylrhodamine ethyl ester (TMRE) fluorescence. Oxidative stress-induced mPTP opening was rescued by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) in a dose-dependent manner at low concentrations...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27888631/autophagy-decreases-alveolar-macrophage-apoptosis-by-attenuating-endoplasmic-reticulum-stress-and-oxidative-stress
#3
Tao Fan, Lei Chen, Zhixin Huang, Zhangfan Mao, Wei Wang, Boyou Zhang, Yao Xu, Shize Pan, Hao Hu, Qing Geng
To study the impact of autophagy on alveolar macrophage apoptosis and its mechanism in the early stages of hypoxia, we established a cell hypoxia-reoxygenation model and orthotopic left lung ischemia-reperfusion model. Rat alveolar macrophages stably expressing RFP-LC3 were treated with autophagy inhibitor (3-methyladenine, 3-MA) or autophagy promoter (rapamycin), followed by hypoxia-reoxygenation treatment 2 h, 4 h or 6 h later. Twenty Sprague-Dawley male rats were randomly divided into four different groups: no blocking of left lung hilum (model group), left lung hilum blocked for 1h with DMSO lavage (control group), left lung hilum blocked for 1 h with 100 ml/kg 3-MA (5 μmol/L) lavage (3-MA group), and left lung hilum blocked for 1 h with 100 ml/kg rapamycin (250 nmol/L) lavage (rapamycin group)...
November 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/27862079/discarded-livers-find-a-new-life-engineered-liver-grafts-using-hepatocytes-recovered-from-marginal-livers
#4
Basak E Uygun, Maria-Louisa Izamis, Maria Jaramillo, Yibin Chen, Gavrielle Price, Sinan Ozer, Martin L Yarmush
Treatment for end-stage liver failure is restricted by the critical shortage of donor organs; about 4000 people die in the USA while waiting for a transplantable organ. This situation has been a major driving force behind the rise of tissue engineering to build artificial tissues/organs. Recent advancements in creating transplantable liver grafts using decellularized liver scaffolds bring the field closer to clinical translation. However, a source of readily available and highly functional adult hepatocytes in adequate numbers for regenerative liver therapies still remains unclear...
November 8, 2016: Artificial Organs
https://www.readbyqxmd.com/read/27854125/apelin-apj-system-a-novel-therapeutic-target-for-myocardial-ischemia-reperfusion-injury
#5
Zhe Chen, Di Wu, Lanfang Li, Linxi Chen
Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Recently, researches indicate that the apelin/APJ system involves in myocardial ischemia-reperfusion injury (MIRI), which is a common pathophysiological process in patients with heart diseases and therapies. The reperfusion induces the expression of apelin and APJ receptor, which play an important role in cardioprotection of MIRI. The apelin/APJ system alleviates MIRI mainly by decreasing mitochondrial reactive oxygen species and delaying the opening of mitochondrial permeability transition pores, which induce the initiation of mitophagy...
November 17, 2016: DNA and Cell Biology
https://www.readbyqxmd.com/read/27824068/sulforaphane-improves-ischemia-induced-detrusor-overactivity-by-downregulating-the-enhancement-of-associated-endoplasmic-reticulum-stress-autophagy-and-apoptosis-in-rat-bladder
#6
Huai-Ching Tai, Shiu-Dong Chung, Chiang-Ting Chien, Hong-Jeng Yu
Atherosclerosis-associated pelvic ischemia has been reported to be a risk factor for bladder dysfunction and subsequent lower urinary tract symptoms (LUTS) in the elderly population. However, the molecular mechanisms of this association remain unclear. We hypothesized that stress-induced cellular responses might play a role in the pathogenesis of ischemia-induced bladder dysfunction. In the present study, the animal model of bladder ischemia was induced by bilateral partial arterial occlusion (BPAO) in rats...
November 8, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27795806/c1q-tnf-related-protein-9-protects-diabetic-rat-heart-against-ischemia-reperfusion-injury-role-of-endoplasmic-reticulum-stress
#7
Sanxing Bai, Liang Cheng, Yang Yang, Chongxi Fan, Dajun Zhao, Zhigang Qin, Xiao Feng, Lin Zhao, Jipeng Ma, Xiaowu Wang, Jian Yang, Xuezeng Xu, Dinghua Yi, Wei Yi
As a newly identified adiponectin paralog, C1q/TNF-related protein 9 (CTRP9) reduces myocardial ischemia reperfusion (IR) injury through partially understood mechanisms. In the present study, we sought to identify the role of endoplasmic reticulum stress (ERS) in CTRP9 induced cardioprotection in diabetic heart. Isolated hearts from high-fat-diet (HFD) induced type 2 diabetic Sprague-Dawley rats were subjected to ex vivo IR protocol via a Langendorff apparatus at the presence of globular CTRP9. CTRP9 significantly improved post-IR heart function and reduced cardiac infarction, cardiomyocytes apoptosis, Caspase-3, Caspase-9, Caspase-12, TNF-α expression, and lactate dehydrogenase activity...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27794481/activated-protein-c-prevents-methylglyoxal-induced-endoplasmic-reticulum-stress-and-cardiomyocyte-apoptosis-via-regulation-of-the-amp-activated-protein-kinase-signaling-pathway
#8
Dae-Hwan Nam, Jung-Hwa Han, Suji Kim, YoungHyun Shin, Jae Hyang Lim, Hyoung Chul Choi, Chang-Hoon Woo
Previous epidemiological studies have shown that methylglyoxal (MGO) levels are highly regulated in diabetic cardiovascular diseases. We have also previously reported that MGO mediates ER stress and apoptosis in cardiomyocytes. Furthermore, activated protein C (APC) has recently been shown to play a protective role against ER stress, as well as a cardioprotective role against ischemia and reperfusion injury by augmenting the AMP-activated protein kinase (AMPK) signaling pathway. Therefore, we hypothesized that APC protects against MGO-induced cardiomyocyte apoptosis through the inhibition of ER stress...
October 26, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27785700/naringenin-ameliorates-hypoxia-reoxygenation-induced-endoplasmic-reticulum-stress-mediated-apoptosis-in-h9c2-myocardial-cells-involvement-in-atf6-ire1%C3%AE-and-perk-signaling-activation
#9
Jia-You Tang, Ping Jin, Qing He, Lin-He Lu, Ji-Peng Ma, Wei-Lun Gao, He-Ping Bai, Jian Yang
Naringenin, a flavanone mainly derived from grapes and citrus fruits, has been reported to exhibit cardioprotective effects. Accumulating evidence has confirmed that endoplasmic reticulum (ER) stress-mediated apoptosis participates in the process of myocardial ischemia/reperfusion injury and inhibiting ER stress is a potential therapeutic target/strategy in preventing cardiovascular diseases. Herein, the current study was designed to investigate whether naringenin protects H9c2 myocardial cells against hypoxia/reoxygenation (H/R) injury via attenuating ER stress or ER stress-mediated apoptosis...
October 26, 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27771898/trehalose-inhibits-protein-aggregation-caused-by-transient-ischemic-insults-through-preservation-of-proteasome-activity-not-via-induction-of-autophagy
#10
Ye Li, Yinan Luo, Tianfei Luo, Bin Lu, Chen Wang, Yanhong Zhang, Meihua Piao, Chunsheng Feng, Pengfei Ge
Protein aggregation has been proved to be a pathological basis accounting for neuronal death caused by either transient global ischemia or oxygen glucose deprivation (OGD), and inhibition of protein aggregation is emerging as a potential strategy of preventing brain damage. Trehalose was found to inhibit protein aggregation caused by neurodegenerative diseases via induction of autophagy, whereas its effect is still elusive on ischemia-induced protein aggregation. In this study, we investigated this issue by using rat model of transient global ischemia and SH-SY5Y model of OGD...
October 22, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27763637/nogo-c-regulates-cardiomyocyte-apoptosis-during-mouse-myocardial-infarction
#11
Shi Jia, Xue Qiao, Jingjing Ye, Xuan Fang, Chunling Xu, Yangpo Cao, Ming Zheng
Myocardial infarction is caused by insufficient coronary blood supply, which leads to myocardial damage and eventually the heart failure. Molecular mechanisms associated with the loss of cardiomyocytes during myocardial infarction (MI) and ischemia-related cardiac diseases are not yet fully understood. Nogo-C is an endoplasmic reticulum protein ubiquitously expressed in tissues including in the heart, however, the cardiac function of Nogo-C is still unknown. In the present study, we found that Nogo-C was upregulated in mouse hearts after MI, and hypoxic treatments also increased Nogo-C protein level in cardiomyocytes...
October 20, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27733676/unfolded-protein-response-in-brain-ischemia-a-timely-update
#12
REVIEW
Wei Yang, Wulf Paschen
Folding and processing newly synthesized proteins are vital functions of the endoplasmic reticulum that are sensitive to a variety of stress conditions. The unfolded protein response is activated to restore endoplasmic reticulum function impaired by stress. While we know that brain ischemia impairs endoplasmic reticulum function, the role of unfolded protein response activation in post-ischemic recovery of neurologic function is only beginning to emerge. Here, we summarize what is known about endoplasmic reticulum stress and unfolded protein response in brain ischemia and discuss recent findings from myocardial ischemia studies that could help to advance research on endoplasmic reticulum stress and unfolded protein response in brain ischemia...
December 2016: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/27667666/suppressors-of-superoxide-h2o2-production-at-site-iq-of-mitochondrial-complex-i-protect-against-stem-cell-hyperplasia-and-ischemia-reperfusion-injury
#13
Martin D Brand, Renata L S Goncalves, Adam L Orr, Leonardo Vargas, Akos A Gerencser, Martin Borch Jensen, Yves T Wang, Simon Melov, Carolina N Turk, Jason T Matzen, Victoria J Dardov, H Michael Petrassi, Shelly L Meeusen, Irina V Perevoshchikova, Heinrich Jasper, Paul S Brookes, Edward K Ainscow
Using high-throughput screening we identified small molecules that suppress superoxide and/or H2O2 production during reverse electron transport through mitochondrial respiratory complex I (site IQ) without affecting oxidative phosphorylation (suppressors of site IQ electron leak, "S1QELs"). S1QELs diminished endogenous oxidative damage in primary astrocytes cultured at ambient or low oxygen tension, showing that site IQ is a normal contributor to mitochondrial superoxide-H2O2 production in cells. They diminished stem cell hyperplasia in Drosophila intestine in vivo and caspase activation in a cardiomyocyte cell model driven by endoplasmic reticulum stress, showing that superoxide-H2O2 production by site IQ is involved in cellular stress signaling...
October 11, 2016: Cell Metabolism
https://www.readbyqxmd.com/read/27630698/heat-shock-protein-70-protects-pc12-cells-against-ischemia-hypoxia-reoxygenation-by-maintaining-intracellular-ca-2-homeostasis
#14
Yuan Liu, Xue-Chun Wang, Dan Hu, Shu-Ran Huang, Qing-Shu Li, Zhi Li, Yan Qu
Heat shock protein 70 (HSP70) maintains Ca(2+) homeostasis in PC12 cells, which may protect against apoptosis; however, the mechanisms of neuroprotection are unclear. Therefore, in this study, we examined Ca(2+) levels in PC12 cells transfected with an exogenous lentiviral HSP70 gene expression construct, and we subsequently subjected the cells to ischemia-hypoxia/reoxygenation injury. HSP70 overexpression increased neuronal viability and ATPase activity, and it decreased cellular reactive oxygen species levels and intracellular Ca(2+) concentration after hypoxia/reoxygenation...
July 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27630541/cerebral-microvascular-endothelial-cell-apoptosis-after-ischemia-role-of-enolase-phosphatase-1-activation-and-aci-reductone-dioxygenase-1-translocation
#15
Yuan Zhang, Ting Wang, Ke Yang, Ji Xu, Lijie Ren, Weiping Li, Wenlan Liu
Enolase-phosphatase 1 (ENOPH1), a newly discovered enzyme of the methionine salvage pathway, is emerging as an important molecule regulating stress responses. In this study, we investigated the role of ENOPH1 in blood brain barrier (BBB) injury under ischemic conditions. Focal cerebral ischemia induced ENOPH1 mRNA and protein expression in ischemic hemispheric microvessels in rats. Exposure of cultured brain microvascular endothelial cells (bEND3 cells) to oxygen-glucose deprivation (OGD) also induced ENOPH1 upregulation, which was accompanied by increased cell death and apoptosis reflected by increased 3-(4, 5-Dimethylthiazol-2-yl)-2, 5- diphenyltetrazolium bromide formation, lactate dehydrogenase release and TUNEL staining...
2016: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/27630065/role-of-the-deubiquitinating-enzyme-ubiquitin-specific-protease-14-in-proteostasis-in-renal-cells
#16
Kapil Sareen-Khanna, Joan Papillon, Simon S Wing, Andrey V Cybulsky
Kidney cell injury may be associated with protein misfolding and induction of endoplasmic reticulum (ER) stress. Examples include complement-induced glomerular epithelial cell (GEC)/podocyte injury in membranous nephropathy, and ischemia-reperfusion injury. Renal cell injury can also result from mutations in integral proteins, which lead to their misfolding and accumulation. Certain nephrin missense mutants misfold, accumulate in the ER, and induce ER stress. We examined if enhancement of ubiquitin-proteasome system (UPS) function may facilitate proteostasis and confer protection against injury...
September 14, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27622292/hypothermia-and-rewarming-activate-a-macroglial-unfolded-protein-response-independent-of-hypoxic-ischemic-brain-injury-in-neonatal-piglets
#17
Jennifer K Lee, Bing Wang, Michael Reyes, Jillian S Armstrong, Ewa Kulikowicz, Polan T Santos, Jeong-Hoo Lee, Raymond C Koehler, Lee J Martin
Therapeutic hypothermia provides incomplete neuroprotection after hypoxia-ischemia (HI)-induced brain injury in neonates. We previously showed that cortical neuron and white matter apoptosis are promoted by hypothermia and early rewarming in a piglet model of HI. The unfolded protein response (UPR) may be one of the potential mediators of this cell death. Here, neonatal piglets underwent HI or sham surgery followed by 29 h of normothermia, 2 h of normothermia + 27 h of hypothermia or 18 h of hypothermia + rewarming...
2016: Developmental Neuroscience
https://www.readbyqxmd.com/read/27608005/mri-dynamically-evaluates-the-therapeutic-effect-of-recombinant-human-manf-on-ischemia-reperfusion-injury-in-rats
#18
Xian-Yun Wang, Meng-Meng Song, Si-Xing Bi, Yu-Jun Shen, Yu-Xian Shen, Yong-Qiang Yu
As an endoplasmic reticulum (ER) stress-inducible protein, mesencephalic astrocyte-derived neurotrophic factor (MANF) has been proven to protect dopaminergic neurons and nondopaminergic cells. Our previous studies had shown that MANF protected against ischemia/reperfusion injury. Here, we developed a magnetic resonance imaging (MRI) technology to dynamically evaluate the therapeutic effects of MANF on ischemia/reperfusion injury. We established a rat focal ischemic model by using middle cerebral artery occlusion (MCAO)...
2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27591867/stress-of-the-endoplasmic-reticulum-of-neurons-in-stroke-can-be-maximally-limited-by-combined-exposure-to-hypercapnia-and-hypoxia
#19
P P Tregub, V P Kulikov, Yu G Motin, M E Nagibaeva, A S Zabrodina
We studied the expression of chaperone GRP-78 and transcription factor NF-kB during the development of ischemic tolerance of the brain after combined and isolated exposure to hypoxia and hypercapnia. Combined exposure to hypoxia and hypercapnia maximally increased the expression of chaperone GRP-78 and transcription factor NF-kB, while the formation of ischemia-induced tolerance under conditions of hypercapnic hypoxia can be associated with activation of adaptive stress mechanisms in the endoplasmic reticulum...
August 2016: Bulletin of Experimental Biology and Medicine
https://www.readbyqxmd.com/read/27587006/mechanisms-of-islet-damage-mediated-by-pancreas-cold-ischemia-rewarming
#20
Keiko Omori, Eiji Kobayashi, Jeffrey Rawson, Masafumi Takahashi, Yoko Mullen
Prolonged pancreas cold ischemia is known to negatively correlate with islet isolation outcomes, hindering successful islet transplantation to treat Type-1 Diabetes. Due to poor islet isolation outcome, pancreata with over 16 h cold ischemia are currently not considered for islet transplantation. Mechanisms involved in pancreas cold ischemia/rewarming mediated islet damage during islet isolation and culture are not well understood. Using an en bloc cold preserved rat pancreas preparation, we attempted to clarify possible mechanisms of islet death associated with prolonged pancreas cold ischemia and subsequent rewarming...
October 2016: Cryobiology
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