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ischemia and endoplasmic reticulum

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https://www.readbyqxmd.com/read/28422872/effect-of-hsp27-and-cofilin-in-the-injury-of-hypoxia-reoxygenation-on-hepatocyte-membrane-f-actin-microfilaments
#1
Yafei Zhang, Jiazhong Wang, Hong Ji, Hongwei Lu, Le Lu, Jinlong Wang, Yiming Li
Hypoxia-reoxygenation (H/R) injury hepatocyte models were established to simulate the ischemia/reperfusion injury of transplanted organ. Through the study of the molecular mechanism of H/R on the F-actin damage of the liver cytomembrane, the mechanism of F-actin damage induced by ischemia and reperfusion was studied from the level of cell and molecule.The hypoxic environment of cells in vitro was simulated by chemical hypoxia agent CoCl2. Liver cells were detected by MTT, H/R group was subdivided into 3 subgroups: H/R 2, 4, and 6 h...
April 2017: Medicine (Baltimore)
https://www.readbyqxmd.com/read/28403128/an-oxygenated-and-transportable-machine-perfusion-system-fully-rescues-liver-grafts-exposed-to-lethal-ischemic-damage-in-a-pig-model-of-dcd-liver-transplantation
#2
Philippe Compagnon, Eric Levesque, Hassen Hentati, Mara Disabato, Julien Calderaro, Cyrille Feray, Anne Corlu, José Laurent Cohen, Ismail Ben Mosbah, Daniel Azoulay
BACKGROUND: Control of warm ischemia (WI) lesions that occur with donation after circulatory death (DCD) would significantly increase the donor pool for liver transplantation. We aimed to determine whether a novel, oxygenated and hypothermic machine perfusion device (HMP Airdrive system) improves the quality of livers derived from DCDs using a large animal model. METHODS: Cardiac arrest was induced in female large white pigs by IV injection of potassium chloride...
April 11, 2017: Transplantation
https://www.readbyqxmd.com/read/28392211/monosialotetrahexosy-1-ganglioside-attenuates-diabetes-associated-cerebral-ischemia-reperfusion-injury-through-suppression-of-the-endoplasmic-reticulum-stress-induced-apoptosis
#3
Danying Su, Jing Ma, Jiachen Yang, Yingying Kang, Manhua Lv, Yang Li
We aimed to assess the neuroprotective mechanism of monosialotetrahexosy-1 ganglioside (GM1) on focal cerebral ischemia/reperfusion (I/R) injury in rats with diabetes. A total of 54 male Wistar rats were induced with diabetes mellitus by administration of streptozotocin (STZ). The rats were then randomized into three groups, including sham group (n=18), I/R group (n=18), and GM1 group (n=18). Focal cerebral ischemia was modeled using the right middle cerebral artery occlusion method. In the GM1 group, diabetic rats were intraperitoneally administered with GM1 (15mg/kg) at 20min prior to reperfusion...
April 6, 2017: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
https://www.readbyqxmd.com/read/28376665/thinking-outside-the-box
#4
Judith Ingles, Chandrashekara N Kyathanahalli, Pancharatnam Jeyasuria, Jennifer C Condon
A broad definition of preconditioning is "the preparation for a subsequent action." Mounting evidence demonstrates that novel remote preconditioning paradigms, in which protective stimuli experienced locally can capacitate systemic tolerance and enhanced cell viability upon exposure to ensuing cellular insults, have been largely successful in the field of cardiovascular ischemia/reperfusion injury. To ensure successful protective preconditioning, some models (including the uterus) have been demonstrated to activate the unfolded protein response (UPR), which is a cellular stress response controlled at the level of the endoplasmic reticulum...
January 1, 2017: Journal of Cardiovascular Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/28320180/mitochondrial-dysfunction-silent-killer-in-cerebral-ischemia
#5
REVIEW
Pramila Bakthavachalam, Prakash Srinivasan Timiri Shanmugam
Mitochondrial dysfunction aggravates ischemic neuronal injury through activation of various pathophysiological and molecular mechanisms. Ischemic neuronal injury is particularly intensified during reperfusion due to impairment of mitochondrial function. Mitochondrial mutilation instigates alterations in calcium homeostasis in neurons, which plays a pivotal role in the maintenance of normal neuronal function. Increase in intracellular calcium level in mitochondria triggers the opening of mitochondrial transition pore and over production of reactive oxygen species (ROS)...
April 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28298952/insights-for-oxidative-stress-and-mtor-signaling-in-myocardial-ischemia-reperfusion-injury-under-diabetes
#6
REVIEW
Dajun Zhao, Jian Yang, Lifang Yang
Diabetes mellitus (DM) displays a high morbidity. The diabetic heart is susceptible to myocardial ischemia/reperfusion (MI/R) injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts more vulnerable to MI/R injury. Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), uncoupling nitric oxide synthase (NOS), and disturbing the mitochondrial quality control may be three major mechanisms of oxidative stress...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28296550/protective-effects-of-salusin-%C3%AE-and-salusin-%C3%AE-on-renal-ischemia-reperfusion-damage-and-their-levels-in-ischemic-acute-renal-failure
#7
M Cakir, H Duzova, A Taslidere, G Orhan, F Ozyalin
Salusin-α and salusin-β are expressed in many tissues including the central nervous system, vessels and kidneys; they have been shown to decrease endoplasmic reticulum stress during heart ischemia/reperfusion (I/R) and to decrease apoptosis. We investigated the relation of salusin-α and salusin-β levels to acute ischemic renal failure. We also investigated whether these peptides are protective against renal I/R damage. Fifty-three rats were divided into six groups: control, I/R, I/R + salusin-α1, I/R + salusin-α10, I/R + salusin-β1 and I/R + salusin-β10...
2017: Biotechnic & Histochemistry: Official Publication of the Biological Stain Commission
https://www.readbyqxmd.com/read/28282906/gsk3%C3%AE-and-vdac-involvement-in-er-stress-and-apoptosis-modulation-during-orthotopic-liver-transplantation
#8
Mohamed Amine Zaouali, Arnau Panisello, Alexandre Lopez, Carlos Castro, Emma Folch, Teresa Carbonell, Anabela Rolo, Carlos Marques Palmeira, Agustin Garcia-Gil, René Adam, Joan Roselló-Catafau
We investigated the involvement of glycogen synthase kinase-3β (GSK3β) and the voltage-dependent anion channel (VDAC) in livers subjected to cold ischemia-reperfusion injury (I/R) associated with orthotopic liver transplantation (OLT). Rat livers were preserved in University of Wisconsin (UW) and Institute Georges Lopez (IGL-1) solution, the latter enriched or not with trimetazidine, and then subjected to OLT. Transaminase (ALT) and HMGB1 protein levels, glutamate dehydrogenase (GLDH), and oxidative stress (MDA) were measured...
March 8, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28277984/neutral-sphingomyelinase-inhibition-alleviates-apoptosis-but-not-er-stress-in-liver-ischemia-reperfusion-injury
#9
Hazal Tuzcu, Betul Unal, Ebru Kırac, Esma Konuk, Filiz Ozcan, Gulsum O Elpek, Necdet Demir, Mutay Aslan
Previous studies have revealed the activation of neutral sphingomyelinase (N-SMase)/ceramide pathway in hepatic tissue following warm liver ischemia reperfusion (IR) injury. Excessive ceramide accumulation is known to potentiate apoptotic stimuli and a link between apoptosis and endoplasmic reticulum (ER) stress has been established in hepatic IR injury. Thus, this study determined the role of selective N-SMase inhibition on ER stress and apoptotic markers in a rat model of liver IR injury. Selective N-SMase inhibitor was administered via intraperitoneal injections...
March 13, 2017: Free Radical Research
https://www.readbyqxmd.com/read/28273718/mechanisms-of-parkinson-s-disease-related-proteins-in-mediating-secondary-brain-damage-after-cerebral-ischemia
#10
TaeHee Kim, Raghu Vemuganti
Both Parkinson's disease (PD) and stroke are debilitating conditions that result in neuronal death and loss of neurological functions. These two conditions predominantly affect aging populations with the deterioration of the quality of life for the patients themselves and a tremendous burden to families. While the neurodegeneration and symptomology of PD develop chronically over the years, post-stroke neuronal death and dysfunction develop rapidly in days. Despite the discrepancy in the pathophysiological time frame and severity, both conditions share common molecular mechanisms that include oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum stress, and activation of various cell death pathways (apoptosis/necrosis/autophagy) that synergistically modulate the neuronal death...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28252345/evidence-of-stress-in-%C3%AE-cells-obtained-with-laser-capture-microdissection-from-pancreases-of-brain-dead-donors
#11
Aref Ebrahimi, Min-Ho Jung, Jonathan M Dreyfuss, Hui Pan, Dennis Sgroi, Susan Bonner-Weir, Gordon C Weir
Isolated islets used for transplantation are known to be stressed, which can result from the circumstances of death, in particular brain death, the preservation of the pancreas with its warm and cold ischemia, from the trauma of the isolation process, and the complex events that occur during tissue culture. The current study focused upon the events that occur before the islet isolation procedure. Pancreases were obtained from brain dead donors (n = 7) with mean age 50 (11) and normal pancreatic tissue obtained at surgery done for pancreatic neoplasms (n = 7), mean age 69 (9)...
March 4, 2017: Islets
https://www.readbyqxmd.com/read/28250763/molecular-chaperones-and-hypoxic-ischemic-encephalopathy
#12
REVIEW
Cong Hua, Wei-Na Ju, Hang Jin, Xin Sun, Gang Zhao
Hypoxic-ischemic encephalopathy (HIE) is a disease that occurs when the brain is subjected to hypoxia, resulting in neuronal death and neurological deficits, with a poor prognosis. The mechanisms underlying hypoxic-ischemic brain injury include excitatory amino acid release, cellular proteolysis, reactive oxygen species generation, nitric oxide synthesis, and inflammation. The molecular and cellular changes in HIE include protein misfolding, aggregation, and destruction of organelles. The apoptotic pathways activated by ischemia and hypoxia include the mitochondrial pathway, the extrinsic Fas receptor pathway, and the endoplasmic reticulum stress-induced pathway...
January 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28242652/glucose-deprivation-induces-atf4-mediated-apoptosis-through-trail-death-receptors
#13
Raffaella Iurlaro, Franziska Püschel, Clara Lucía León-Annicchiarico, Hazel O'Connor, Seamus J Martin, Daniel Palou-Gramón, Estefanía Lucendo, Cristina Muñoz-Pinedo
Metabolic stress occurs frequently in tumors and in normal tissues undergoing transient ischemia. Nutrient deprivation triggers, among many potential cell death-inducing pathways, an endoplasmic reticulum (ER) stress response with induction of the Integrated Stress Response transcription factor ATF4. However, how this results in cell death remains unknown. Here we show that glucose deprivation triggered ER stress and induced the Unfolded Protein Response transcription factors ATF4 and CHOP. This was associated with non-transcriptional accumulation of the TRAIL receptor TRAIL-R1 (DR4) and with ATF4-mediated, CHOP-independent induction of TRAIL-R2 (DR5), suggesting that cell death in this context may involve death receptor signaling...
February 27, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28228736/stress-signal-network-between-hypoxia-and-er-stress-in-chronic-kidney-disease
#14
REVIEW
Hiroshi Maekawa, Reiko Inagi
Chronic kidney disease (CKD) is characterized by an irreversible decrease in kidney function and induction of various metabolic dysfunctions. Accumulated findings reveal that chronic hypoxic stress and endoplasmic reticulum (ER) stress are involved in a range of pathogenic conditions, including the progression of CKD. Because of the presence of an arteriovenous oxygen shunt, the kidney is thought to be susceptible to hypoxia. Chronic kidney hypoxia is induced by a number of pathogenic conditions, including renal ischemia, reduced peritubular capillary, and tubulointerstitial fibrosis...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28212798/protein-kinase-c-as-regulator-of-vascular-smooth-muscle-function-and-potential-target-in-vascular-disorders
#15
H C Ringvold, R A Khalil
Vascular smooth muscle (VSM) plays an important role in maintaining vascular tone. In addition to Ca(2+)-dependent myosin light chain (MLC) phosphorylation, protein kinase C (PKC) is a major regulator of VSM function. PKC is a family of conventional Ca(2+)-dependent α, β, and γ, novel Ca(2+)-independent δ, ɛ, θ, and η, and atypical ξ, and ι/λ isoforms. Inactive PKC is mainly cytosolic, and upon activation it undergoes phosphorylation, maturation, and translocation to the surface membrane, the nucleus, endoplasmic reticulum, and other cell organelles; a process facilitated by scaffold proteins such as RACKs...
2017: Advances in Pharmacology
https://www.readbyqxmd.com/read/28205129/remifentanil-postconditioning-ameliorates-histone-h3-acetylation-modification-in-h9c2-cardiomyoblasts-after-hypoxia-reoxygenation-via-attenuating-endoplasmic-reticulum-stress
#16
Manli Chen, Qin Liu, Lijian Chen, Lei Zhang, Erwei Gu
Remifentanil postconditioning (RPC) elicits cardioprotection against ischemia/reperfusion injury (IRI) by attenuating apoptosis associated with endoplasmic reticulum stress (ERS). Histone H3, acetylation modifications of histone H3, and histone deacetylases (HDAC) also have key roles in the mediation of the survival and apoptosis of cardiomyocytes. In this study, an in vitro IRI model was established with H9c2 cardiomyoblasts to investigate the role of histone H3 acetylation and HDAC3 in RPC-induced attenuation of ERS-associated apoptosis...
February 16, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28178380/pre-ischemia-melatonin-treatment-alleviated-acute-neuronal-injury-after-ischemic-stroke-by-inhibiting-endoplasmic-reticulum-stress-dependent-autophagy-via-perk-and-ire1-signalings
#17
Dayun Feng, Bao Wang, Lei Wang, Neeta Abraham, Kai Tao, Lu Huang, Wei Shi, Yushu Dong, Yan Qu
Melatonin has demonstrated a potential protective effect in central nervous system. Thus, it is interesting to determine whether pre-ischemia melatonin administration could protect against cerebral ischemia/reperfusion (IR)-related injury and the underlying molecular mechanisms. In this study, we revealed that IR injury significantly activated endoplasmic reticulum (ER) stress and autophagy in a middle cerebral artery occlusion mouse model. Pre-ischemia melatonin treatment was able to attenuate IR-induced ER stress and autophagy...
February 8, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28135002/ischemia-reperfusion
#18
Theodore Kalogeris, Christopher P Baines, Maike Krenz, Ronald J Korthuis
Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload)...
December 6, 2016: Comprehensive Physiology
https://www.readbyqxmd.com/read/28134810/acidosis-activates-endoplasmic-reticulum-stress-pathways-through-gpr4-in-human-vascular-endothelial-cells
#19
Lixue Dong, Elizabeth A Krewson, Li V Yang
Acidosis commonly exists in the tissue microenvironment of various pathophysiological conditions such as tumors, inflammation, ischemia, metabolic disease, and respiratory disease. For instance, the tumor microenvironment is characterized by acidosis and hypoxia due to tumor heterogeneity, aerobic glycolysis (the "Warburg effect"), and the defective vasculature that cannot efficiently deliver oxygen and nutrients or remove metabolic acid byproduct. How the acidic microenvironment affects the function of blood vessels, however, is not well defined...
January 27, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28112174/2-3-5-4-tetrahydroxystilbene-2-o-%C3%AE-d-glucoside-protects-murine-hearts-against-ischemia-reperfusion-injury-by-activating-notch1-hes1-signaling-and-attenuating-endoplasmic-reticulum-stress
#20
Meng Zhang, Li-Ming Yu, Hang Zhao, Xuan-Xuan Zhou, Qian Yang, Fan Song, Li Yan, Meng-En Zhai, Bu-Ying Li, Bin Zhang, Zhen-Xiao Jin, Wei-Xun Duan, Si-Wang Wang
2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG) is a water-soluble active component extracted from Polygonum multiflorum Thunb. A number of studies demonstrate that TSG exerts cardioprotective effects. Since endoplasmic reticulum (ER) stress plays a key role in myocardial ischemia/reperfusion (MI/R)-induced cell apoptosis, we sought to determine whether modulation of the ER stress during MI/R injury was involved in the cardioprotective action of TSG. Male mice were treated with TSG (60 mg·kg(-1)·d(-1), ig) for 2 weeks and then were subjected to MI/R surgery...
March 2017: Acta Pharmacologica Sinica
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