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https://www.readbyqxmd.com/read/29331396/autophagy-in-ischemic-stroke
#1
REVIEW
Pei Wang, Bo-Zong Shao, Zhiqiang Deng, Shi Chen, Zhenyu Yue, Chao-Yu Miao
Autophagy is a self-eating cellular catabolic pathway, through which long-lived proteins, damaged organelles and misfolded proteins are degraded and recycled for the maintenance of cellular homeostasis and normal cellular functions. Autophagy plays an important homeostatic role in the regulation of cell survival. Accumulating evidence shows that autophagy is activated in various cell types in the brain such as neurons, glia cells, and brain microvascular cells upon ischemic stroke. However, the exact role and molecular mechanisms of autophagy process that is implicated in ischemic stroke have yet to be elucidated...
January 10, 2018: Progress in Neurobiology
https://www.readbyqxmd.com/read/29301204/proteasome-and-organs-ischemia-reperfusion-injury
#2
REVIEW
Joan Oliva
The treatment of organ failure on patients requires the transplantation of functional organs, from donors. Over time, the methodology of transplantation was improved by the development of organ preservation solutions. The storage of organs in preservation solutions is followed by the ischemia of the organ, resulting in a shortage of oxygen and nutrients, which damage the tissues. When the organ is ready for the transplantation, the reperfusion of the organ induces an increase of the oxidative stress, endoplasmic reticulum stress, and inflammation which causes tissue damage, resulting in a decrease of the transplantation success...
December 30, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29288332/essential-role-for-egfr-tyrosine-kinase-and-er-stress-in-myocardial-infarction-in-type-2-diabetes
#3
Vishal Mali, Samuel Haddox, Corey Hornersmith, Khalid Matrougui, Souad Belmadani
We previously reported that EGFR tyrosine kinase (EGFRtk) activity and endoplasmic reticulum (ER) stress are enhanced in type 2 diabetic (T2D) mice and cause vascular dysfunction. In the present study, we determined the in vivo contribution of EGFRtk and ER stress in acute myocardial infarction induced by acute ischemia (40 min)-reperfusion (24 h) (I/R) injury in T2D (db-/db-) mice. We treated db-/db- mice with EGFRtk inhibitor (AG1478, 10 mg/kg/day) for 2 weeks. Mice were then subjected to myocardial I/R injury...
December 29, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29278321/design-and-evaluation-of-lyophilized-fibroblast-growth-factor-21-and-its-protection-against-ischemia-cerebral-injury
#4
Xuanxin Yang, Qi Hui, Bingjie Yu, Zhen Huang, Peipei Zhou, Panfeng Wang, Zhitao Wang, Shucai Pang, Jinghang Li, Hanshi Wang, Li Lin, Xiaokun Li, Xiaojie Wang
This study investigated the effect of the excipients, including glycine, mannitol, arginine, trehalose, sorbitol, and poloxamer188 on the stability of recombinant human fibroblast growth factor 21(FGF21) during the process of lyophilization and storage. The glass transition temperature (Tg), protein secondary structure, aggregation ratio and the bioactivity of lyophilized FGF21 were measured. We furthermore investigated the effect of FGF21 against ischemia cerebral injury using the middle cerebral artery occlusion (MCAO) model in rats...
December 26, 2017: Bioconjugate Chemistry
https://www.readbyqxmd.com/read/29277709/granulocyte-colony-stimulating-factor-protects-against-endoplasmic-reticulum-stress-in-an-experimental-model-of-stroke
#5
Janet M Menzie-Suderam, Payam Mohammad-Gharibani, Jigar Modi, Zea Ma, Rui Tao, Howard Prentice, Jang-Yen Wu
Granulocyte-colony stimulating factor (G-CSF) is an endogenous growth factor that exhibits a diverse range of neuroprotective mechanisms against a variety of neurological disorders including ischemic stroke. We investigated the anti-apoptotic mechanisms of G-CSF against endoplasmic reticulum (ER) stress induced apoptosis. Sprague-Dawley rats were subjected to transient occlusion of the middle cerebral artery (MCAO) for 90 minutes. Rats were injected with G-CSF (n= 15; 50ug/kg body weight s.c.) for 4 days, starting 24 hours post-MCAO and brains were harvested after 4 days reperfusion (n=16)...
December 22, 2017: Brain Research
https://www.readbyqxmd.com/read/29215059/protective-effect-of-mesenchymal-stem-cells-on-the-pressure-ulcer-formation-by-the-regulation-of-oxidative-and-endoplasmic-reticulum-stress
#6
Sei-Ichiro Motegi, Akiko Sekiguchi, Akihiko Uchiyama, Akihito Uehara, Chisako Fujiwara, Sahori Yamazaki, Buddhini Perera, Hideharu Nakamura, Sachiko Ogino, Yoko Yokoyama, Ryoko Akai, Takao Iwawaki, Osamu Ishikawa
Cutaneous ischemia-reperfusion (I/R) injury is associated with the early pathogenesis of cutaneous pressure ulcers (PUs). The objective of this study was to investigate the effect of mesenchymal stem cells (MSCs) injection on the formation of PUs after I/R injury and determine the underlying mechanisms. We found that the subcutaneous injection of MSCs into areas of I/R injured skin significantly suppressed the formation of PUs. I/R-induced vascular damage, hypoxia, oxidative DNA damage, and apoptosis were decreased by MSCs injection...
December 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29212948/elevated-urinary-creld2-is-associated-with-endoplasmic-reticulum-stress-mediated-kidney-disease
#7
Yeawon Kim, Sun-Ji Park, Scott R Manson, Carlos Af Molina, Kendrah Kidd, Heather Thiessen-Philbrook, Rebecca J Perry, Helen Liapis, Stanislav Kmoch, Chirag R Parikh, Anthony J Bleyer, Ying Maggie Chen
ER stress has emerged as a signaling platform underlying the pathogenesis of various kidney diseases. Thus, there is an urgent need to develop ER stress biomarkers in the incipient stages of ER stress-mediated kidney disease, when a kidney biopsy is not yet clinically indicated, for early therapeutic intervention. Cysteine-rich with EGF-like domains 2 (CRELD2) is a newly identified protein that is induced and secreted under ER stress. For the first time to our knowledge, we demonstrate that CRELD2 can serve as a sensitive urinary biomarker for detecting ER stress in podocytes or renal tubular cells in murine models of podocyte ER stress-induced nephrotic syndrome and tunicamycin- or ischemia-reperfusion-induced acute kidney injury (AKI), respectively...
December 7, 2017: JCI Insight
https://www.readbyqxmd.com/read/29169992/hax-1-regulates-serca2a-oxidation-and-degradation
#8
Philip A Bidwell, Guan-Sheng Liu, Narayani Nagarajan, Chi Keung Lam, Kobra Haghighi, George Gardner, Wen-Feng Cai, Wen Zhao, Luke Mugge, Elizabeth Vafiadaki, Despina Sanoudou, Jack Rubinstein, Djamel Lebeche, Roger Hajjar, Junichi Sadoshima, Evangelia G Kranias
Ischemia/reperfusion injury is associated with contractile dysfunction and increased cardiomyocyte death. Overexpression of the hematopoietic lineage substrate-1-associated protein X-1 (HAX-1) has been shown to protect from cellular injury but the function of endogenous HAX-1 remains obscure due to early lethality of the knockout mouse. Herein we generated a cardiac-specific and inducible HAX-1 deficient model, which uncovered an unexpected role of HAX-1 in regulation of sarco/endoplasmic reticulum Ca-ATPase (SERCA2a) in ischemia/reperfusion injury...
November 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29141573/liver-protective-effects-of-extra-virgin-olive-oil-interaction-between-its-chemical-composition-and-the-cell-signaling-pathways-involved-in-protection
#9
Sandra A Soto-Alarcon, Rodrigo Valenzuela, Alfonso Valenzuela, Luis A Videla
BACKGROUND AND OBJECTIVE: The liver is an organ susceptible to a multitude of injuries that causes liver damage, like steatosis, non-alcoholic steatohepatitis, cirrhosis, hepatocellular carcinoma, and ischemia-reperfusion injury. Extra virgin olive oil (EVOO), presents several protective effects on the liver, reducing hepatic steatosis, hepatocyte ballooning, fibrogenesis, preventing lipid peroxidation, among other effects. Due to its high levels of monounsaturated fatty acids, mainly oleic acid and phenolic compounds, such as hydroxytyrosol and oleuropein, EVOO is able to participate in the activation of different signaling pathways in the hepatocytes involved in the prevention of inflammation, oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, and insulin resistance, allowing the prevention or resolution of liver damage...
November 14, 2017: Endocrine, Metabolic & Immune Disorders Drug Targets
https://www.readbyqxmd.com/read/29137244/microrna-423-5p-facilitates-hypoxia-reoxygenation-induced-apoptosis-in-renal-proximal-tubular-epithelial-cells-by-targeting-gstm1-via-endoplasmic-reticulum-stress
#10
Xiao-Peng Yuan, Long-Shan Liu, Chuan-Bao Chen, Jian Zhou, Yi-Tao Zheng, Xiao-Ping Wang, Ming Han, Chang-Xi Wang
It has been reported that microRNAs (miRs) can regulate renal response to acute injury and members of them are believed to be important in maintenance of renal function and development of renal injury. We investigated the actions of microRNA-423-5p (miR-423-5p) and glutathione-S-transferase (GST) M1 after acute kidney injury. MiR-423-5p was up-regulated and GSTM1 was down-regulated in human kidney (HK-2) cells subjected to hypoxia/reoxygenation (H/R) and in rat kidneys subjected to ischemia/reperfusion (I/R) injury...
October 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/29122608/thioredoxin-albumin-fusion-protein-prevents-copper-enhanced-zinc-induced-neurotoxicity-via-its-antioxidative-activity
#11
Ken-Ichiro Tanaka, Mikako Shimoda, Victor T G Chuang, Kento Nishida, Masahiro Kawahara, Tatsuhiro Ishida, Masaki Otagiri, Toru Maruyama, Yu Ishima
Zinc (Zn) is a co-factor for a vast number of enzymes, and functions as a regulator for immune mechanism and protein synthesis. However, excessive Zn release induced in pathological situations such as stroke or transient global ischemia is toxic. Previously, we demonstrated that the interaction of Zn and copper (Cu) is involved in the pathogenesis of Alzheimer's disease and vascular dementia. Furthermore, oxidative stress has been shown to play a significant role in the pathogenesis of various metal ions induced neuronal death...
November 6, 2017: International Journal of Pharmaceutics
https://www.readbyqxmd.com/read/29105479/-progress-of-acupuncture-and-moxibustion-research-on-the-signal-transduction-pathways-involved-in-cell-apoptosis-in-myocardial-ischemia-reperfusion-injury
#12
Yan Xiao, Liang Ding, Yi-Huang Gu
Myocardial cell apoptosis is very common in the clinic, and is caused by myocardial ischemia reperfusion injury (MIRI). There are different degrees of cell apoptosis in MIRI. However, initiation of the signal transduction mechanism of myocardial cell apoptosis is unclear. The present research confirmed that acupuncture and moxibustion are effective interventions for cell apoptosis in MIRI through three approaches:the death receptor pathway, mitochondrial pathway and endoplasmic reticulum pathway. In this paper, the authors summarize the mechanism characteristics of acupuncture and moxibustion in MIRI cell apoptosis, and discuss the signal transduction pathways involved in the effects of acupuncture and moxibustion in MIRI cell apoptosis, in order to provide new ideas and evidence for the clinical application of acupuncture and moxibustion to prevent cell apoptosis in MIRI...
October 25, 2017: Zhen Ci Yan Jiu, Acupuncture Research
https://www.readbyqxmd.com/read/29101309/biochemical-targets-of-drugs-mitigating-oxidative-stress-via-redox-independent-mechanisms
#13
REVIEW
Bernd Gesslbauer, Valery Bochkov
Acute or chronic oxidative stress plays an important role in many pathologies. Two opposite approaches are typically used to prevent the damage induced by reactive oxygen and nitrogen species (RONS), namely treatment either with antioxidants or with weak oxidants that up-regulate endogenous antioxidant mechanisms. This review discusses options for the third pharmacological approach, namely amelioration of oxidative stress by 'redox-inert' compounds, which do not inactivate RONS but either inhibit the basic mechanisms leading to their formation (i...
November 3, 2017: Biochemical Society Transactions
https://www.readbyqxmd.com/read/29081777/hyperglycemia-aggravates-hepatic-ischemia-and-reperfusion-injury-by-inhibiting-liver-resident-macrophage-m2-polarization-via-c-ebp-homologous-protein-mediated-endoplasmic-reticulum-stress
#14
Zhuqing Rao, Jie Sun, Xiongxiong Pan, Ziyang Chen, Heliang Sun, Panpan Zhang, Mei Gao, Zhengnian Ding, Cunming Liu
Aggravated liver ischemia and reperfusion (IR) injury has been observed in hyperglycemic hosts, but its underlying mechanism remains undefined. Liver-resident macrophages (Kupffer cells, KCs) and endoplasmic reticulum (ER) stress play crucial roles in the pathogenesis of liver IR injury. In this study, we evaluated the role of ER stress in regulating KC activation and liver IR injury in a streptozotocin-induced hyperglycemic/diabetic mouse model. Compared to the control group (CON group), hyperglycemic mice exhibited a significant increase in liver injury and intrahepatic inflammation following IR...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/29067098/curcumin-inhibits-endoplasmic-reticulum-stress-induced-by-cerebral-ischemia-reperfusion-injury-in-rats
#15
Haiying Zhu, Yanxia Fan, Hongyu Sun, Liyan Chen, Xiao Man
The aim of the present study was to observe the dynamic changes of the growth arrest and DNA damage-inducible 153 (GADD153) gene and caspase-12 in the brain tissue of rats with cerebral ischemia-reperfusion injury (CIRI) and the impact of curcumin pretreatment. A total of 60 rats were randomly divided into the normal group (N), the sham operation group (S), the dimethyl sulfoxide control group (D) and the curcumin treatment group (C). For group D and C, 12 (T1), 24 (T2) and 72 h (T3) of reperfusion were performed after 2 h ischemia...
November 2017: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29045568/loss-of-protein-kinase-novel-1-pkn1-is-associated-with-mild-systolic-and-diastolic-contractile-dysfunction-increased-phospholamban-thr17-phosphorylation-and-exacerbated-ischaemia-reperfusion-injury
#16
Asvi A Francois, Kofo Obasanjo-Blackshire, James E Clark, Andrii Boguslavskyi, Mark R Holt, Peter Parker, Michael S Marber, Richard J Heads
Aims: PKN1 is a stress-responsive protein kinase acting downstream of small GTP-binding proteins of the Rho/Rac family. The aim was to determine its role in endogenous cardioprotection. Methods and Results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischemia and reperfusion (I/R). Myocardial infarct size was doubled in PKN1 KO hearts compared to WT hearts. PKN1 was basally phosphorylated on the activation loop Thr778 PDK1 target site which was unchanged during I/R...
October 16, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/29045036/endoplasmic-reticulum-stress-regulates-oxygen-glucose-deprivation-induced-parthanatos-in-human-sh-sy5y-cells-via-improvement-of-intracellular-ros
#17
Hai-Feng Wang, Zong-Qi Wang, Ye Ding, Mei-Hua Piao, Chun-Sheng Feng, Guang-Fan Chi, Yi-Nan Luo, Peng-Fei Ge
AIMS: Endoplasmic reticulum (ER) stress has been demonstrated to regulate neuronal death caused by ischemic insults via activation of apoptosis, but it still remains unclear whether ER stress participates in regulation of parthanatos, a new type of programmed cell death characterized by PARP-1 overactivation and intracellular accumulation of PAR polymer. METHODS: we used oxygen-glucose deprivation (OGD) and human SH-SY5Y cells to simulate neuronal damage caused by ischemia...
October 16, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/29040818/metformin-attenuates-er-stress-induced-mitochondrial-dysfunction
#18
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress, a disturbance of the ER function, contributes to cardiac injury. ER and mitochondria are closely connected organelles within cells. ER stress contributes to mitochondrial dysfunction, which is a key factor to increase cardiac injury. Metformin, a traditional anti-diabetic drug, decreases cardiac injury during ischemia-reperfusion. Metformin also inhibits ER stress in cultured cells. We hypothesized that metformin can attenuate the ER stress-induced mitochondrial dysfunction and subsequent cardiac injury...
September 28, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/29035876/hydrogen-gas-attenuates-myocardial-ischemia-reperfusion-injury-independent-of-postconditioning-in-rats-by-attenuating-endoplasmic-reticulum-stress-induced-autophagy
#19
Yunan Gao, Hongxiao Yang, Jing Chi, Qiannan Xu, Luqi Zhao, Weijia Yang, Weifan Liu, Wei Yang
BACKGROUND/AIMS: To study the effect of inhaling hydrogen gas on myocardial ischemic/reperfusion(I/R) injury in rats. METHODS: Seventy male Wistar albino rats were divided into five groups at random as the sham group (Sham). The I/R group (I/R), The ischemic postconditioning group (IPo), The I/R plus hydrogen group (IH2) and the ischemic postconditioning plus hydrogen group (IPoH2). The Sham group was without coronary occlusion. In I/R group, Ischemic/reperfusion injury was induced by coronary occlusion for 1 hour...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29031902/chrysophanol-inhibits-endoplasmic-reticulum-stress-in-cerebral-ischemia-and-reperfusion-mice
#20
Yongmei Zhao, Yalan Fang, Haiping Zhao, Jincheng Li, Yunxia Duan, Wenjuan Shi, Yuyou Huang, Li Gao, Yumin Luo
Endoplasmic reticulum (ER) stress plays a critical role in mediating ischemia/reperfusion (I/R) damage in the brain. Our previous study showed that Chrysophanol (CHR) alleviated cerebral ischemic injury in mice and nuclear factor-κB (NF-κB) involved in its neuroprotective effect, but the precise mechanism remains not fully understood. The present study investigated the effect of CHR treatment on I/R-induced ER stress. Mice were subjected to middle cerebral artery occlusion (MCAO) for 45min and received either vehicle or CHR (0...
October 12, 2017: European Journal of Pharmacology
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