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ischemia and endoplasmic reticulum and autophagy

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
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
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
Yan-Ying Fan, Wei-Wei Hu, Fang Nan, Zhong Chen
Ischemic postconditioning (PostC) is defined as a series of rapid intermittent interruptions of blood flow at the phase of reperfusion, which produces neuroprotection against cerebral ischemia/reperfusion injury via mobilizing the brain's own endogenous adaptive mechanisms. Now the concept of conventional ischemic PostC has been extended to limb remote ischemic PostC and chemical PostC with hypoxia, volatile anesthetic, CO2, etc. According to the different temporal profile of PostC, it is divided into rapid and delayed PostC...
January 10, 2017: Neurochemistry International
Antero Salminen, Anu Kauppinen, Kai Kaarniranta
Alzheimer's disease (AD) is associated with deficiencies in cerebrovascular functions, e.g. reduced cerebral blood flow and capillary amyloid angiopathy, both of which are evident during the early phase of AD, thus local hypoxia/ischemia could augment the pathogenesis of AD. There is abundant literature revealing that exposures to hypoxia/ischemia increase the amyloidogenic processing of amyloid-β precursor protein (APP) leading to the accumulation of amyloid-β peptides in brain. This hypoxia-induced response has been attributed to a significant increase in the activities of β- and γ-secretases, whereas α-secretase activity decreases in hypoxia...
December 17, 2016: Journal of Neurochemistry
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)...
December 27, 2016: Oncotarget
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
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
Tao Fan, Zhixin Huang, Lei Chen, Wei Wang, Boyou Zhang, Yao Xu, Shize Pan, Zhangfan Mao, Hao Hu, Qing Geng
The activation of autophagy has been demonstrated to exert protective roles during hypoxia-reoxygenation (H/R)-induced brain injuries. This study aimed to investigate whether and how preconditioning with a proteasome inhibitor (MG-132), a proteasome promoter (Adriamycin, ADM), an autophagy inhibitor (3-methyladenine, 3-MA) and an autophagy promoter (Rapamycin, Rap) affected endoplasmic reticulum stress (ERS), the ubiquitin-proteasome system (UPS), autophagy, inflammation and apoptosis. Ubiquitin protein and 26S proteasome activity levels were decreased by MG-132 pretreatment but increased by ADM pretreatment at 2h, 4h and 6h following H/R treatment...
November 15, 2016: European Journal of Pharmacology
Xuemei Bai, Song Liu, Lin Yuan, Yunkai Xie, Tong Li, Lingxiao Wang, Xueer Wang, Tiantian Zhang, Shucun Qin, Guohau Song, Li Ge, Zhen Wang
Hydrogen as a new medical gas exerts organ-protective effects through regulating oxidative stress, inflammation and apoptosis. Multiple lines of evidence reveal the protective effects of hydrogen in various models of brain injury. However, the exact mechanism underlying this protective effect of hydrogen against hypoxic-ischemic brain damage (HIBD) is not fully understood. The present study was designed to investigate whether hydrogen-rich saline (HS) attenuates HIBD in neonatal mice and whether the observed protection is associated with reduced endoplasmic reticulum (ER) stress and regulated autophagy...
September 1, 2016: Brain Research
Gur P Kaushal, Sudhir V Shah
Autophagy is a conserved multistep pathway that degrades and recycles damaged organelles and macromolecules to maintain intracellular homeostasis. The autophagy pathway is upregulated under stress conditions including cell starvation, hypoxia, nutrient and growth-factor deprivation, endoplasmic reticulum stress, and oxidant injury, most of which are involved in the pathogenesis of acute kidney injury (AKI). Recent studies demonstrate that basal autophagy in the kidney is vital for the normal homeostasis of the proximal tubules...
April 2016: Kidney International
Liya Liu, Youxi Wu, Xiulan Huang
Orientin, a flavonoid exists in Chinese traditional herbal Polygonum orientale L., has been previously demonstrated to protect against myocardial ischemia reperfusion injury (MIRI) through inhibition of apoptosis. However, the underlying mechanisms remain to be elucidated and we therefore in this study investigated the effects of orientin on autophagy during MIRI in rats. The results indicate that orientin, at the concentrations of 10 and 30 μM in the cultures of neonatal rat cardiomyocytes, promoted the induction of autophagy, increasing the formation of autophagosomes and enhancing the expression of LC3 puncta, LC3-II/LC3-I ratio and Beclin 1 after hypoxia/reoxygenation...
April 5, 2016: European Journal of Pharmacology
Ben He, Yichao Zhao, Longwei Xu, Lingchen Gao, Yuanyuan Su, Nan Lin, Jun Pu
Circadian rhythm disruption or decrease in levels of circadian hormones such as melatonin increases ischemic heart disease risk. The nuclear melatonin receptors RORs are pivotally involved in circadian rhythm regulation and melatonin effects mediation. However, the functional roles of RORs in the heart have never been investigated and were therefore the subject of this study on myocardial ischemia/reperfusion (MI/R) injury pathogenesis. RORα and RORγ subtypes were detected in the adult mouse heart, and RORα but not RORγ was downregulated after MI/R...
April 2016: Journal of Pineal Research
Dong Liu, Xing Liu, Ti Zhou, William Yao, Jun Zhao, Zhigang Zheng, Wei Jiang, Fengsong Wang, Felix O Aikhionbare, Donald L Hill, Nerimah Emmett, Zhen Guo, Dongmei Wang, Xuebiao Yao, Yong Chen
Endoplasmic reticulum (ER) stress is involved in ischemic preconditioning that protects various organs from ischemia/reperfusion (I/R) injury. We established an in vivo ER stress preconditioning model in which tunicamycin was injected into rats before hepatic I/R. The hepatic I/R injury, demonstrated by serum aminotransferase level and the ultra-structure of the liver, was alleviated by administration of tunicamycin, which induced ER stress in rat liver by activating inositol-requiring enzyme 1 (IRE1) and upregulating 78 kDa glucose-regulated protein (GRP78)...
April 2016: Journal of Molecular Cell Biology
Haomming Zhou, Jianjun Zhu, Shi Yue, Ling Lu, Ronald W Busuttil, Jerzy W Kupiec-Weglinski, Xuehao Wang, Yuan Zhai
Endoplasmic reticulum (ER) stress plays critical roles in the pathogenesis of liver ischemia-reperfusion injury (IRI). As ER stress triggers an adaptive cellular response, the question of what determines its functional outcome in liver IRI remains to be defined. In a murine liver partial warm ischemia model, we studied how transient (30 minutes) or prolonged (90 minutes) liver ischemia regulated local ER stress response and autophagy activities and their relationship with liver IRI. Effects of chemical chaperon 4-phenylbutyrate (4-PBA) or autophagy inhibitor 3-methyladenine (3-MA) were evaluated...
February 2016: Transplantation
Xiaoyu Tian, Suling Ma, Yaqi Wang, Lianguo Hou, Yun Shi, Min Yao, Xiaoning Wang, Huifeng Zhang, Lingling Jiang
We evaluated the effects of administration of 1,25-dihydroxyvitamin D (1,25(OH)2D) during pregnancy on relieving adverse outcomes of preeclampsia and the pathologic and biochemical changes in reduction in uteroplacental perfusion (RUPP) model of rats. On day 1, 7, and 14 of pregnancy, rats in pregnant RUPP plus 1,25(OH)2D (RUPP+VD) group (n = 15) received 120 ng/100 g body weight/week of 1,25(OH)2D by subcutaneous injection, while rats in normal pregnant (n = 12) and the RUPP group (n = 14) received 1,25(OH)2D vehicle (saline solution)...
February 2016: DNA and Cell Biology
Rong Hu, Zhi-Feng Chen, Jia Yan, Qi-Fang Li, Yan Huang, Hui Xu, Xiao-Ping Zhang, Hong Jiang
Diverse clinical factors, including intestinal ischemia, contribute to acute lung injury (ALI), which has up to a 40% mortality rate. During the development of lung injury an immune response is elicited that exacerbates the lung insult. Neutrophils have been well studied in mediating the pulmonary insults through an assortment of mechanisms, such as release of granule contents and production of proinflammatory cytokines due to the overactivation of complement and cytokines. In this study, we found that enhanced endoplasmic reticulum (ER) stress was observed in infiltrated neutrophils in the early stage of an ALI mice model...
November 15, 2015: Journal of Immunology: Official Journal of the American Association of Immunologists
Fanmuyi Yang, Jia Luo
Ethanol abuse affects virtually all organ systems and the central nervous system (CNS) is particularly vulnerable to excessive ethanol exposure. Ethanol exposure causes profound damages to both the adult and developing brain. Prenatal ethanol exposure induces fetal alcohol spectrum disorders (FASD) which is associated with mental retardation and other behavioral deficits. A number of potential mechanisms have been proposed for ethanol-induced brain damage; these include the promotion of neuroinflammation, interference with signaling by neurotrophic factors, induction of oxidative stress, modulation of retinoid acid signaling, and thiamine deficiency...
October 14, 2015: Biomolecules
Bhavya B Chandrika, Cheng Yang, Yang Ou, Xiaoke Feng, Djamali Muhoza, Alexandrea F Holmes, Sue Theus, Sarika Deshmukh, Randy S Haun, Gur P Kaushal
We examined whether endoplasmic reticulum (ER) stress-induced autophagy provides cytoprotection from renal tubular epithelial cell injury due to oxidants and chemical hypoxia in vitro, as well as from ischemia-reperfusion (IR) injury in vivo. We demonstrate that the ER stress inducer tunicamycin triggers an unfolded protein response, upregulates ER chaperone Grp78, and activates the autophagy pathway in renal tubular epithelial cells in culture. Inhibition of ER stress-induced autophagy accelerated caspase-3 activation and cell death suggesting a pro-survival role of ER stress-induced autophagy...
2015: PloS One
Peng Wang, Nan Zhang, Jia Liang, Jiefei Li, Song Han, Junfa Li
Micro-RNAs (miRs) have emerged as key gene regulators in many diseases, including stroke. We recently reported that miR-30a protects N2A cells against ischemic injury, in part through enhancing beclin 1-mediated autophagy. The present study explores further the involvement of miR-30a in ischemia-induced apoptosis and its possible mechanisms in primary cortical neurons and stroked mouse brain. We demonstrate that miR-30a level is significantly decreased in cortical neurons after 1-hr oxygen-glucose deprivation (OGD)/24-hr reoxygenation...
November 2015: Journal of Neuroscience Research
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