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endoplasmic reticulum and autophagy

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https://www.readbyqxmd.com/read/27905509/the-er-stress-regulator-bip-mediates-cadmium-induced-autophagy-and-neuronal-senescence
#1
Tao Wang, Yan Yuan, Hui Zou, Jinlong Yang, Shiwen Zhao, Yonggang Ma, Yi Wang, Jianchun Bian, Xuezhong Liu, Jianhong Gu, Zongping Liu, Jiaqiao Zhu
Autophagy is protective in cadmium (Cd)-induced oxidative damage. Endoplasmic reticulum (ER) stress has been shown to induce autophagy in a process requiring the unfolded protein response signalling pathways. Cd treatment significantly increased senescence in neuronal cells, which was aggravated by 3-MA or silencing of Atg5 and abolished by rapamycin. Cd increased expression of ER stress regulators Bip, chop, eIf2α, and ATF4, and activated autophagy as evidenced by upregulated LC3. Moreover, the ER stress inhibitor mithramycin inhibited the expression of ER stress protein chaperone Bip and blocked autophagic flux...
December 1, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27899413/calcium-channel-regulator-mid1-links-torc2-mediated-changes-in-mitochondrial-respiration-to-autophagy
#2
Ariadne Vlahakis, Nerea Lopez Muniozguren, Ted Powers
Autophagy is a catabolic process that recycles cytoplasmic contents and is crucial for cell survival during stress. The target of rapamycin (TOR) kinase regulates autophagy as part of two distinct protein complexes, TORC1 and TORC2. TORC1 negatively regulates autophagy according to nitrogen availability. In contrast, TORC2 functions as a positive regulator of autophagy during amino acid starvation, via its target kinase Ypk1, by repressing the activity of the calcium-dependent phosphatase calcineurin and promoting the general amino acid control (GAAC) response...
November 29, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27896021/lithocholic-acid-induces-endoplasmic-reticulum-stress-autophagy-and-mitochondrial-dysfunction-in-human-prostate-cancer-cells
#3
Ahmed A Gafar, Hossam M Draz, Alexander A Goldberg, Mohamed A Bashandy, Sayed Bakry, Mahmoud A Khalifa, Walid AbuShair, Vladimir I Titorenko, J Thomas Sanderson
Lithocholic acid (LCA) is a secondary bile acid that is selectively toxic to human neuroblastoma, breast and prostate cancer cells, whilst sparing normal cells. We previously reported that LCA inhibited cell viability and proliferation and induced apoptosis and necrosis of androgen-dependent LNCaP and androgen-independent PC-3 human prostate cancer cells. In the present study, we investigated the roles of endoplasmic reticulum (ER) stress, autophagy and mitochondrial dysfunction in the toxicity of LCA in PC-3 and autophagy deficient, androgen-independent DU-145 cells...
2016: PeerJ
https://www.readbyqxmd.com/read/27888631/autophagy-decreases-alveolar-macrophage-apoptosis-by-attenuating-endoplasmic-reticulum-stress-and-oxidative-stress
#4
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/27881436/knockdown-of-histidine-rich-calcium-binding-protein-hrc-suppresses-liver-fibrosis-by-inhibiting-the-activation-of-hepatic-stellate-cells
#5
Jingmei Liu, Mengke Li, Jin Gong, Ping Han, Yunwu Wang, Dean Tian, Jiazhi Liao
The histidine-rich calcium binding protein (HRC) is a regulator of Ca(2+)- homeostasis and it plays a significant role in hepatocellular carcinoma (HCC) progression. However, the relationship between HRC and liver fibrogenesis is still unknown. Our data demonstrated that HRC was upregulated in fibrotic liver and activated HSCs. TGF-β treatment increased α-SMA and HRC expression dose-dependently in HSCs. Repression of HRC reduced α-SMA, CTGF and collagens expression, and inhibited HSCs proliferation and migration...
November 23, 2016: Biology Open
https://www.readbyqxmd.com/read/27877136/novel-role-of-er-stress-and-autophagy-in-microcystin-lr-induced-apoptosis-in-chinese-hamster-ovary-cells
#6
Shenshen Zhang, Chuanrui Liu, Yang Li, Mustapha U Imam, Hui Huang, Haohao Liu, Yongjuan Xin, Huizhen Zhang
Microcystin-LR (MC-LR) is a ubiquitous peptide that exhibits strong reproductive toxicity, although the mechanistic basis for such toxicity remains largely unknown. The present study was conducted to investigate the mechanisms underlying the adverse effects of exposure to MC-LR in Chinese hamster ovary (CHO) cells. The results showed that MC-LR inhibited the in vitro proliferation of CHO cells significantly, with an IC50 of 10 μM. Moreover, MC-LR-treated CHO cells revealed strong induction of cell cycle arrest and apoptosis...
2016: Frontiers in Physiology
https://www.readbyqxmd.com/read/27871116/glucocorticoid-signaling-and-bone-biology
#7
T Komori
Since glucocorticoids remain an effective therapeutic option for the treatment of many inflammatory and autoimmune diseases, glucocorticoid-induced osteoporosis is the most common form of secondary osteoporosis. Fractures may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Under physiological conditions, glucocorticoids are required for normal bone development due to their regulation of osteoblast differentiation, possibly via the Wnt/β-catenin pathway and TSC22D3. However, serum levels of endogenous corticosterone are elevated in aged mice and glucocorticoids exert negative effects on the survival of osteoblasts and osteocytes as well as angiogenesis...
November 2016: Hormone and Metabolic Research, Hormon- und Stoffwechselforschung, Hormones et Métabolisme
https://www.readbyqxmd.com/read/27865347/gestational-food-restriction-decreases-placental-interleukin-10-expression-and-markers-of-autophagy-and-endoplasmic-reticulum-stress-in-murine-intrauterine-growth-restriction
#8
Alison Chu, Shanthie Thamotharan, Amit Ganguly, Madhuri Wadehra, Matteo Pellegrini, Sherin U Devaskar
Intrauterine growth restriction (IUGR) affects up to 10% of pregnancies and often results in short- and long-term sequelae for offspring. The mechanisms underlying IUGR are poorly understood, but it is known that healthy placentation is essential for nutrient provision to fuel fetal growth, and is regulated by immunologic inputs. We hypothesized that in pregnancy, maternal food restriction (FR) resulting in IUGR would decrease the overall immunotolerant milieu in the placenta, leading to increased cellular stress and death...
October 2016: Nutrition Research
https://www.readbyqxmd.com/read/27861594/vmp1-establishes-er-microdomains-that-regulate-membrane-contact-sites-and-autophagy
#9
Luis-Carlos Tábara, Ricardo Escalante
The endoplasmic reticulum (ER) regulates organelle dynamics through the formation of membrane contact sites (MCS). Here we describe that VMP1, a multispanning ER-resident protein involved in autophagy, is enriched in ER micro-domains that are in close proximity to diverse organelles in HeLa and Cos-7 cells. These VMP1 puncta are highly dynamic, moving in concert with lipid droplets, mitochondria and endosomes. Some of these micro-domains are associated with ER sliding events and also with fission events of mitochondria and endosomes...
2016: PloS One
https://www.readbyqxmd.com/read/27855785/sec24-phosphorylation-regulates-autophagosome-abundance-during-nutrient-deprivation
#10
Saralin Davis, Juan Wang, Ming Zhu, Kyle Stahmer, Ramya Lakshminarayan, Majid Ghassemian, Yu Jiang, Elizabeth A Miller, Susan Ferro-Novick
Endoplasmic Reticulum (ER)-derived COPII coated vesicles constitutively transport secretory cargo to the Golgi. However, during starvation-induced stress, COPII vesicles have been implicated as a membrane source for autophagosomes, distinct organelles that engulf cellular components for degradation by macroautophagy (hereafter called autophagy). How cells regulate core trafficking machinery to fulfill dramatically different cellular roles in response to environmental cues is unknown. Here we show that phosphorylation of conserved amino acids on the membrane-distal surface of the Saccharomyces cerevisiae COPII cargo adaptor, Sec24, reprograms COPII vesicles for autophagy...
November 18, 2016: ELife
https://www.readbyqxmd.com/read/27851986/blocking-wnt-secretion-reduces-growth-of-hepatocellular-carcinoma-cell-lines-mostly-independent-of-%C3%AE-catenin-signaling
#11
Wenhui Wang, Lei Xu, Pengyu Liu, Kiran Jairam, Yuebang Yin, Kan Chen, Dave Sprengers, Maikel P Peppelenbosch, Qiuwei Pan, Ron Smits
Aberrant activation of Wnt/β-catenin signaling plays a key role in the onset and development of hepatocellular carcinomas (HCC), with about half of them acquiring mutations in either CTNNB1 or AXIN1. However, it remains unclear whether these mutations impose sufficient β-catenin signaling or require upstream Wnt ligand activation for sustaining optimal growth, as previously suggested for colorectal cancers. Using a panel of nine HCC cell lines, we show that siRNA-mediated knockdown of β-catenin impairs growth of all these lines...
November 13, 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27848175/glucocorticoids-prevent-enterovirus-71-capsid-protein-vp1-induced-calreticulin-surface-exposure-by-alleviating-neuronal-er-stress
#12
Dan-Dan Hu, Jian-Ning Mai, Li-Ya He, Pei-Qing Li, Wen-Xiong Chen, Jian-Jiang Yan, Wei-Dong Zhu, Li Deng, Dan Wei, Di-Hui Liu, Si-Da Yang, Zhi-Bin Yao
Severe hand-foot-and-mouth disease (HFMD) caused by Enterovirus 71 (EV71) always accompanies with inflammation and neuronal damage in the central nervous system (CNS). During neuronal injuries, cell surface-exposed calreticulin (Ecto-CRT) is an important mediator for primary phagocytosis of viable neurons by microglia. Our data confirmed that brainstem neurons underwent neuronophagia by glia in EV71-induced death cases of HFMD. EV71 capsid proteins VP1, VP2, VP3, or VP4 did not induce apoptosis of brainstem neurons...
November 15, 2016: Neurotoxicity Research
https://www.readbyqxmd.com/read/27825129/late-stage-inhibition-of-autophagy-enhances-calreticulin-surface-exposure
#13
Dan-Dan Li, Bo Xie, Xiao-Jun Wu, Jing-Jing Li, Ya Ding, Xi-Zhi Wen, Xing Zhang, Shu-Guang Zhu, Wei Liu, Xiao-Shi Zhang, Rui-Qing Peng
Calreticulin (CRT) exposure on the cell surface is essential for inducing immunogenic cell death by chemotherapy. Recent studies have shown conflicting effects of chemotherapy-induced autophagy on CRT exposure in cancer cells. Our data revealed that surface-exposed CRT (Ecto-CRT) emission was attenuated by inhibition of autophagy at early stages; however, inhibition of autophagy at late stages resulted in increased Ecto-CRT. Furthermore, neither autophagy activation nor endoplasmic reticulum (ER) stress induction alone was sufficient for CRT surface exposure...
November 4, 2016: Oncotarget
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
#14
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/27814649/nitric-oxide-mediated-pathways-and-its-role-in-the-degenerative-diseases
#15
Nan Zhang, Yu Diao, Rongrong Hua, Jun Wang, Song Han, Junfa Li, Yanling Yin
Nitric oxide (NO) is a relatively short-lived inorganic free radical, which can be produced by different types of cells in multi-cellular organisms. This diffusible messenger functions as either an effector or a second messenger in many intercellular communications or intracellular signaling pathways. NO becomes noxious if it is produced in excess. These effects are mainly mediated by the reactivity of NO with various reactive oxygen species, which can be countered by antioxidant enzymes. In addition, NO can directly modify biological molecules via S-nitrosylation and lead to altered signaling responses...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/27814589/er-chaperone-grp78-regulates-autophagy-by-modulation-of-p53-localization
#16
Mohd Kamil, Ejazul Haque, Safia Irfan, Saba Sheikh, Adria Hasan, Aamir Nazir, Mohtashim Lohani, Snober S Mir
GRP78 (glucose regulated protein 78) is a major Endoplasmic Reticulum (ER) chaperone that plays a pivotal role in normal ER functioning. Its increased expression also works as an indicator of ER stress. Its anti-apoptotic and pro-autophagic activity makes it an intriguing target to study the relationship between GRP78 and p53, which is also a major regulator of apoptosis and autophagy. Here, we studied the effect of Rotenone and Parathion on human lung cancer cells (A549 cell line) specifically with respect to ER stress and its association with different cell death pathways...
January 1, 2017: Frontiers in Bioscience (Elite Edition)
https://www.readbyqxmd.com/read/27812546/%C3%AE-cell-specific-increased-expression-of-calpastatin-prevents-diabetes-induced-by-islet-amyloid-polypeptide-toxicity
#17
Tatyana Gurlo, Safia Costes, Jonathan D Hoang, Jacqueline F Rivera, Alexandra E Butler, Peter C Butler
The islet in type 2 diabetes (T2D) shares many features of the brain in protein misfolding diseases. There is a deficit of β cells with islet amyloid derived from islet amyloid polypeptide (IAPP), a protein coexpressed with insulin. Small intracellular membrane-permeant oligomers, the most toxic form of IAPP, are more frequent in β cells of patients with T2D and rodents expressing human IAPP. β Cells in T2D, and affected cells in neurodegenerative diseases, share a comparable pattern of molecular pathology, including endoplasmic reticulum stress, mitochondrial dysfunction, attenuation of autophagy, and calpain hyperactivation...
November 3, 2016: JCI Insight
https://www.readbyqxmd.com/read/27810915/regulation-of-morphine-induced-synaptic-alterations-role-of-oxidative-stress-er-stress-and-autophagy
#18
Yu Cai, Lu Yang, Guoku Hu, Xufeng Chen, Fang Niu, Li Yuan, Han Liu, Huangui Xiong, Jyothi Arikkath, Shilpa Buch
Our findings suggest that morphine dysregulates synaptic balance in the hippocampus, a key center for learning and memory, via a novel signaling pathway involving reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, and autophagy. We demonstrate in this study that exposure of morphine to hippocampal neurons leads to a reduction in excitatory synapse densities with a concomitant enhancement of inhibitory synapse densities via activation of the μ opioid receptor. Furthermore, these effects of morphine are mediated by up-regulation of intracellular ROS from NADPH oxidase, leading, in turn, to sequential induction of ER stress and autophagy...
October 24, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27805250/autophagy-eliminates-er-membrane-reorganization-induced-by-bcl-2-inhibitor-in-hela-cells
#19
Xiaoning Li, Yongwei Kang, Bingxuan Jiao, Meihui Xia, Yao Wu, Liankun Sun
The endoplasmic reticulum (ER) is a membranous network within cells that is important for several cellular functions including translation and folding of secretory and membrane proteins, lipid biogenesis and sequestration of Ca2+. Disruption of ER structure might affect the normal physiology of the cells. In yeast, expansion of the ER is observed under unfolded protein response (UPR) and subsequently induces autophagy initiated from the ER. In this study, we demonstrated a drastic and specific ER membrane reorganization (EMR), characterized by the clustering of the ER membrane into large and compact aggregates and occurring independent of UPR in HeLa cells treated with S1 combined with ABT-737...
October 27, 2016: Oncology Reports
https://www.readbyqxmd.com/read/27803675/subcellular-evidence-for-biogenesis-of-autophagosomal-membrane-during-spermiogenesis-in-vivo
#20
Yufei Huang, Ping Yang, Tengfei Liu, Hong Chen, Xiaoya Chu, Nisar Ahmad, Qian Zhang, Quanfu Li, Lisi Hu, Yi Liu, Qiusheng Chen
Although autophagosome formation has attracted substantial attention, the origin and the source of the autophagosomal membrane remains unresolved. The present study was designed to investigate in vivo subcellular evidence for the biogenesis of autophagosomal membrane during spermiogenesis using transmission-electron microscopy (TEM), Western blots and immunohistochemistry in samples from the Chinese soft-shelled turtle. The testis expressed LC3-II protein, which was located within spermatids at different stages of differentiation and indicated active autophagy...
2016: Frontiers in Physiology
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