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https://www.readbyqxmd.com/read/28425987/biological-activity-of-tumor-treating-fields-in-preclinical-glioma-models
#1
Manuela Silginer, Michael Weller, Roger Stupp, Patrick Roth
Glioblastoma is the most common and aggressive form of intrinsic brain tumor with a very poor prognosis. Thus, novel therapeutic approaches are urgently needed. Tumor-treating fields (TTFields) may represent such a novel treatment option. The aim of this study was to investigate the effects of TTFields on glioma cells, as well as the functional characterization of the underlying mechanisms. Here, we assessed the anti-glioma activity of TTFields in several preclinical models. Applying TTFields resulted in the induction of cell death in a frequency- and intensity-dependent manner in long-term glioma cell lines, as well as glioma-initiating cells...
April 20, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28423682/rip3-deficiency-ameliorates-inflammatory-response-in-mice-infected-with-influenza-h7n9-virus-infection
#2
Yu-Lin Xu, Hai-Lin Tang, Hao-Ran Peng, Ping Zhao, Zhong-Tian Qi, Wen Wang
Influenza H7N9 virus infection causes an acute, highly contagious respiratory illness that triggers cell death of infected cells and airway epithelial destruction. RIP3 is a key regulator of cell death responses to a growing number of viral and microbial agents. This study aimed to investigate the role of RIP3 in inflammation of influenza H7N9 virus infection. Here, RIP3 knock out (RIP3-/-) mice and littermate wild type mice were infected intranasally with influenza H7N9 virus (A/Fujian/S03/2015) to determine the contribution of RIP3 to the inflammatory response of influenza H7N9 virus infection...
March 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28421813/hemin-causes-lung-microvascular-endothelial-barrier-dysfunction-by-necroptotic-cell-death
#3
Sunit Singla, Justin R Sysol, Benjamin Dille, Nicole Jones, Jiwang Chen, Roberto F Machado
Hemin, the oxidized prosthetic moiety of hemoglobin, has been implicated in the pathogenesis of acute chest syndrome (ACS) in sickle cell patients by virtue of its endothelial-activating properties. In this study, we examined whether hemin can cause lung microvascular endothelial barrier dysfunction. By assessing transendothelial resistance using electrical cell impedance sensing, and by directly measuring trans-monolayer FITC-dextran flux, we found that hemin does cause endothelial barrier dysfunction in a concentration-dependent manner...
April 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28414098/cytosolic-calcium-mediates-rip1-rip3-complex-dependent-necroptosis-through-jnk-activation-and-mitochondrial-ros-production-in-human-colon-cancer-cells
#4
Wen Sun, Xiaxia Wu, Hongwei Gao, Jie Yu, Wenwen Zhao, Jin-Jian Lu, Jinhua Wang, Guanhua Du, Xiuping Chen
Necroptosis is a form of programmed necrosis mediated by signaling complexes with receptor-interacting protein 1 (RIP1) and RIP3 kinases as the main mediators. However, the underlying execution pathways of this phenomenon have yet to be elucidated in detail. In this study, a RIP1/RIP3 complex was formed in 2-methoxy-6-acetyl-7-methyljuglone (MAM)-treated HCT116 and HT29 colon cancer cells. With this formation, mitochondrial reactive oxygen species (ROS) levels increased, mitochondrial depolarization occurred, and ATP concentrations decreased...
April 14, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28412393/adhesion-induced-eosinophil-cytolysis-requires-the-ripk3-mlkl-signaling-pathway-which-is-counter-regulated-by-autophagy
#5
Susanne Radonjic-Hoesli, Xiaoliang Wang, Elisabeth de Graauw, Christina Stoeckle, Beata Styp-Rekowska, Ruslan Hlushchuk, Dagmar Simon, Peter J Spaeth, Shida Yousefi, Hans-Uwe Simon
BACKGROUND: Eosinophils are a subset of granulocytes which can be involved in the pathogenesis of different diseases, including allergy. Their effector functions are closely linked to their cytotoxic granule proteins. The release takes place by several different mechanisms, one of which is cytolysis, which is associated with the release of intact granules, so-called clusters of free eosinophil granules. The mechanism underlying this activation-induced form of cell death in eosinophils has remained unclear...
April 12, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28410401/ripk3-interacts-with-mavs-to-regulate-type-i-ifn-mediated-immunity-to-influenza-a-virus-infection
#6
Jeffrey Downey, Erwan Pernet, François Coulombe, Benoit Allard, Isabelle Meunier, Joanna Jaworska, Salman Qureshi, Donald C Vinh, James G Martin, Philippe Joubert, Maziar Divangahi
The type I interferon pathway plays a critical role in both host defense and tolerance against viral infection and thus requires refined regulatory mechanisms. RIPK3-mediated necroptosis has been shown to be involved in anti-viral immunity. However, the exact role of RIPK3 in immunity to Influenza A Virus (IAV) is poorly understood. In line with others, we, herein, show that Ripk3-/- mice are highly susceptible to IAV infection, exhibiting elevated pulmonary viral load and heightened morbidity and mortality...
April 14, 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28406433/diversity-of-amyloid-motifs-in-nlr-signaling-in-fungi
#7
REVIEW
Antoine Loquet, Sven J Saupe
Amyloid folds not only represent the underlying cause of a large class of human diseases but also display a variety of functional roles both in prokaryote and eukaryote organisms. Among these roles is a recently-described activity in signal transduction cascades functioning in host defense and programmed cell death and involving Nod-like receptors (NLRs). In different fungal species, prion amyloid folds convey activation signals from a receptor protein to an effector domain by an amyloid templating and propagation mechanism...
April 13, 2017: Biomolecules
https://www.readbyqxmd.com/read/28401906/acrolein-acts-as-a-neurotoxin-in-the-nigrostriatal-dopaminergic-system-of-rat-involvement-of-%C3%AE-synuclein-aggregation-and-programmed-cell-death
#8
Yi-Ting Wang, Hui-Ching Lin, Wei-Zhong Zhao, Hui-Ju Huang, Yu-Li Lo, Hsiang-Tsui Wang, Anya Maan-Yuh Lin
Clinical studies report significant increases in acrolein (an α,β-unsaturated aldehyde) in the substantia nigra (SN) of patients with Parkinson's disease (PD). In the present study, acrolein-induced neurotoxicity in the nigrostriatal dopaminergic system was investigated by local infusion of acrolein (15, 50, 150 nmoles/0.5 μl) in the SN of Sprague-Dawley rats. Acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was delineated by reductions in tyrosine hydroxylase (TH) levels, dopamine transporter levels and TH-positive neurons in the infused SN as well as in striatal dopamine content...
April 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28397069/licl-treatment-induces-programmed-cell-death-of-schwannoma-cells-through-akt-and-mtor-mediated-necroptosis
#9
Ying Wang, Qi Zhang, Bo Wang, Peng Li, Pinan Liu
Lithium is considered a first-line therapy for the treatment of bipolar disorder and was recently shown to be associated with a reduced overall cancer risk. A growing body of evidence has indicated the potential antitumor benefits of this drug. Lithium likely functions as an antitumor agent. In this study, we found that lithium chloride (LiCl) significantly inhibits the proliferation of both RT4 cells and human NF2-associated primary schwannoma cells by inhibiting the expression of apoptosis-related proteins...
April 10, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28396243/mechanical-force-mediated-pathological-cartilage-thinning-is-regulated-by-necroptosis-and-apoptosis
#10
C Zhang, S Lin, T Li, Y Jiang, Z Huang, J Wen, W Cheng, H Li
OBJECTIVE: This study aimed to identify the mechanisms underlying mandibular chondrocyte cell death and cartilage thinning in response to mechanical force. MATERIAL AND METHODS: An in vivo model (compressive mechanical force) and an in vitro model (TNF-α+cycloheximide) were used to induce mandibular chondrocyte necroptosis. Hematoxylin and eosin staining and transmission electron microscopy were used to assess histological and subcellular changes in mandibular chondrocyte...
April 7, 2017: Osteoarthritis and Cartilage
https://www.readbyqxmd.com/read/28388412/escrt-iii-acts-downstream-of-mlkl-to-regulate-necroptotic-cell-death-and-its-consequences
#11
Yi-Nan Gong, Cliff Guy, Hannes Olauson, Jan Ulrich Becker, Mao Yang, Patrick Fitzgerald, Andreas Linkermann, Douglas R Green
The activation of mixed lineage kinase-like (MLKL) by receptor-interacting protein kinase-3 (RIPK3) results in plasma membrane (PM) disruption and a form of regulated necrosis, called necroptosis. Here, we show that, during necroptosis, MLKL-dependent calcium (Ca(2+)) influx and phosphatidylserine (PS) exposure on the outer leaflet of the plasma membrane preceded loss of PM integrity. Activation of MLKL results in the generation of broken, PM "bubbles" with exposed PS that are released from the surface of the otherwise intact cell...
April 6, 2017: Cell
https://www.readbyqxmd.com/read/28388403/escrting-necroptosis
#12
Hongyan Guo, William J Kaiser
Necroptosis is a highly inflammatory form of programmed cell death that results from MLKL-mediated disruption of the cell membrane. In this issue of Cell, Gong et al. challenge the notion that MLKL activation is a point of no return by identifying mechanisms to counterbalance necroptosis, sustain plasma membrane integrity, and prolong cell viability.
April 6, 2017: Cell
https://www.readbyqxmd.com/read/28387756/pore-forming-toxin-mediated-ion-dysregulation-leads-to-death-receptor-independent-necroptosis-of-lung-epithelial-cells-during-bacterial-pneumonia
#13
Norberto González-Juarbe, Kelley Margaret Bradley, Anukul Taranath Shenoy, Ryan Paul Gilley, Luis Felipe Reyes, Cecilia Anahí Hinojosa, Marcos Ignacio Restrepo, Peter Herman Dube, Molly Ann Bergman, Carlos Javier Orihuela
We report that pore-forming toxins (PFTs) induce respiratory epithelial cell necroptosis independently of death receptor signaling during bacterial pneumonia. Instead, necroptosis was activated as a result of ion dysregulation arising from membrane permeabilization. PFT-induced necroptosis required RIP1, RIP3 and MLKL, and could be induced in the absence or inhibition of TNFR1, TNFR2 and TLR4 signaling. We detected activated MLKL in the lungs from mice and nonhuman primates experiencing Serratia marcescens and Streptococcus pneumoniae pneumonia, respectively...
April 7, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28387136/the-protective-effect-of-aucubin-from-eucommia-ulmoides-against-status-epilepticus-by-inducing-autophagy-and-inhibiting-necroptosis
#14
Jin Wang, Ying Li, Wei-Hua Huang, Xiang-Chang Zeng, Xiao-Hui Li, Jian Li, Jun Zhou, Jian Xiao, Bo Xiao, Dong-Sheng Ouyang, Kai Hu
Eucommia ulmoides Oliv. is a famous traditional Chinese medicine which exhibits anti-oxidative stress ability and neuro-protective effects. Aucubin is the predominant component of Eucommia ulmoides Oliv. Our present study is intended to investigate aucubin's potential protective effects on neurons against epilepsy in the hippocampus by establishing the lithium-pilocarpine induced status epilepticus (SE) rat model in vivo. Aucubin (at a low dose and a high dose of 5[Formula: see text]mg/kg and 10[Formula: see text]mg/kg, respectively) was administered through gavage for two weeks before lithium-pilocarpine injection...
April 7, 2017: American Journal of Chinese Medicine
https://www.readbyqxmd.com/read/28382594/the-contribution-of-necroptosis-in-neurodegenerative-diseases
#15
REVIEW
Lifei Shao, Shuping Yu, Wei Ji, Haizhen Li, Yilu Gao
Over the past decades, cell apoptosis has been significantly reputed as an accidental, redundant and alternative manner of cell demise which partakes in homeostasis in the development of extensive diseases. Nevertheless, necroptosis, another novel manner of cell death through a caspase-independent way, especially in neurodegenerative diseases remains ambiguous. The cognition of this form of cell demise is helpful to understand other forms of morphological resemblance of necrosis. Additionally, the concrete signal mechanism in the regulation of necroptosis is beneficial to the diagnosis and treatment of neurodegenerative diseases...
April 5, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28380356/necroptosis-execution-is-mediated-by-plasma-membrane-nanopores-independent-of-calcium
#16
Uris Ros, Aida Peña-Blanco, Kay Hänggi, Ulrich Kunzendorf, Stefan Krautwald, W Wei-Lynn Wong, Ana J García-Sáez
Necroptosis is a form of regulated necrosis that results in cell death and content release after plasma membrane permeabilization. However, little is known about the molecular events responsible for the disruption of the plasma membrane. Here, we find that early increase in cytosolic calcium in TNF-induced necroptosis is mediated by treatment with a Smac mimetic via the TNF/RIP1/TAK1 survival pathway. This does not require the activation of the necrosome and is dispensable for necroptosis. Necroptosis induced by the activation of TLR3/4 pathways does not trigger early calcium flux...
April 4, 2017: Cell Reports
https://www.readbyqxmd.com/read/28377599/chemically-different-non-thermal-plasmas-target-distinct-cell-death-pathways
#17
Oleg Lunov, Vitalii Zablotskii, Olexander Churpita, Mariia Lunova, Milan Jirsa, Alexandr Dejneka, Šárka Kubinová
A rigorous biochemical analysis of interactions between non-thermal plasmas (NTPs) and living cells has become an important research topic, due to recent developments in biomedical applications of non-thermal plasmas. Here, we decouple distinct cell death pathways targeted by chemically different NTPs. We show that helium NTP cells treatment, results in necrosome formation and necroptosis execution, whereas air NTP leads to mTOR activation and autophagy inhibition, that induces mTOR-related necrosis. On the contrary, ozone (abundant component of air NTP) treatment alone, exhibited the highest levels of reactive oxygen species production leading to CypD-related necrosis via the mitochondrial permeability transition...
April 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28374134/the-p38-cyld-pathway-is-involved-in-necroptosis-induced-by-oxygen-glucose-deprivation-combined-with-zvad-in-primary-cortical-neurons
#18
Tao Feng, WeiWei Chen, CaiYi Zhang, Jie Xiang, HongMei Ding, LianLian Wu, DeQin Geng
Recently, necroptosis, a form of programmed necrosis, has been widely studied. It has previously been shown that knockout of lysine 63 deubiquitinase CYLD significantly inhibits necroptosis in other cell lines, and serum response factor (SRF) could regulate CYLD gene expression through p38 mitogen-activated protein kinase (p38 MAPK). In the following study, we show oxygen-glucose deprivation (OGD) combined with a caspase inhibitor, ZVAD (OGD/ZVAD), induced CYLD protein expression in a time-dependent manner...
April 4, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28368460/the-capacity-of-pneumococci-to-activate-macrophage-nf-kb-determines-necroptosis-and-pneumonia-severity
#19
Fadie T Coleman, Matthew T Blahna, Hirofumi Kamata, Kazuko Yamamoto, Mary C Zabinski, Igor Kramnik, Andrew A Wilson, Darrell N Kotton, Lee J Quinton, Matthew R Jones, Stephen I Pelton, Joseph P Mizgerd
During pneumococcal pneumonia, antibacterial defense requires the orchestrated expression of innate immunity mediators, initiated by alveolar macrophages and dependent on transcription driven by Nuclear Factor-kB (NF-kB). Such immune pressure may select for pneumococci which avoid or subvert macrophage NF-kB activation. Analyzing pneumococci collected from children in Massachusetts, we find that the activation of macrophage NF-kB by S. pneumoniae is highly diverse, with a preponderance of low NF-kB activators that associate particularly with complicated pneumonia...
March 25, 2017: Journal of Infectious Diseases
https://www.readbyqxmd.com/read/28368457/low-nf-kb-activation-and-necroptosis-in-alveolar-macrophages-a-new-virulence-property-of-streptococcus-pneumoniae
#20
Anders P Hakansson, Caroline Bergenfelz
No abstract text is available yet for this article.
March 25, 2017: Journal of Infectious Diseases
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