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https://www.readbyqxmd.com/read/27909314/controlled-detonation-evolution-of-necroptosis-in-pathogen-defense
#1
REVIEW
Michelle Brault, Andrew Oberst
Necroptosis is a lytic form of programmed cell death that involves the swelling and rupture of dying cells. While several necroptosis-inducing stimuli have been defined, in most cells this pathway is kept in check by the action of the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases. How and when necroptosis is triggered under physiological conditions therefore remains a persistent question. Because necroptosis likely arose as a defensive mechanism against viral infection, exploration of this question requires a consideration of host-pathogen interactions, and how the sensing of infection could sensitize cells to necroptosis...
December 2, 2016: Immunology and Cell Biology
https://www.readbyqxmd.com/read/27904666/ad-hgf-improves-the-cardiac-remodeling-of-rat-following-myocardial-infarction-by-upregulating-autophagy-and-necroptosis-and-inhibiting-apoptosis
#2
Jiabao Liu, Peng Wu, Yunle Wang, Yingqiang Du, Nan A, Shuiyuan Liu, Yiming Zhang, Ningtian Zhou, Zhihui Xu, Zhijian Yang
Cell death in MI is the most critical determinant of subsequent left ventricular remodeling and heart failure. Besides apoptosis, autophagy and necroptosis have been recently found to be another two regulated cell death styles. HGF has been reported to have a protective role in MI, but its impact on the three death styles remains unclear. Thus, our study was performed to investigate the distribution of autophagy, apoptosis and necroptosis in cardiac tissues after MI and explore the role and mechanism of Ad-HGF on cardiac remodeling by regulating the three death styles...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27904150/regulating-the-balance-between-necroptosis-apoptosis-and-inflammation-by-inhibitors-of-apoptosis-proteins
#3
REVIEW
Lazaros Vasilikos, Lisanne M Spilgies, Janin Knop, WWei-Lynn Wong
Understanding how Inhibitors of APoptosis proteins (IAPs) regulate apoptosis and necroptosis has been fast-forwarded by the use of Smac mimetics to deplete or inhibit the IAPs, specifically cIAP1& 2 and XIAP. The loss or inhibition of cIAP1, cIAP2 and XIAP causes the majority of cells to be sensitized to death receptor induced cell death, particularly tumour necrosis factor (TNF). Mouse genetics shows that there is some functional redundancy and the use of Smac mimetics has allowed us to understand how changing the composition of proteins recruited to TNF receptor 1 upon TNF ligation can alter protein complex formation and activation of apoptosis or necroptosis, particularly when caspases are inhibited...
December 1, 2016: Immunology and Cell Biology
https://www.readbyqxmd.com/read/27902929/necroptosis-in-amyotrophic-lateral-sclerosis-and-other-neurological-disorders
#4
REVIEW
Jessica R Morrice, Cheryl Y Gregory-Evans, Christopher A Shaw
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the progressive degeneration of upper and lower motor neurons. Cell death in ALS and in general was previously believed to exist as a dichotomy between apoptosis and necrosis. Most research investigating cell death mechanisms in ALS was conducted before the discovery of programmed necrosis thus did not use selective cell death pathway-specific markers. Recently, a new form of programmed cell death, termed "necroptosis", has been characterized and has been recently implicated in ALS as a primary mechanism driving motor neuron cell death in different forms of ALS...
November 27, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27901113/programmed-necrosis-a-new-mechanism-of-steroidogenic-luteal-cell-death-and-elimination-during-luteolysis-in-cows
#5
Takuo Hojo, Marta J Siemieniuch, Karolina Lukasik, Katarzyna K Piotrowska-Tomala, Agnieszka W Jonczyk, Kiyoshi Okuda, Dariusz J Skarzynski
Programmed necrosis (necroptosis) is an alternative form of programmed cell death that is regulated by receptor-interacting protein kinase (RIPK) 1 and 3-dependent, but is a caspase (CASP)-independent pathway. In the present study, to determine if necroptosis participates in bovine structural luteolysis, we investigated RIPK1 and RIPK3 expression throughout the estrous cycle, during prostaglandin F2α (PGF)-induced luteolysis in the bovine corpus luteum (CL), and in cultured luteal steroidogenic cells (LSCs) after treatment with selected luteolytic factors...
November 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27900566/autophagy-regulates-death-of-retinal-pigment-epithelium-cells-in-age-related-macular-degeneration
#6
REVIEW
Kai Kaarniranta, Paulina Tokarz, Ali Koskela, Jussi Paterno, Janusz Blasiak
Age-related macular degeneration (AMD) is an eye disease underlined by the degradation of retinal pigment epithelium (RPE) cells, photoreceptors, and choriocapillares, but the exact mechanism of cell death in AMD is not completely clear. This mechanism is important for prevention of and therapeutic intervention in AMD, which is a hardly curable disease. Present reports suggest that both apoptosis and pyroptosis (cell death dependent on caspase-1) as well as necroptosis (regulated necrosis dependent on the proteins RIPK3 and MLKL, caspase-independent) can be involved in the AMD-related death of RPE cells...
November 29, 2016: Cell Biology and Toxicology
https://www.readbyqxmd.com/read/27899821/activation-of-tnfr2-sensitizes-macrophages-for-tnfr1-mediated-necroptosis
#7
Daniela Siegmund, Juliane Kums, Martin Ehrenschwender, Harald Wajant
Macrophages express TNFR1 as well as TNFR2 and are also major producers of tumor necrosis factor (TNF), especially upon contact with pathogen-associated molecular patterns. Consequently, TNF not only acts as a macrophage-derived effector molecule but also regulates the activity and viability of macrophages. Here, we investigated the individual contribution of TNFR1 and TNFR2 to TNF-induced cell death in macrophages. Exclusive stimulation of TNFR1 showed no cytotoxic effect whereas selective stimulation of TNFR2 displayed mild cytotoxicity...
September 22, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27895479/cationic-pegylated-liposomes-incorporating-an-antimicrobial-peptide-tilapia-hepcidin-2-3-an-adjuvant-of-epirubicin-to-overcome-multidrug-resistance-in-cervical-cancer-cells
#8
Vivian Juang, Hsin-Pin Lee, Anya Maan-Yuh Lin, Yu-Li Lo
Antimicrobial peptides (AMPs) have been recently evaluated as a new generation of adjuvants in cancer chemotherapy. In this study, we designed PEGylated liposomes encapsulating epirubicin as an antineoplastic agent and tilapia hepcidin 2-3, an AMP, as a multidrug resistance (MDR) transporter suppressor and an apoptosis/autophagy modulator in human cervical cancer HeLa cells. Cotreatment of HeLa cells with PEGylated liposomal formulation of epirubicin and hepcidin 2-3 significantly increased the cytotoxicity of epirubicin...
2016: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/27886851/the-role-of-necroptosis-in-pulmonary-diseases
#9
REVIEW
Kenji Mizumura, Shuichiro Maruoka, Yasuhiro Gon, Augustine M K Choi, Shu Hashimoto
By regulating the cell number and eliminating harmful cells, programmed cell death plays a critical role in development, homeostasis, and disease. While apoptosis is a recognized form of programmed cell death, necrosis was considered a type of uncontrolled cell death induced by extreme physical or chemical stress. However, recent studies have revealed the existence of a genetically programmed and regulated form of necrosis, termed necroptosis. Necroptosis is defined as necrotic cell death that is dependent on receptor-interacting protein kinase 3 (RIPK3)...
November 2016: Respiratory Investigation
https://www.readbyqxmd.com/read/27882947/arginase-2-promotes-neurovascular-degeneration-during-ischemia-reperfusion-injury
#10
Esraa Shosha, Zhimin Xu, Harumasa Yokota, Alan Saul, Modesto Rojas, R William Caldwell, Ruth B Caldwell, S Priya Narayanan
Retinal ischemia is a major cause of visual impairment and blindness and is involved in various disorders including diabetic retinopathy, glaucoma, optic neuropathies and retinopathy of prematurity. Neurovascular degeneration is a common feature of these pathologies. Our lab has previously reported that the ureahydrolase arginase 2 (A2) is involved in ischemic retinopathies. Here, we are introducing A2 as a therapeutic target to prevent neurovascular injury after retinal ischemia/reperfusion (I/R) insult. Studies were performed with mice lacking both copies of A2 (A2(-/-)) and wild-type (WT) controls (C57BL6J)...
November 24, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27880732/ceramide-activates-lysosomal-cathepsin-b-and-cathepsin-d-to-attenuate-autophagy-and-induces-er-stress-to-suppress-myeloid-derived-suppressor-cells
#11
Feiyan Liu, Xia Li, Chunwan Lu, Aiping Bai, Jacek Bielawski, Alicja Bielawska, Brendan Marshall, Patricia V Schoenlein, Iryna O Lebedyeva, Kebin Liu
Myeloid-derived suppressor cells (MDSCs) are immune suppressive cells that are hallmarks of human cancer. MDSCs inhibit cytotoxic T lymphocytes (CTLs) and NK cell functions to promote tumor immune escape and progression, and therefore are considered key targets in cancer immunotherapy. Recent studies determined a key role of the apoptosis pathways in tumor-induced MDSC homeostasis and it is known that ceramide plays a key role in regulation of mammalian cell apoptosis. In this study, we aimed to determine the efficacy and underlying molecular mechanism of ceramide in suppression of MDSCs...
November 17, 2016: Oncotarget
https://www.readbyqxmd.com/read/27875900/effects-of-necrostatin-1-an-inhibitor-of-necroptosis-and-its-inactive-analogue-nec-1i-on-basal-cardiovascular-function
#12
A Szobi, T Rajtik, A Adameova
Inhibition of receptor-interacting serine/threonine-protein kinase 1 (RIP1) by necrostatin-1 (Nec-1) alleviates cardiac injury due to prevention of necroptotic cell death. Its inactive analogue necrostatin-1i (Nec-1i), lacking RIP1 activity, serves as a suitable control. It is unknown if these agents influence the heart function in the absence of damaging stimuli. For this purpose, we measured intraarterial blood pressure (systolic - sBP and diastolic - dBP) and ECG parameters after a bolus administration of Nec-1 and Nec-1i in rats during 30 min...
November 23, 2016: Physiological Research
https://www.readbyqxmd.com/read/27869161/therapeutic-targeting-of-necroptosis-by-smac-mimetic-bypasses-apoptosis-resistance-in-acute-myeloid-leukemia-cells
#13
C Safferthal, K Rohde, S Fulda
Resistance to apoptosis, for example due to overexpression of Inhibitor of Apoptosis (IAP) proteins, is associated with poor prognosis in acute myeloid leukemia (AML). Here, we identify that Smac mimetics such as BV6, which antagonizes IAP proteins, elicit necroptosis in AML cells, in which apoptosis is inhibited pharmacologically by caspase inhibitors or genetically by caspase-8 knockdown. Importantly, BV6 triggers necroptosis also in apoptosis-resistant patient-derived AML blasts, underlining the clinical relevance of our findings...
November 21, 2016: Oncogene
https://www.readbyqxmd.com/read/27857075/linear-ubiquitin-chain-assembly-complex-coordinates-late-thymic-t-cell-differentiation-and-regulatory-t-cell-homeostasis
#14
Charis E Teh, Najoua Lalaoui, Reema Jain, Antonia N Policheni, Melanie Heinlein, Silvia Alvarez-Diaz, Julie M Sheridan, Eva Rieser, Stefanie Deuser, Maurice Darding, Hui-Fern Koay, Yifang Hu, Fiona Kupresanin, Lorraine A O'Reilly, Dale I Godfrey, Gordon K Smyth, Philippe Bouillet, Andreas Strasser, Henning Walczak, John Silke, Daniel H D Gray
The linear ubiquitin chain assembly complex (LUBAC) is essential for innate immunity in mice and humans, yet its role in adaptive immunity is unclear. Here we show that the LUBAC components HOIP, HOIL-1 and SHARPIN have essential roles in late thymocyte differentiation, FOXP3(+) regulatory T (Treg)-cell development and Treg cell homeostasis. LUBAC activity is not required to prevent TNF-induced apoptosis or necroptosis but is necessary for the transcriptional programme of the penultimate stage of thymocyte differentiation...
November 18, 2016: Nature Communications
https://www.readbyqxmd.com/read/27850980/1344-plasma-rip3-a-regulator-of-necroptosis-is-associated-with-mortality-organ-dysfunction-in-sepsis
#15
John Reilly, Michael Shashaty, Brian Anderson, Jessica Palakshappa, Meghan Hotz, Jason Christie, Nuala Meyer, Nilam Mangalmurti
No abstract text is available yet for this article.
December 2016: Critical Care Medicine
https://www.readbyqxmd.com/read/27847551/caspase-3-deletion-promotes-necrosis-in-atherosclerotic-plaques-of-apoe-knockout-mice
#16
Mandy O J Grootaert, Dorien M Schrijvers, Marthe Hermans, Viviane O Van Hoof, Guido R Y De Meyer, Wim Martinet
Apoptosis of macrophages and vascular smooth muscle cells (VSMCs) in advanced atherosclerotic plaques contributes to plaque progression and instability. Caspase-3, a key executioner protease in the apoptotic pathway, has been identified in human and mouse atherosclerotic plaques but its role in atherogenesis is not fully explored. We therefore investigated the impact of caspase-3 deletion on atherosclerosis by crossbreeding caspase-3 knockout (Casp3(-/-)) mice with apolipoprotein E knockout (ApoE(-/-)) mice...
2016: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/27845194/human-albumin-attenuates-excessive-innate-immunity-via-inhibition-of-microglial-mincle-syk-signaling-in-subarachnoid-hemorrhage
#17
Yi Xie, Hongquan Guo, Liumin Wang, Lili Xu, Xiaohao Zhang, Linjie Yu, Qian Liu, Yunzi Li, Nana Zhao, Nan Zhao, Ruidong Ye, Xinfeng Liu
Subarachnoid hemorrhage (SAH) is a devastating subtype of stroke. Microglial macrophage-inducible C-type lectin (Mincle) receptor launches microglial innate immunity after SAH, and thereby achieves a key step of early cerebral injury in SAH. We previously revealed albumin could improve long-term neurological outcomes after SAH. In this study, we examined the role of microglia-mediated innate immunity in the salutary effects of albumin. SAH was induced by endovascular perforation in rats. We found that albumin can significantly mitigate early neurovascular dysfunction of SAH rats...
November 10, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27843441/the-janus-face-of-death-receptor-signaling-during-tumor-immunoediting
#18
REVIEW
Eimear O' Reilly, Andrea Tirincsi, Susan E Logue, Eva Szegezdi
Cancer immune surveillance is essential for the inhibition of carcinogenesis. Malignantly transformed cells can be recognized by both the innate and adaptive immune systems through different mechanisms. Immune effector cells induce extrinsic cell death in the identified tumor cells by expressing death ligand cytokines of the tumor necrosis factor ligand family. However, some tumor cells can escape immune elimination and progress. Acquisition of resistance to the death ligand-induced apoptotic pathway can be obtained through cleavage of effector cell expressed death ligands into a poorly active form, mutations or silencing of the death receptors, or overexpression of decoy receptors and pro-survival proteins...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27834956/a-bak-dependent-mitochondrial-amplification-step-contributes-to-smac-mimetic-glucocorticoid-induced-necroptosis
#19
Katharina Rohde, Lara Kleinesudeik, Stefanie Roesler, Oliver Löwe, Juliana Heidler, Katrin Schröder, Ilka Wittig, Stefan Dröse, Simone Fulda
Necroptosis is a form of programmed cell death that critically depends on RIP3 and MLKL. However, the contribution of mitochondria to necroptosis is still poorly understood. In the present study, we discovered that mitochondrial perturbations play a critical role in Smac mimetic/Dexamethasone (Dexa)-induced necroptosis independently of death receptor ligands. We demonstrate that the Smac mimetic BV6 and Dexa cooperate to trigger necroptotic cell death in acute lymphoblastic leukemia (ALL) cells that are deficient in caspase activation due to absent caspase-8 expression or pharmacological inhibition by the caspase inhibitor zVAD...
November 11, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27832584/getting-a-grip-on-flu-by-casting-the-dai
#20
Danielle M Clancy, Seamus J Martin
Influenza A initiates host cell death through unknown mechanisms. Thapa et al. (2016) in this issue of Cell Host & Microbe, along with recent work by Kuriakose et al. (2016), indicate that this virus provokes divergent modes of cell death, including apoptosis and necroptosis, via the nucleic acid sensor, DAI.
November 9, 2016: Cell Host & Microbe
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