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https://www.readbyqxmd.com/read/28524164/ripped-for-neuroinflammation
#1
Bart Tummers, Douglas R Green
Activation of the receptor interacting serine/threonine kinase (RIPK) 3 mediates an inflammatory type of cell death called necroptosis; in addition, RIPK3 has necroptosis-independent roles in inflammation, although these are not well defined. In a recent study published in Cell, Daniels and colleagues demonstrate that RIPK3 controls West Nile virus infection by promoting neuroinflammation in the central nervous system without affecting neuronal death.
May 19, 2017: Cell Research
https://www.readbyqxmd.com/read/28511054/synthesis-and-in-vitro-anticancer-activity-of-new-2-thioxo-oxazolidin-4-one-derivatives
#2
Júlia Furtado Campos, Michelly Cristiny Pereira, Wanessa Layssa Batista de Sena, Caio Gomes de Barros Martins, Jamerson Ferreira de Oliveira, Cezar Augusto da Cruz Amorim, Moacyr Jesus Barreto de Melo Rêgo, Marina Galdino da Rocha Pitta, Maria do Carmo Alves de Lima, Maira Galdino da Rocha Pitta, Ivan da Rocha Pitta
BACKGROUND: Oxazolidinones derivatives exhibit different biological properties, including anticancer activity. This work aimed to investigate the anticancer potential of five novel 2-Thioxo-oxazolidin-4-one derivatives. METHODS: Cytotoxicity assays were performed in human peripheral blood mononuclear cells (PBMCs) from healthy individuals and seven tumor cell lines. Apoptosis detection and cell cycle were evaluated by flow cytometry and the expression of genes involved in cell death processes by Real-Time PCR...
March 18, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/28506461/mk2-phosphorylates-ripk1-to-prevent-tnf-induced-cell-death
#3
Isabel Jaco, Alessandro Annibaldi, Najoua Lalaoui, Rebecca Wilson, Tencho Tenev, Lucie Laurien, Chun Kim, Kunzah Jamal, Sidonie Wicky John, Gianmaria Liccardi, Diep Chau, James M Murphy, Gabriela Brumatti, Rebecca Feltham, Manolis Pasparakis, John Silke, Pascal Meier
TNF is an inflammatory cytokine that upon binding to its receptor, TNFR1, can drive cytokine production, cell survival, or cell death. TNFR1 stimulation causes activation of NF-κB, p38α, and its downstream effector kinase MK2, thereby promoting transcription, mRNA stabilization, and translation of target genes. Here we show that TNF-induced activation of MK2 results in global RIPK1 phosphorylation. MK2 directly phosphorylates RIPK1 at residue S321, which inhibits its ability to bind FADD/caspase-8 and induce RIPK1-kinase-dependent apoptosis and necroptosis...
May 10, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28501693/necrostatin-1-protects-hippocampal-neurons-against-ischemia-reperfusion-injury-via-the-rip3-daxx-signaling-pathway-in-rats
#4
Rongli Yang, Kun Hu, Jieyun Chen, Shiguang Zhu, Lei Li, Hailong Lu, Pingjing Li, Ruiguo Dong
Global cerebral ischemia/reperfusion (I/R) induces selective neuronal injury in CA1 region of hippocampus, leading to severe impairment in behavior, learning and memory functions. However, the molecular mechanism underlying the processes was not elucidated clearly. RIP3 is a key molecular switch connecting apoptosis, necrosis and necroptosis. DAXX, as a novel substrate of RIP3, plays a vital role in ischemia-induced neuronal death. The aim of this study is to investigate the role and mechanism of RIP3/DAXX signaling pathway on neurons in CA1 region of the rat hippocampus after cerebral I/R...
May 10, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28498367/initiation-and-execution-mechanisms-of-necroptosis-an-overview
#5
REVIEW
Sasker Grootjans, Tom Vanden Berghe, Peter Vandenabeele
Necroptosis is a form of regulated cell death, which is induced by ligand binding to TNF family death domain receptors, pattern recognizing receptors and virus sensors. The common feature of these receptor systems is the implication of proteins, which contain a receptor interaction protein kinase (RIPK) homology interaction motif (RHIM) mediating recruitment and activation of receptor-interacting protein kinase 3 (RIPK3), which ultimately activates the necroptosis executioner mixed lineage kinase domain-like (MLKL)...
May 12, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28492546/cold-inducible-rna-binding-protein-through-tlr4-signaling-induces-mitochondrial-dna-fragmentation-and-regulates-macrophage-cell-death-after-trauma
#6
Zhigang Li, Erica K Fan, Jinghua Liu, Melanie J Scott, Yuehua Li, Song Li, Wen Xie, Timothy R Billiar, Mark A Wilson, Yong Jiang, Ping Wang, Jie Fan
Trauma is a major cause of systemic inflammatory response syndrome and multiple organ dysfunction syndrome. Macrophages (Mφ) direct trauma-induced inflammation, and Mφ death critically influences the progression of the inflammatory response. In the current study, we explored an important role of trauma in inducing mitochondrial DNA (mtDNA) damage in Mφ and the subsequent regulation of Mφ death. Using an animal pseudo-fracture trauma model, we demonstrated that tissue damage induced NADPH oxidase activation and increased the release of reactive oxygen species via cold-inducible RNA-binding protein (CIRP)-TLR4-MyD88 signaling...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28487950/flow-control-effect-of-necrostatin-1-on-cell-death-of-the-nrk-52e-renal-tubular-epithelial-cell-line
#7
Jialun Luo, Yiming Tao, Xinling Liang, Yuanhan Chen, Li Zhang, Fen Jiang, Shuangxin Liu, Zhiming Ye, Zhilian Li, Wei Shi
Apoptosis and necroptosis occur in renal tubular epithelial cell (RTEC) death in acute kidney injury (AKI), and may be regulated by several methods. The present study identified a protective effect of necrostatin‑1 (Nec‑1) on RTECs via a flow-control-like effect. The results established a hypoxic‑ischemic injury model of rat NRK‑52E RTECs using tumour necrosis factor‑α followed by ATP depletion with antimycin A and the pan-caspase pathway blocker, benzyloxycarbonyl-Val-Ala-Asp-fluoro-methylketone...
May 9, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28485476/necroptosis-resumes-apoptosis-in-hippocampus-but-not-in-frontal-cortex
#8
Sara Nikseresht, Fariba Khodagholi, Leila Dargahi, Abolhassan Ahmadiani
Cell death subsequent to concurrent with neuroinflammation results in some damages like neuron loss and spatial memory impairment. In this study we demonstrate the temporal pattern of neuroinflammation, necroptotic and apoptotic cell deaths in hippocampus and frontal cortex following intracerebroventricular administration of lipopolysaccharide (LPS). We evaluated receptor interacting protein kinase 1 (RIP1), RIP3 and two related metabolic enzymes including glutamate-ammonia ligase (GLUL) and glutamate dehydrogenase (GLUD) as necroptosis factors...
May 9, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28480338/the-role-of-necroptosis-in-atherosclerotic-disease
#9
Nicholas J Leeper
It is now known that cells don't always die by apoptosis, but can also undergo a process known as programmed cell necrosis, or necroptosis. In a study recently published in Science Advances, investigators reported that this pro-inflammatory process is active in human atherosclerosis, may promote growth of the necrotic core, and may serve as a novel molecular imaging and translational therapeutic target. These findings represent a major step in our goal to reduce coronary disease and stroke.
October 2016: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/28476895/regression-of-apoptosis-resistant-colorectal-tumors-by-induction-of-necroptosis-in-mice
#10
Gui-Wei He, Claudia Günther, Veronika Thonn, Yu-Qiang Yu, Eva Martini, Barbara Buchen, Markus F Neurath, Michael Stürzl, Christoph Becker
Cancer cells often acquire capabilities to evade cell death induced by current chemotherapeutic treatment approaches. Caspase-8, a central initiator of death receptor-mediated apoptosis, for example, is frequently inactivated in human cancers via multiple mechanisms such as mutation. Here, we show an approach to overcome cell death resistance in caspase-8-deficient colorectal cancer (CRC) by induction of necroptosis. In both a hereditary and a xenograft mouse model of caspase-8-deficient CRC, second mitochondria-derived activator of caspase (SMAC) mimetic treatment induced massive cell death and led to regression of tumors...
May 5, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28476074/down-the-rabbit-hole-is-necroptosis-truly-an-innate-response-to-infection
#11
Jaclyn S Pearson, James M Murphy
Pathogenic microbes have evolved countless sophisticated mechanisms to subvert host immune responses and cause disease. Understanding evasion strategies employed by pathogens has led to numerous discoveries on specific host cell processes that are critical for controlling infection. Programmed cell death (PCD) is a key host defense to microbial infection, as well as being critical for organ development and cellular homeostasis in multicellular organisms. Much of our current understanding of PCD as a host response to infection has stemmed from the discovery and study of viral inhibitors of apoptosis, and more recently viral inhibition of the newly characterised from of PCD termed necroptosis, the mechanisms of which are still under intense investigation...
May 5, 2017: Cellular Microbiology
https://www.readbyqxmd.com/read/28473408/lysis-of-human-neutrophils-by-community-associated-methicillin-resistant-staphylococcus-aureus
#12
Mallary C Greenlee-Wacker, Silvie Kremserová, William M Nauseef
Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) cause infections associated with extensive tissue damage and necrosis. In vitro, human neutrophils fed CA-MRSA lyse by an unknown mechanism that is inhibited by necrostatin-1, an allosteric inhibitor of receptor-interacting serine/threonine kinase 1 (RIPK-1). RIPK-1 figures prominently in necroptosis, a specific form of programmed cell death dependent on RIPK-1, RIPK-3 and the mixed lineage kinase-like protein (MLKL). We previously reported that necrostatin-1 inhibits lysis of human neutrophils fed CA-MRSA and attributed the process to necroptosis...
May 4, 2017: Blood
https://www.readbyqxmd.com/read/28472590/evidence-of-necroptosis-in-hearts-subjected-to-various-forms-of-ischemic-insults
#13
Adriana Adameova, Jaroslav Hrdlicka, Adrian Szobi, Veronika Ledvényiová-Farkašová, Katarina Kopaskova, Martina Murarikova, Jan Neckar, Frantisek Kolar, Táňa Ravingerová, Naranjan S Dhalla
Long-lasting ischemia can result in cell loss; however, repeated episodes of brief ischemia increase the resistance of the heart against deleterious effects of subsequent prolonged ischemic insult and promote cell survival. Traditionally, it is believed that the supply of blood to the ischemic heart is associated with release of cytokines, activation of inflammatory response and induction of necrotic cell death. In the past few years, this paradigm of passive necrosis as an uncontrolled cell death has been re-examined and the existence of a strictly regulated form of necrotic cell death, necroptosis, has been documented...
May 4, 2017: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28462531/the-interplay-of-ikk-nf-%C3%AE%C2%BAb-and-ripk1-signaling-in-the-regulation-of-cell-death-tissue-homeostasis-and-inflammation
#14
REVIEW
Vangelis Kondylis, Snehlata Kumari, Katerina Vlantis, Manolis Pasparakis
Regulated cell death pathways have important functions in host defense and tissue homeostasis. Studies in genetic mouse models provided evidence that cell death could cause inflammation in different tissues. Inhibition of RIPK3-MLKL-dependent necroptosis by FADD and caspase-8 was identified as a key mechanism preventing inflammation in epithelial barriers. Moreover, the interplay between IKK/NF-κB and RIPK1 signaling was recognized as a critical determinant of tissue homeostasis and inflammation. NEMO was shown to regulate RIPK1 kinase activity-mediated apoptosis by NF-κB-dependent and -independent functions, which are critical for averting chronic tissue injury and inflammation in the intestine and the liver...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462529/ferroptosis-bug-or-feature
#15
REVIEW
Scott J Dixon
Ferroptosis is an iron-dependent, oxidative form of non-apoptotic cell death. This form of cell death does not share morphological, biochemical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non-apoptotic cell death. Ferroptosis can be triggered by depleting the cell of the amino acid cysteine, or by inhibiting the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Why certain stimuli trigger ferroptosis instead of another form of cell death, and whether this process could be adaptive in vivo, are two major unanswered questions concerning this process...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462528/the-in-vivo-evidence-for-regulated-necrosis
#16
REVIEW
Wulf Tonnus, Andreas Linkermann
Necrosis is a hallmark of several widespread diseases or their direct complications. In the past decade, we learned that necrosis can be a regulated process that is potentially druggable. RIPK3- and MLKL-mediated necroptosis represents by far the best studied pathway of regulated necrosis. During necroptosis, the release of damage-associated molecular patterns (DAMPs) drives a phenomenon referred to as necroinflammation, a common consequence of necrosis. However, most studies of regulated necrosis investigated cell lines in vitro in a cell autonomous manner, which represents a non-physiological situation...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462525/caspase-8-regulating-life-and-death
#17
REVIEW
Bart Tummers, Douglas R Green
Roles for cell death in development, homeostasis, and the control of infections and cancer have long been recognized. Although excessive cell damage results in passive necrosis, cells can be triggered to engage molecular programs that result in cell death. Such triggers include cellular stress, oncogenic signals that engage tumor suppressor mechanisms, pathogen insults, and immune mechanisms. The best-known forms of programmed cell death are apoptosis and a recently recognized regulated necrosis termed necroptosis...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462524/ripk3-driven-cell-death-during-virus-infections
#18
REVIEW
Jason W Upton, Maria Shubina, Siddharth Balachandran
The programmed self-destruction of infected cells is a powerful antimicrobial strategy in metazoans. For decades, apoptosis represented the dominant mechanism by which the virus-infected cell was thought to undergo programmed cell death. More recently, however, new mechanisms of cell death have been described that are also key to host defense. One such mechanism in vertebrates is programmed necrosis, or "necroptosis", driven by receptor-interacting protein kinase 3 (RIPK3). Once activated by innate immune stimuli, including virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which then disrupts cellular membranes to effect necroptosis...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462521/ripk3-in-cell-death-and-inflammation-the-good-the-bad-and-the-ugly
#19
REVIEW
Susana Orozco, Andrew Oberst
Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases-1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28461585/upregulated-ectonucleotidases-in-fadd-and-rip1-deficient-jurkat-leukemia-cells-counteract-extracellular-atp-amp-accumulation-via-pannexin-1-channels-during-chemotherapeutic-drug-induced-apoptosis
#20
Andrea M Boyd-Tressler, Graham S Lane, George R Dubyak
Pannexin-1 (Panx1) channels mediate the efflux of ATP and AMP from cancer cells in response to induction of extrinsic apoptosis by death receptors or intrinsic apoptosis by chemotherapeutic agents. We previously described the accumulation of extracellular ATP /AMP during chemotherapy-induced apoptosis in Jurkat human leukemia cells. In this study, we compared how different signaling pathways determine extracellular nucleotide pools in control Jurkat cells versus Jurkat lines that lack the FADD or RIP1 cell death regulatory proteins...
May 1, 2017: Molecular Pharmacology
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