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https://www.readbyqxmd.com/read/29681455/the-structure-of-the-necrosome-ripk1-ripk3-core-a-human-hetero-amyloid-signaling-complex
#1
Miguel Mompeán, Wenbo Li, Jixi Li, Ségolène Laage, Ansgar B Siemer, Gunes Bozkurt, Hao Wu, Ann E McDermott
The RIPK1-RIPK3 necrosome is an amyloid signaling complex that initiates TNF-induced necroptosis, serving in human immune defense, cancer, and neurodegenerative diseases. RIPK1 and RIPK3 associate through their RIP homotypic interaction motifs with consensus sequences IQIG (RIPK1) and VQVG (RIPK3). Using solid-state nuclear magnetic resonance, we determined the high-resolution structure of the RIPK1-RIPK3 core. RIPK1 and RIPK3 alternately stack (RIPK1, RIPK3, RIPK1, RIPK3, etc.) to form heterotypic β sheets...
April 16, 2018: Cell
https://www.readbyqxmd.com/read/29666472/caspase-8-deficiency-in-mouse-embryos-triggers-chronic-ripk1-dependent-activation-of-inflammatory-genes-independently-of-ripk3
#2
Tae-Bong Kang, Ju-Seong Jeong, Seung-Hoon Yang, Andrew Kovalenko, David Wallach
Deletion of the Casp8 gene in epithelial tissues of mice results in severe inflammatory pathologies. Its ubiquitous deletion, or its specific deletion in endothelial cells, results in intrauterine death associated with capillary damage. These pathologies are all preventable by co-deletion of Casp8 and the genes encoding either the RIPK1 or the RIPK3 protein kinase. Since activation of RIPK3 in Caspase-8-deficient cells can trigger necroptotic cell death, and since RIPK1 can activate RIPK3, it is widely assumed that the inflammatory states resulting from Caspase-8 deficiency occur as a consequence of RIPK3-induced necroptosis...
April 17, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29643440/bacterial-pore-forming-toxins-promote-the-activation-of-caspases-in-parallel-to-necroptosis-to-enhance-alarmin-release-and-inflammation-during-pneumonia
#3
Norberto Gonzalez-Juarbe, Kelley M Bradley, Ashleigh N Riegler, Luis F Reyes, Terry Brissac, Sang-Sang Park, Marcos I Restrepo, Carlos J Orihuela
Pore-forming toxins are the most common virulence factor in pathogenic bacteria. They lead to membrane permeabilization and cell death. Herein, we show that respiratory epithelial cells (REC) undergoing bacterial pore-forming toxin (PFT)-induced necroptosis simultaneously experienced caspase activation independently of RIPK3. MLKL deficient REC treated with a pan-caspase inhibitor were protected in an additive manner against PFT-induced death. Subsequently, cleaved versions of caspases-2, -4 and -10 were detected within REC undergoing necroptosis by immunoblots and monoclonal antibody staining...
April 11, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29621771/low-necroptosis-process-predicts-poor-treatment-outcome-of-human-papillomavirus-positive-cervical-cancers-by-decreasing-tumor-associated-macrophages-m1-polarization
#4
Lin Li, Song Yu, Chunyi Zang
BACKGROUND/AIM: The aim of this study was to assess the functions of the necroptosis process on the prognosis of high-risk human papillomavirus (HR-HPV)-related cervical cancer. METHODS: PCR and western blotting were used to demonstrate the expression of the necroptosis marker, mixed lineage kinase domain-like protein (MLKL), in whole blood and peripheral blood mononuclears (PBMCs) of 89 cervical cancer patients and 15 healthy volunteers. Necroptosis levels and M1 polarization were determined in tumor co-cultured macrophages...
April 5, 2018: Gynecologic and Obstetric Investigation
https://www.readbyqxmd.com/read/29621753/necroptosis-contributes-to-urban-particulate-matter-induced-airway-epithelial-injury
#5
Feng Xu, Man Luo, Lulu He, Yuan Cao, Wen Li, Songmin Ying, Zhihua Chen, Huahao Shen
BACKGROUND/AIMS: Necroptosis, a form of programmed necrosis, is involved in the pathologic process of several kinds of pulmonary diseases. However, the role of necroptosis in particulate matter (PM)-induced pulmonary injury remains unclear. The objective of this study is to investigate the involvement of necroptosis in the pathogenesis of PM-induced toxic effects in pulmonary inflammation and mucus hyperproduction, both in vitro and in vivo. METHODS: PM was administered into human bronchial epithelial (HBE) cells or mouse airways, and the inflammatory response and mucus production were assessed...
March 29, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29598451/novel-drug-discovery-strategies-for-atherosclerosis-that-target-necrosis-and-necroptosis
#6
Isabelle Coornaert, Sam Hofmans, Lars Devisscher, Koen Augustyns, Pieter Van Der Veken, Guido R Y De Meyer, Wim Martinet
Formation and enlargement of a necrotic core play a pivotal role in atherogenesis. Since the discovery of necroptosis, which is a regulated form of necrosis, prevention of necrotic cell death has become an attractive therapeutic goal to reduce plaque formation. Areas covered: This review highlights the triggers and consequences of (unregulated) necrosis and necroptosis in atherosclerosis. The authors discuss different pharmacological strategies to inhibit necrotic cell death in advanced atherosclerotic plaques...
March 29, 2018: Expert Opinion on Drug Discovery
https://www.readbyqxmd.com/read/29593066/necroptosis-in-development-and-diseases
#7
REVIEW
Bing Shan, Heling Pan, Ayaz Najafov, Junying Yuan
Necroptosis, a form of regulated necrotic cell death mediated by RIPK1 (receptor-interacting protein kinase 1) kinase activity, RIPK3, and MLKL (mixed-lineage kinase domain-like pseudokinase), can be activated under apoptosis-deficient conditions. Modulating the activation of RIPK1 by ubiquitination and phosphorylation is critical to control both necroptosis and apoptosis. Mutant mice with kinase-dead RIPK1 or RIPK3 and MLKL deficiency show no detrimental phenotype in regard to development and adult homeostasis...
March 1, 2018: Genes & Development
https://www.readbyqxmd.com/read/29588419/tweak-and-ripk1-mediate-a-second-wave-of-cell-death-during-aki
#8
Diego Martin-Sanchez, Miguel Fontecha-Barriuso, Susana Carrasco, Maria Dolores Sanchez-Niño, Anne von Mässenhausen, Andreas Linkermann, Pablo Cannata-Ortiz, Marta Ruiz-Ortega, Jesus Egido, Alberto Ortiz, Ana Belen Sanz
Acute kidney injury (AKI) is characterized by necrotic tubular cell death and inflammation. The TWEAK/Fn14 axis is a mediator of renal injury. Diverse pathways of regulated necrosis have recently been reported to contribute to AKI, but there are ongoing discussions on the timing or molecular regulators involved. We have now explored the cell death pathways induced by TWEAK/Fn14 activation and their relevance during AKI. In cultured tubular cells, the inflammatory cytokine TWEAK induces apoptosis in a proinflammatory environment...
March 27, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29581579/restoration-of-e-cadherin-by-ppbica-protects-against-cisplatin-induced-acute-kidney-injury-by-attenuating-inflammation-and-programmed-cell-death
#9
Li Gao, Ming-Ming Liu, Hong-Mei Zang, Qiu-Ying Ma, Qin Yang, Ling Jiang, Gui-Ling Ren, Hai-Di Li, Wei-Feng Wu, Jia-Nan Wang, Biao Wei, Xue-Qi Liu, Cheng Jiang, Cheng Huang, Jun Li, Xiao-Ming Meng
E-cadherin is a major component of tubular adherent proteins that maintain intercellular contacts and cell polarity in epithelial tissue. It is involved in pathological processes of renal cell carcinoma and fibrotic diseases via epithelial-mesenchymal transition. Although studies have shown E-cadherin is significantly downregulated in acute kidney injury (AKI), its function in AKI is unknown. Here, we evaluated cell damage and inflammation in cisplatin-stimulated tubular epithelial cell lines after disrupting E-cadherin and restoring it with PPBICA, a small molecule identified by high-throughput screening...
March 26, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29560122/the-enhanced-susceptibility-of-adam-17-hypomorphic-mice-to-dss-induced-colitis-is-not-ameliorated-by-loss-of-ripk3-revealing-an-unexpected-function-of-adam-17-in-necroptosis
#10
Johaiber Fuchslocher Chico, Maren Falk-Paulsen, Anne Luzius, Carina Saggau, Barbara Ruder, Julia Bolik, Dirk Schmidt-Arras, Andreas Linkermann, Christoph Becker, Philip Rosenstiel, Stefan Rose-John, Dieter Adam
The disintegrin metalloprotease ADAM17 has a critical role in intestinal inflammation and regeneration in mice, as illustrated by the dramatically increased susceptibility of ADAM17 hypomorphic (ADAM17ex/ex ) mice to dextran sulfate sodium (DSS)-induced colitis. Similarly, necroptosis has been implicated in inflammatory responses in the intestine. In this study, we have investigated the contribution of necroptosis to ADAM17-regulated intestinal inflammation in vivo by crossing ADAM17ex/ex mice with mice that lack the necroptotic core protein RIPK3...
February 27, 2018: Oncotarget
https://www.readbyqxmd.com/read/29557374/dabrafenib-an-inhibitor-of-rip3-kinase-dependent-necroptosis-reduces-ischemic-brain-injury
#11
Shelly A Cruz, Zhaohong Qin, Alexandre F R Stewart, Hsiao-Huei Chen
Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases (RIPK) associated with the tumor necrosis factor-alpha (TNF-α)/death receptor. Recent evidence shows RIPK inhibitors are neuroprotective and alleviate ischemic brain injury in a number of animal models, however, most have not yet undergone clinical trials and safety in humans remains in question. Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar concentrations...
February 2018: Neural Regeneration Research
https://www.readbyqxmd.com/read/29550813/a-role-for-receptor-interacting-protein-kinase-1-in-neutrophil-extracellular-trap-formation-in-patients-with-systemic-lupus-erythematosus-a-preliminary-study
#12
Ruru Guo, Yang Tu, Shaowei Xie, Xue Song Liu, Yang Song, Suli Wang, Xiaoxiang Chen, Liangjing Lu
BACKGROUND/AIMS: Neutrophil extracellular traps (NETs) are known to play an important role in systemic lupus erythematosus (SLE) by triggering innate and adaptive immune responses. The molecular mechanisms responsible for their formation in SLE are still unclear. In this study, we aim to characterize the role of the receptor-interacting protein kinase-1 (RIPK1), a homologous serine/threonine kinase previously implicated in the regulation of necroptosis and tissue injury, in decreasing neutrophil death and formation of NETs, and to investigate the clinical implications of RIPK1 in SLE...
March 13, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29540580/intracellular-nucleic-acid-sensing-triggers-necroptosis-through-synergistic-type-i-ifn-and-tnf-signaling
#13
Michelle Brault, Tayla M Olsen, Jennifer Martinez, Daniel B Stetson, Andrew Oberst
The sensing of viral nucleic acids within the cytosol is essential for the induction of innate immune responses following infection. However, this sensing occurs within cells that have already been infected. The death of infected cells can be beneficial to the host by eliminating the virus's replicative niche and facilitating the release of inflammatory mediators. In this study, we show that sensing of intracellular DNA or RNA by cGAS-STING or RIG-I-MAVS, respectively, leads to activation of RIPK3 and necroptosis in bone marrow-derived macrophages...
March 14, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29540162/ripk3-deficient-mice-were-not-protected-from-nephrotoxic-nephritis
#14
N R Hill, H T Cook, C D Pusey, R M Tarzi
BACKGROUND: Necrotizing glomerular lesions are a feature of severe glomerulonephritis. Unlike apoptosis, cellular necrosis has the potential to release damage-associated proteins into the microenvironment, thereby potentiating inflammation. Until recently necrosis was thought to be an unregulated cellular response to injury. However, recent evidence suggests that under certain circumstances receptor mediated necrosis occurs in response to death ligand signalling, one form of which is termed necroptosis...
March 14, 2018: BMC Nephrology
https://www.readbyqxmd.com/read/29528059/cationic-peroxidase-from-proso-millet-induces-human-colon-cancer-cell-necroptosis-by-regulating-autocrine-tnf-%C3%AE-and-ripk3-demethylation
#15
Xiaodong Cui, Ru Wang, Zhuanhua Wang
A cationic peroxidase (POD) was purified from proso millet seeds (PmPOD) using ammonium sulfate fractionation, cation exchange, and size exclusion chromatography. The purified PmPOD showed toxicity to normal cells and tumor cells, but was more sensitive in HT29 cells. Furthermore, the mechanism driving HCT116 and HT29 cell death by PmPOD was the induction of receptor interacting protein kinase 1 (RIPK1)- and RIPK3-dependent necroptosis, independent of apoptosis. More importantly, PmPOD could induce tumor necrosis factor-α (TNF-α) production through transcriptional upregulation...
March 12, 2018: Food & Function
https://www.readbyqxmd.com/read/29527209/receptor-interacting-protein-kinases-1-and-3-and-mixed-lineage-kinase-domain-like-protein-are-activated-by-sublytic-complement-and-participate-in-complement-dependent-cytotoxicity
#16
Michal Lusthaus, Niv Mazkereth, Natalie Donin, Zvi Fishelson
The complement system participates in the pathogenesis of many diseases. Complement activation produces several active protein complexes and peptides, including the terminal C5b-9 complexes. It was reported that C5b-9 complexes insert into the plasma membrane and cause membrane perturbation, intracellular calcium surge, metabolic depletion, and osmotic lysis. Previously, we showed that complement-dependent cytotoxicity (CDC) is regulated by JNK and Bid. Here, we demonstrate that three mediators in TNFα-induced necroptosis (regulated necrosis), the receptor-interacting protein kinases, receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3), and mixed-lineage kinase domain-like protein (MLKL), are activated by complement and contribute to CDC...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29520026/intestinal-epithelial-caspase-8-signaling-is-essential-to-prevent-necroptosis-during-salmonella-typhimurium-induced-enteritis
#17
Manuela Hefele, Iris Stolzer, Barbara Ruder, Gui-Wei He, Mousumi Mahapatro, Stefan Wirtz, Markus F Neurath, Claudia Günther
Although induction of host cell death is a pivotal step during bacteria-induced gastroenteritis, the molecular regulation remains to be fully characterized. To expand our knowledge, we investigated the role of the central cell death regulator Caspase-8 in response to Salmonella Typhimurium. Here, we uncovered that intestinal salmonellosis was associated with strong upregulation of members of the host cell death machinery in intestinal epithelial cells (IECs) as an early event, suggesting that elimination of infected IECs represents a host defense strategy...
March 8, 2018: Mucosal Immunology
https://www.readbyqxmd.com/read/29502045/ripk3-promotes-er-stress-induced-necroptosis-in-cardiac-ir-injury-a-mechanism-involving-calcium-overload-xo-ros-mptp-pathway
#18
Pingjun Zhu, Shunying Hu, Qinhua Jin, Dandan Li, Feng Tian, Sam Toan, Yang Li, Hao Zhou, Yundai Chen
Receptor-interacting protein 3 (Ripk3)-mediated necroptosis contributes to cardiac ischaemia-reperfusion (IR) injury through poorly defined mechanisms. Our results demonstrated that Ripk3 was strongly upregulated in murine hearts subjected to IR injury and cardiomyocytes treated with LPS and H2 O2 . The higher level of Ripk3 was positively correlated to the infarction area expansion, cardiac dysfunction and augmented cardiomyocytes necroptosis. Function study further illustrated that upregulated Ripk3 evoked the endoplasmic reticulum (ER) stress, which was accompanied with an increase in intracellular Ca2+ level ([Ca2+ ]c) and xanthine oxidase (XO) expression...
March 1, 2018: Redox Biology
https://www.readbyqxmd.com/read/29500402/phenytoin-inhibits-necroptosis
#19
Anne von Mässenhausen, Wulf Tonnus, Nina Himmerkus, Simon Parmentier, Danish Saleh, Diego Rodriquez, Jiraporn Ousingsawat, Rosalind L Ang, Joel M Weinberg, Ana B Sanz, Alberto Ortiz, Adrian Zierleyn, Jan Ulrich Becker, Blandine Baratte, Nathalie Desban, Stéphane Bach, Ina Maria Schiessl, Shoko Nogusa, Siddharth Balachandran, Hans Joachim Anders, Adrian T Ting, Markus Bleich, Alexei Degterev, Karl Kunzelmann, Stefan R Bornstein, Douglas R Green, Christian Hugo, Andreas Linkermann
Receptor-interacting protein kinases 1 and 3 (RIPK1/3) have best been described for their role in mediating a regulated form of necrosis, referred to as necroptosis. During this process, RIPK3 phosphorylates mixed lineage kinase domain-like (MLKL) to cause plasma membrane rupture. RIPK3-deficient mice have recently been demonstrated to be protected in a series of disease models, but direct evidence for activation of necroptosis in vivo is still limited. Here, we sought to further examine the activation of necroptosis in kidney ischemia-reperfusion injury (IRI) and from TNFα-induced severe inflammatory response syndrome (SIRS), two models of RIPK3-dependent injury...
March 2, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29497034/proteasome-inhibition-blocks-necroptosis-by-attenuating-death-complex-aggregation
#20
Mohammad Ali, Edward S Mocarski
Proteasome inhibitors have achieved clinical success because they trigger intrinsic and extrinsic cell death to eliminate susceptible human cancers. The ubiquitin-proteasome protein degradation system regulates signaling pathways by controlling levels of components such as cellular inhibitor of apoptosis (cIAP)1 and cIAP2 in TNF-mediated cell death. Here, we sought to evaluate the contribution of necroptosis to the cell death pattern induced by the specific proteasome inhibitor Carfilzomib (Cf). Proteasome inhibitor-sensitive multiple myeloma cell lines die in response to Cf by apoptosis in combination with serine protease-dependent death, without any contribution of RIPK3-dependent necroptosis...
March 1, 2018: Cell Death & Disease
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