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https://www.readbyqxmd.com/read/28230861/ripk3-interactions-with-mlkl-and-camkii-mediate-oligodendrocytes-death-in-the-developing-brain
#1
Yi Qu, Jun Tang, Huiqing Wang, Shiping Li, Fengyan Zhao, Li Zhang, Q Richard Lu, Dezhi Mu
Oligodendrocyte progenitor cells (OPCs) death is a key contributor to cerebral white matter injury (WMI) in the developing brain. A previous study by our group indicated that receptor-interacting proteins (RIPs) are crucial in mediating necroptosis in developing neurons. However, whether this mechanism is involved in OPCs death is unclear. We aimed to explore the mechanisms of RIP-mediated oligodendrocytes (OLs) death in the developing brain. Oligodendrocytes necroptosis was induced by oxygen-glucose deprivation plus caspase inhibitor zVAD treatment (OGD/zVAD) in vitro...
February 23, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28218266/crystal-nephropathies-mechanisms-of-crystal-induced-kidney-injury
#2
REVIEW
Shrikant R Mulay, Hans-Joachim Anders
Crystals can trigger a wide range of kidney injuries that can lead to acute kidney injury, chronic kidney disease, renal colic or nephrocalcinosis, depending on the localization and dynamics of crystal deposition. Studies of the biology of crystal handling by the kidney have shown that the formation of different crystals and other microparticles and the associated mechanisms of renal damage share molecular mechanisms, such as stimulation of the NLRP3 inflammasome or direct cytotoxicity through activation of the necroptosis signalling pathway...
February 20, 2017: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/28211563/cytotoxic-analysis-and-chemical-characterization-of-fractions-of-the-hydroalcoholic-extract-of-the-euterpe-oleracea-mart-seed-in-the-mcf-7-cell-line
#3
Dayanne da S Freitas, José A Morgado-Díaz, Adriana S Gehren, Flávia C B Vidal, Raquel Maria T Fernandes, Wanderson Romão, Lilian V Tose, Fabiola N S Frazão, Maria Célia P Costa, Dulcelena F Silva, Maria do Desterro S B Nascimento
OBJECTIVES: To analyse the antineoplastic activity of fractions derived from the hydroalcoholic extract of Euterpe oleracea Mart. seed in the MCF-7 cell line and to identify the compounds responsible for the antineoplastic action. METHODS: Cells were treated with 10, 20, 40 and 60 μg/ml with the hexane, chloroform and ethyl acetate fraction (EAF) of the hydroalcoholic extract of açaí seed, for 24 and 48 h. After treatment, cell viability was measured using MTT assay and cell death was assessed using the Annexin-Pi assay...
February 17, 2017: Journal of Pharmacy and Pharmacology
https://www.readbyqxmd.com/read/28204973/iaps-and-cell-death
#4
John Silke, James Vince
IAPs were named as inhibitors of apoptosis, programmed cell death, but it has become apparent that they are regulators of other types of cell death too. Because they inhibit cell death in cancer cells there has been an intense interest in developing inhibitors of these proteins to induce or sensitise cancer cells to death. In this article, we will discuss the involvement of IAPs in the apoptosis, necroptosis and pyroptosis programmed cell death paradigms. All these types of cell death are intimately involved with causing or repressing inflammation and it should perhaps therefore come as no surprise that IAPs are also involved in regulating inflammation directly...
February 16, 2017: Current Topics in Microbiology and Immunology
https://www.readbyqxmd.com/read/28199887/killing-colon-cancer-cells-through-pcd-pathways-by-a-novel-hyaluronic-acid-modified-shell-core-nanoparticle-loaded-with-rip3-in-combination-with-chloroquine
#5
Xueyan Hou, Chengli Yang, Lijing Zhang, Tingting Hu, Dan Sun, Hua Cao, Fan Yang, Gang Guo, Changyang Gong, Xiaoning Zhang, Aiping Tong, Rui Li, Yu Zheng
Due to extensive apoptosis defects and multidrug resistance, there is great interest regarding non-apoptotic programmed cell death (PCD) pathways, such as lysosomal-mediated programmed cell death (LM-PCD), necroptosis and autophagy. Because there is an intricate effector network among these PCD pathways, it is expected that they may act synergistically in cancer therapy. In this study, chloroquine (CQ) was found to significantly upregulate receptor-interacting protein kinase 3 (RIP3) expression, and RIP3 were involved in CQ-related autophagy...
January 2, 2017: Biomaterials
https://www.readbyqxmd.com/read/28197335/caspase-8-not-so-silently-deadly
#6
REVIEW
Rebecca Feltham, James E Vince, Kate E Lawlor
Apoptosis is a caspase-dependent programmed form of cell death, which is commonly believed to be an immunologically silent process, required for mammalian development and maintenance of cellular homoeostasis. In contrast, lytic forms of cell death, such as RIPK3- and MLKL-driven necroptosis, and caspase-1/11-dependent pyroptosis, are postulated to be inflammatory via the release of damage associated molecular patterns (DAMPs). Recently, the function of apoptotic caspase-8 has been extended to the negative regulation of necroptosis, the cleavage of inflammatory interleukin-1β (IL-1β) to its mature bioactive form, either directly or via the NLRP3 inflammasome, and the regulation of cytokine transcriptional responses...
January 2017: Clinical & Translational Immunology
https://www.readbyqxmd.com/read/28191895/erratum-espl-is-a-bacterial-cysteine-protease-effector-that-cleaves-rhim-proteins-to-block-necroptosis-and-inflammation
#7
Jaclyn S Pearson, Cristina Giogha, Sabrina Mühlen, Ueli Nachbur, Chi L L Pham, Ying Zhang, Joanne M Hildebrand, Clare V Oates, Tania Wong Fok Lung, Danielle Ingle, Laura F Dagley, Aleksandra Bankovacki, Emma J Petrie, Gunnar N Schroeder, Valerie F Crepin, Gad Frankel, Seth L Masters, James Vince, James M Murphy, Margaret Sunde, Andrew I Webb, John Silke, Elizabeth L Hartland
No abstract text is available yet for this article.
February 13, 2017: Nature Microbiology
https://www.readbyqxmd.com/read/28186202/inhibition-of-receptor-interacting-protein-kinase-1-with-necrostatin-1s-ameliorates-disease-progression-in-elastase-induced-mouse-abdominal-aortic-aneurysm-model
#8
Qiwei Wang, Ting Zhou, Zhenjie Liu, Jun Ren, Noel Phan, Kartik Gupta, Danielle M Stewart, Stephanie Morgan, Carmel Assa, K Craig Kent, Bo Liu
Abdominal aortic aneurysm (AAA) is a common aortic disease with a progressive nature. There is no approved pharmacological treatment to effectively slow aneurysm growth or prevent rupture. Necroptosis is a form of programmed necrosis that is regulated by receptor-interacting protein kinases (RIPs). We have recently demonstrated that the lack of RIP3 in mice prevented aneurysm formation. The goal of the current study is to test whether perturbing necroptosis affects progression of existing aneurysm using the RIP1 inhibitors Necrostatin-1 (Nec-1) and an optimized form of Nec-1, 7-Cl-O-Nec-1 (Nec-1s)...
February 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28179994/matrine-induces-rip3-dependent-necroptosis-in-cholangiocarcinoma-cells
#9
Beibei Xu, Minying Xu, Yuan Tian, Qiang Yu, Yujie Zhao, Xiong Chen, Panying Mi, Hanwei Cao, Bing Zhang, Gang Song, Yan-Yan Zhan, Tianhui Hu
The development of acquired resistance to pro-apoptotic antitumor agents is a major impediment to the cure of cholangiocarcinoma (CCA). Antitumor drugs inducing non-apoptotic cell death are considered as a new approach to overcome such drug resistance. Here, we reported for the first time that matrine-induced necroptosis in CCA cell lines, differing from its classical role to induce apoptosis in many other kinds of cancer cells. CCA cells under matrine treatment exhibited typical necrosis-like but not apoptotic morphologic change...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28177687/curcumin-protects-neuronal-cells-against-status-epilepticus-induced-hippocampal-damage-through-induction-of-autophagy-and-inhibition-of-necroptosis
#10
Jin Wang, Yuan Liu, Xiao-Hui Li, Xiang-Chang Zeng, Jian Li, Jun Zhou, Bo Xiao, Kai Hu
Status epilepticus, the most severe form of epilepsy, is characterized by progressive functional and structural damage in the hippocampus, ultimately leading to the development and clinical appearance of spontaneous, recurrent seizures. Though the pathogenesis underlying epileptogenesis processes remains unclear, a substantial body of evidence has shown that status epilepticus acts as an important initial factor in triggering epileptogenesis. Notably, besides classical cell death mechanisms such as apoptosis and necrosis, two novel regulators of cell fate known as necroptosis and autophagy, are demonstrated to be involved in neuronal damage in various neurodegenerative and neuropsychiatric disorders...
December 9, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28176780/rip1-autophosphorylation-is-promoted-by-mitochondrial-ros-and-is-essential-for-rip3-recruitment-into-necrosome
#11
Yingying Zhang, Sheng Sean Su, Shubo Zhao, Zhentao Yang, Chuan-Qi Zhong, Xin Chen, Qixu Cai, Zhang-Hua Yang, Deli Huang, Rui Wu, Jiahuai Han
Necroptosis is a type of programmed cell death with great significance in many pathological processes. Tumour necrosis factor-α(TNF), a proinflammatory cytokine, is a prototypic trigger of necroptosis. It is known that mitochondrial reactive oxygen species (ROS) promote necroptosis, and that kinase activity of receptor interacting protein 1 (RIP1) is required for TNF-induced necroptosis. However, how ROS function and what RIP1 phosphorylates to promote necroptosis are largely unknown. Here we show that three crucial cysteines in RIP1 are required for sensing ROS, and ROS subsequently activates RIP1 autophosphorylation on serine residue 161 (S161)...
February 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28174728/necrosis-apoptosis-necroptosis-pyroptosis-it-matters-how-acinar-cells-die-during-pancreatitis
#12
EDITORIAL
Matthias Sendler, Julia Mayerle, Markus M Lerch
No abstract text is available yet for this article.
July 2016: Cellular and Molecular Gastroenterology and Hepatology
https://www.readbyqxmd.com/read/28151659/discovery-of-a-first-in-class-receptor-interacting-protein-1-rip1-kinase-specific-clinical-candidate-gsk2982772-for-the-treatment-of-inflammatory-diseases
#13
Philip A Harris, Scott B Berger, Jae U Jeong, Rakesh Nagilla, Deepak Bandyopadhyay, Nino Campobasso, Carol A Capriotti, Julie A Cox, Lauren Dare, Xiaoyang Dong, Patrick M Eidam, Joshua N Finger, Sandra J Hoffman, James Kang, Viera Kasparcova, Bryan W King, Ruth Lehr, Yunfeng Lan, Lara K Leister, John D Lich, Thomas T MacDonald, Nathan A Miller, Michael T Ouellette, Christina S Pao, Attiq Rahman, Michael A Reilly, Alan R Rendina, Elizabeth J Rivera, Michelle C Schaeffer, Clark A Sehon, Robert R Singhaus, Helen H Sun, Barbara A Swift, Rachel D Totoritis, Anna Vossenkämper, Paris Ward, David D Wisnoski, Daohua Zhang, Robert W Marquis, Peter J Gough, John Bertin
RIP1 regulates necroptosis and inflammation and may play an important role in contributing to a variety of human pathologies, including immune-mediated inflammatory diseases. Small-molecule inhibitors of RIP1 kinase that are suitable for advancement into the clinic have yet to be described. Herein, we report our lead optimization of a benzoxazepinone hit from a DNA-encoded library and the discovery and profile of clinical candidate GSK2982772 (compound 5), currently in phase 2a clinical studies for psoriasis, rheumatoid arthritis, and ulcerative colitis...
February 10, 2017: Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28151480/ripk1-ripk3-promotes-vascular-permeability-to-allow-tumor-cell-extravasation-independent-of-its-necroptotic-function
#14
Kay Hänggi, Lazaros Vasilikos, Aida Freire Valls, Rosario Yerbes, Janin Knop, Lisanne M Spilgies, Kristy Rieck, Tvisha Misra, John Bertin, Peter J Gough, Thomas Schmidt, Carmen Ruiz de Almodòvar, W Wei-Lynn Wong
Necroptosis is an inflammatory form of programmed cell death requiring receptor-interacting protein kinase 1, 3 (RIPK1, RIPK3) and mixed lineage kinase domain-like protein (MLKL). The kinase of RIPK3 phosphorylates MLKL causing MLKL to form a pore-like structure, allowing intracellular contents to release and cell death to occur. Alternatively, RIPK1 and RIPK3 have been shown to regulate cytokine production directly influencing inflammatory immune infiltrates. Recent data suggest that necroptosis may contribute to the malignant transformation of tumor cells in vivo and we asked whether necroptosis may have a role in the tumor microenvironment altering the ability of the tumor to grow or metastasize...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28151467/augmented-trophoblast-cell-death-in-preeclampsia-can-proceed-via-ceramide-mediated-necroptosis
#15
Liane Jennifer Bailey, Sruthi Alahari, Andrea Tagliaferro, Martin Post, Isabella Caniggia
Preeclampsia, a serious hypertensive disorder of pregnancy, is characterized by elevated ceramide (CER) content that is responsible for heightened trophoblast cell death rates via apoptosis and autophagy. Whether trophoblast cells undergo necroptosis, a newly characterized form of regulated necrosis, and the potential role of CER in this process remain to be established. Herein, we report that exposure of both JEG3 cells and primary isolated cytotrophoblasts to C16:0 CER in conjunction with a caspase-8 inhibitor (Q-VD-OPh) promoted necroptotic cell death, as evidenced by increased expression and association of receptor-interacting protein kinases RIP1 and RIP3, as well as phosphorylation of mixed lineage kinase domain-like (MLKL) protein...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28145813/alteration-in-long-non-coding-rna-expression-after-traumatic-brain-injury-in-rats
#16
Chuan-Fang Wang, Cheng-Cheng Zhao, Wei-Ji Weng, Jin Lei, Yong Lin, Qing Mao, Guo-Yi Gao, Jun-Feng Feng, Ji-Yao Jiang
Traumatic brain injury (TBI) causes a primary insult and initiates a secondary injury cascade. The mechanisms underlying the secondary injury are multifactorial and may include the aberrant expression of long non-coding RNA (lncRNA) post-TBI. Here, lncRNA microarray analysis was performed to profile the altered lncRNAs in the rat hippocampus after TBI. A total of 271 lncRNA probe sets and 1046 mRNA probe sets were differentially expressed after TBI. Gene ontology analysis showed that the main components of the most significantly changed categories were inflammation, DNA transcription, apoptosis and necroptosis...
February 1, 2017: Journal of Neurotrauma
https://www.readbyqxmd.com/read/28140659/protective-effect-of-mild-induced-hypothermia-against-moderate-traumatic-brain-injury-in-rats-involved-in-necroptotic-and-apoptotic-pathways
#17
Hai-Bo Zhang, Shi-Xiang Cheng, Yue Tu, Sai Zhang, Shi-Ke Hou, Zhen Yang
AIM: To investigate the protective effect of hypothermia (HT) on brain injury in moderate traumatic brain injury (TBI) rat models and the potential mechanisms, especially the involvement of RIPK1 in apoptosis and necroptosis. METHODS: Adult Sprague-Dawley rats were randomized to four groups: sham+normothermia (sham+NT), sham+hypothermia (sham+HT), moderate TBI+normothermia (TBI+NT) and moderate TBI+hypothermia (TBI+HT). The sham+HT and TBI+HT groups were submitted to 32°C for 6 hours...
January 31, 2017: Brain Injury: [BI]
https://www.readbyqxmd.com/read/28139717/deferasirox-induced-iron-depletion-promotes-bclxl-downregulation-and-death-of-proximal-tubular-cells
#18
Diego Martin-Sanchez, Angel Gallegos-Villalobos, Miguel Fontecha-Barriuso, Susana Carrasco, Maria Dolores Sanchez-Niño, Francisco J Lopez-Hernandez, Marta Ruiz-Ortega, Jesus Egido, Alberto Ortiz, Ana Belén Sanz
Iron deficiency has been associated with kidney injury. Deferasirox is an oral iron chelator used to treat blood transfusion-related iron overload. Nephrotoxicity is the most serious and common adverse effect of deferasirox and may present as an acute or chronic kidney disease. However, scarce data are available on the molecular mechanisms of nephrotoxicity. We explored the therapeutic modulation of deferasirox-induced proximal tubular cell death in culture. Deferasirox induced dose-dependent tubular cell death and AnexxinV/7AAD staining showed features of apoptosis and necrosis...
January 31, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28138137/programmed-cell-death-as-a-defence-against-infection
#19
REVIEW
Ine Jorgensen, Manira Rayamajhi, Edward A Miao
Eukaryotic cells can die from physical trauma, which results in necrosis. Alternatively, they can die through programmed cell death upon the stimulation of specific signalling pathways. In this Review, we discuss the role of different cell death pathways in innate immune defence against bacterial and viral infection: apoptosis, necroptosis, pyroptosis and NETosis. We describe the interactions that interweave different programmed cell death pathways, which create complex signalling networks that cross-guard each other in the evolutionary 'arms race' with pathogens...
January 31, 2017: Nature Reviews. Immunology
https://www.readbyqxmd.com/read/28134664/the-walking-dead-macrophage-inflammation-and-death-in-atherosclerosis
#20
Mary M Kavurma, Katey J Rayner, Denuja Karunakaran
PURPOSE OF REVIEW: To highlight recent studies that describe novel inflammatory and signaling mechanisms that regulate macrophage death in atherosclerosis. RECENT FINDINGS: Macrophages contribute to all stages of atherosclerosis. The traditional dogma states that in homeostatic conditions, macrophages undergo apoptosis and are efficiently phagocytosed to be cleared by a process called efferocytosis. In advanced atherosclerosis, however, defective efferocytosis results in secondary necrosis of these uncleared apoptotic cells, which ultimately contributes to the formation of the characteristic necrotic core and the vulnerable plaque...
January 27, 2017: Current Opinion in Lipidology
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