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necroptosis

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https://www.readbyqxmd.com/read/28342910/receptor-interacting-protein-kinase-3-controls-keratinocyte-activation-in-a-necroptosis-independent-manner-and-promotes-psoriatic-dermatitis-in-mice
#1
Tetsuya Honda, Osamu Yamamoto, Yu Sawada, Gyohei Egawa, Akihiko Kitoh, Atsushi Otsuka, Teruki Dainichi, Saeko Nakajima, Yoshiki Miyachi, Kenji Kabashima
RIPK3 in keratinocytes facilitates psoriatic inflammation by promoting cytokine and chemokine production, independent of the induction of necroptosis. Control of RIPK3 activation may be a novel therapeutic target for psoriasis.
March 22, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/28342712/therapeutic-targets-in-the-selective-killing-of-cancer-cells-by-nanomaterials
#2
REVIEW
Mohd Javed Akhtar, Maqusood Ahamed, Hisham A Alhadlaq
Cancer is the result of numerous defects in key regulatory proteins and pathways, and targeting them with anticancer agents is associated with severe systemic toxicity. Increased levels of reactive oxygen species (ROS) and compensatory antioxidant levels in cancer cells have emerged as broad spectrum targets for therapeutic interventions. The biochemical features of cancer provide multiple but overlapping opportunities that could be efficiently exploited by the optimally engineered particulate characteristics of nanomaterials (NMs)...
March 22, 2017: Clinica Chimica Acta; International Journal of Clinical Chemistry
https://www.readbyqxmd.com/read/28335619/over-expression-of-the-x-linked-inhibitor-of-apoptosis-protects-against-retinal-degeneration-in-a-feline-model-of-retinal-detachment
#3
Sarah Wassmer, Brian Leonard, Stuart Coupland, Adam Baker, John Hamilton, William W Hauswirth, Catherine Tsilfidis
Retinal detachment is an acute disorder in humans that is caused by trauma or disease, and it can often lead to permanent visual deficits that result from the death of photoreceptors in the retina. The final pathway for photoreceptor cell death is apoptosis and necroptosis. The X-linked inhibitor of apoptosis (XIAP) has been shown to block both of these cell death pathways. We tested the effects of XIAP on photoreceptor survival in a feline model of retinal detachment. The study was performed in 12 cats, divided into 2 experimental groups...
March 23, 2017: Human Gene Therapy
https://www.readbyqxmd.com/read/28330474/hypercholesterolemia-downregulates-autophagy-in-the-rat-heart
#4
Zoltán Giricz, Gábor Koncsos, Tomáš Rajtík, Zoltán V Varga, Tamás Baranyai, Csaba Csonka, Adrián Szobi, Adriana Adameová, Roberta A Gottlieb, Péter Ferdinandy
BACKGROUND: We have previously shown that efficiency of ischemic conditioning is diminished in hypercholesterolemia and that autophagy is necessary for cardioprotection. However, it is unknown whether isolated hypercholesterolemia disturbs autophagy or the mammalian target of rapamycin (mTOR) pathways. Therefore, we investigated whether isolated hypercholesterolemia modulates cardiac autophagy-related pathways or programmed cell death mechanisms such as apoptosis and necroptosis in rat heart...
March 23, 2017: Lipids in Health and Disease
https://www.readbyqxmd.com/read/28320320/antiviral-activity-of-pha767491-against-human-herpes-simplex-virus-in-vitro-and-in-vivo
#5
Jue Hou, Zili Zhang, Qiang Huang, Jun Yan, Xiaohu Zhang, Xiaoliang Yu, Guihua Tan, Chunfu Zheng, Feng Xu, Sudan He
BACKGROUND: Herpes simplex virus (HSV) is a common human pathogen that causes a variety of diseases, including oral-labial, genital lesions and life-threatening encephalitis. The antiviral nucleoside analogues such as acyclovir are currently used in anti-HSV therapies; however, clinical overuse of these drugs has led to the emergence of drug-resistant viral strains. Hence, there is an urgent need to develop new anti-HSV agents. METHODS: To identify novel anti-HSV-1 compounds, we screened the LOPAC small scale library of 1280 bioactive compounds to identify inhibitors of HSV-1-induced necroptosis...
March 20, 2017: BMC Infectious Diseases
https://www.readbyqxmd.com/read/28315674/dichotomy-between-receptor-interacting-protein-1-and-receptor-interacting-protein-3-mediated-necroptosis-in-experimental-pancreatitis
#6
Jianghong Wu, Tunike Mulatibieke, Jianbo Ni, Xiao Han, Bin Li, Yue Zeng, Rong Wan, Xingpeng Wang, Guoyong Hu
Pancreatic acinar cell necrosis and inflammatory responses are two key pathologic processes in acute pancreatitis (AP), which determines the severity and outcome of the disease. Recent studies suggest that necroptosis, a programed form of necrosis, is involved in the pathogenesis of AP, but the underlying mechanisms remain unknown. We investigated the expression of necrosome components, including receptor-interacting protein (RIP) 1, RIP3, and mixed lineage kinase domain-like (MLKL), and the molecular mechanisms in pancreatitis-associated necroptosis...
March 15, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28306512/an-inflammatory-perspective-on-necroptosis
#7
REVIEW
Conor J Kearney, Seamus J Martin
Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals" that promote inflammation. However, because most pro-necroptotic stimuli are intrinsically highly pro-inflammatory-due to their ability to initiate the synthesis of numerous cytokines and chemokines-the inflammatory consequences of necroptosis are complex...
March 16, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28301240/necroptosis-of-splenic-macrophages-induced-by-streptococcus-gallolyticus-subsp-pasteurianus
#8
Meixia Li, Bo Liu, Changqin Gu, Wanpo Zhang, Jun Yang, Guofu Cheng, Cuiping Liu, Xueying Hu
A previous study demonstrated that a highly virulent strain of Streptococcus gallolyticus subsp. pasteurianus, designated as the AL101002 strain, induced high mortality in ducklings with splenic lesions. In this study, 42 ducklings were subcutaneously inoculated with the AL101002 strain to study changes in splenic lesions over time. The spleens from these ducklings were significantly enlarged by congestion and edema, and/or showed multiple marbled areas 14 days postinoculation (dpi). The AL101002 strain was reisolated from the spleens and blood and confirmed by immunohistochemistry (IHC) with the use of anti-AL101002 antibody...
March 2017: Avian Diseases
https://www.readbyqxmd.com/read/28297660/progesterone-prevents-high-grade-serous-ovarian-cancer-by-inducing-necroptosis-of-p53-defective-fallopian-tube-epithelial-cells
#9
Na-Yiyuan Wu, Hsuan-Shun Huang, Tung Hui Chao, Hsien Ming Chou, Chao Fang, Chong-Zhen Qin, Chueh-Yu Lin, Tang-Yuan Chu, Hong Hao Zhou
High-grade serous ovarian carcinoma (HGSOC) originates mainly from the fallopian tube (FT) epithelium and always carries early TP53 mutations. We previously reported that tumors initiate in the FT fimbria epithelium because of apoptotic failure and the expansion of cells with DNA double-strand breaks (DSB) caused by bathing of the FT epithelial cells in reactive oxygen species (ROSs) and hemoglobin-rich follicular fluid (FF) after ovulation. Because ovulation is frequent and HGSOC is rare, we hypothesized that luteal-phase progesterone (P4) could eliminate p53-defective FT cells...
March 14, 2017: Cell Reports
https://www.readbyqxmd.com/read/28297565/rationale-for-determining-the-functional-potency-of-mesenchymal-stem-cells-in-preventing-regulated-cell-death-for-therapeutic-use
#10
Abderrahim Naji, Narufumi Suganuma, Nicolas Espagnolle, Ken-Ichi Yagyu, Nobuyasu Baba, Luc Sensebé, Frédéric Deschaseaux
Mesenchymal stem (stromal) cells (MSCs) are being investigated for treating degenerative and inflammatory disorders because of their reparative and immunomodulatory properties. Intricate mechanisms relate cell death processes with immune responses, which have implications for degenerative and inflammatory conditions. We review the therapeutic value of MSCs in terms of preventing regulated cell death (RCD). When cells identify an insult, specific intracellular pathways are elicited for execution of RCD processes, such as apoptosis, necroptosis, and pyroptosis...
March 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28294381/cd3-cd8-nkg2d-t-lymphocytes-induce-apoptosis-and-necroptosis-in-hla-negative-cells-via-fasl-fas-interaction
#11
O K Ivanova, T N Sharapova, E A Romanova, L P Sashchenko, D V Yashin
An important problem in cellular immunology is to identify new populations of cytotoxic lymphocytes capable of killing tumor cells that have lost classical components of MHC-machinery and to understand mechanisms of the death of these cells. We have previously found that CD4(+) CD25(+) lymphocytes appear in the lymphokine-activated killer (LAK) cell culture, which carry Tag7 (PGRP-S) and FasL proteins on their surface and can kill Hsp70- and Fas-expressing HLA-negative cells. In this work, we have continued to study the mechanisms of killing of the HLA-negative tumor cells, focusing this time on the CD8+ lymphocytes...
March 15, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28293227/mlkl-mediated-necroptosis-accelerates-jev-induced-neuroinflammation-in-mice
#12
Peiyu Bian, Xuyang Zheng, Li Wei, Chuantao Ye, Hong Fan, Yanhui Cai, Ying Zhang, Fanglin Zhang, Zhansheng Jia, Yingfeng Lei
Japanese encephalitis virus (JEV) is the most prevalent cause of viral encephalitis in Asia and the western Pacific. Neuronal death caused by JEV infection and inflammation induced cytotoxicity leads to progression and deterioration of Japanese encephalitis (JE). Mixed-lineage kinase domain-like protein (MLKL) mediated necroptosis is a newly discovered pathway of programmed cell death and participates in many inflammatory diseases. In this study, we demonstrated for the first time that necroptosis was involved in the neuronal loss during JE via immune-electron microscopy and immunochemistry...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28292903/mouse-cytomegalovirus-m36-and-m45-death-suppressors-cooperate-to-prevent-inflammation-resulting-from-antiviral-programmed-cell-death-pathways
#13
Lisa P Daley-Bauer, Linda Roback, Lynsey N Crosby, A Louise McCormick, Yanjun Feng, William J Kaiser, Edward S Mocarski
The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood. Murine cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8 activity (M36) and RIP3 signaling (M45) suppress these antiviral responses. Here, we report that this virus activates caspase-8 in macrophages to trigger apoptosis that gives rise to secondary necroptosis. Infection with double-mutant ΔM36/M45mutRHIM virus reveals a signaling pattern in which caspase-8 activates caspase-3 to drive apoptosis with subsequent RIP3-dependent activation of mixed lineage kinase domain-like (MLKL) leading to necroptosis...
March 14, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28292463/key-players-of-the-necroptosis-pathway-ripk1-and-sirt2-are-altered-in-placenta-from-preeclampsia-and-fetal-growth-restriction
#14
Natalie J Hannan, Sally Beard, Natalie K Binder, Kenji Onda, Tu'uhevaha J Kaitu'u-Lino, Qi Chen, Laura Tuohey, Manarangi De Silva, Stephen Tong
INTRODUCTION: Preeclampsia (PE) and fetal growth restriction (FGR) are among the leading causes of perinatal morbidity and mortality. Placental insufficiency is central to these conditions. The mechanisms underlying placental insufficiency are poorly understood. Apoptosis has long been considered the only form of regulated cell death, recent research has identified an alternate process of programmed cell death known as necroptosis [1]. Necroptosis is distinct from apoptosis, relying on the deacetylase sirtuin-2 [2], receptor interacting kinases RIPK1 and 3, and the pseudokinase MLKL [3]...
March 2017: Placenta
https://www.readbyqxmd.com/read/28291959/the-opening-of-atp-sensitive-k-channels-protects-h9c2-cardiac-cells-against-the-high-glucose-induced-injury-and-inflammation-by-inhibiting-the-ros-tlr4-necroptosis-pathway
#15
Weijie Liang, Meiji Chen, Dongdan Zheng, Jianhao Li, Mingcai Song, Wenzhu Zhang, Jianqiang Feng, Jun Lan
BACKGROUND/AIMS: Hyperglycemia activates multiple signaling molecules, including reactive oxygen species (ROS), toll-like receptor 4 (TLR4), receptor-interacting protein 3 (RIP3, a kinase promoting necroptosis), which mediate hyperglycemia-induced cardiac injury. This study explored whether inhibition of ROS-TLR4-necroptosis pathway contributed to the protection of ATP-sensitive K+ (KATP) channel opening against high glucose-induced cardiac injury and inflammation. METHODS: H9c2 cardiac cells were treated with 35 mM glucose (HG) to establish a model of HG-induced insults...
February 22, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28289909/ripk1-ripk3-mlkl-mediated-necroptosis-contributes-to-compression-induced-rat-nucleus-pulposus-cells-death
#16
Songfeng Chen, Xiao Lv, Binwu Hu, Zengwu Shao, Baichuan Wang, Kaige Ma, Hui Lin, Min Cui
The aim of this study was to systematically investigate the role of necroptosis in compression-induced rat nucleus pulposus (NP) cells death, as well as explore the underlying mechanisms involved. Rat NP cells underwent various periods of exposure to 1.0 MPa pressure. Cell viability and cell death were quantified by using cell counting kit-8 (CCK-8), and Calcein-AM/propidium iodine (PI) staining respectively. Necroptosis-associated target molecules receptor-interacing protein kinase 1 (RIPK1), phosphorylated RIPK1 (pRIPK1), receptor-interacing protein kinase 3 (RIPK3), phosphorylated RIPK3 (pRIPK3) and mixed lineage kinase domain-like (MLKL) were analyzed by Western-blot and RT-PCR...
March 13, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28285358/fluoroquinolones-and-propionic-acid-derivatives-induce-inflammatory-responses-in-vitro
#17
Akira Nakajima, Hiroki Sato, Shingo Oda, Tsuyoshi Yokoi
Fluoroquinolones and propionic acid derivatives are widely used antibacterials and non-steroidal anti-inflammatory drugs, respectively, which have been reported to frequently trigger drug hypersensitivity reactions. Such reactions are induced by inflammatory mediators such as cytokines and chemokines. The present study investigated whether levofloxacin, a fluoroquinolone, and loxoprofen, a propionic acid derivative, have the potential to induce immune-related gene expression in dendritic cell-like cell lines such as HL-60, K562, and THP-1, and immortalized keratinocytes such as HaCaT...
March 11, 2017: Cell Biology and Toxicology
https://www.readbyqxmd.com/read/28279333/dai-another-way-necroptotic-control-of-viral-infection
#18
Jason W Upton, William J Kaiser
Interrogation of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necroptosis functions as a trap door to eliminate virally infected cells. This crucial host defense pathway is orchestrated by the sensing of infection by DAI/ZBP-1, engagement of the kinase RIPK3, and subsequent membrane permeablization by the pseudokinase MLKL.
March 8, 2017: Cell Host & Microbe
https://www.readbyqxmd.com/read/28274274/a-novel-form-of-necrosis-triad-occurs-in-human-huntington-s-disease
#19
Emiko Yamanishi, Kazuko Hasegawa, Kyota Fujita, Shizuko Ichinose, Saburo Yagishita, Miho Murata, Kazuhiko Tagawa, Takumi Akashi, Yoshinobu Eishi, Hitoshi Okazawa
We previously reported transcriptional repression-induced atypical cell death of neuron (TRIAD), a new type of necrosis that is mainly regulated by Hippo pathway signaling and distinct from necroptosis regulated by RIP1/3 pathway. Here, we examined the ultrastructural and biochemical features of neuronal cell death in the brains of human HD patients in parallel with the similar analyses using mutant Htt-knock-in (Htt-KI) mice. LATS1 kinase, the critical regulator and marker of TRIAD, is actually activated in cortical neurons of postmortem human HD and of Htt-KI mouse brains, while apoptosis promoter kinase Plk1 was inactivated in human HD brains...
March 8, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28273458/distinct-kinase-independent-role-of-ripk3-in-cd11c-mononuclear-phagocytes-in-cytokine-induced-tissue-repair
#20
Kenta Moriwaki, Sakthi Balaji, John Bertin, Peter J Gough, Francis Ka-Ming Chan
Receptor interacting protein kinase 3 (RIPK3) induces necroptosis, a type of regulated necrosis, through its kinase domain and receptor interacting protein (RIP) homotypic interaction motif (RHIM). In addition, RIPK3 has been shown to regulate NLRP3 inflammasome and nuclear factor κB (NF-κB) activation. However, the relative contribution of these signaling pathways to RIPK3-dependent inflammation in distinct immune effectors is unknown. To investigate these questions, we generated RIPK3-GFP reporter mice...
March 7, 2017: Cell Reports
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