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https://www.readbyqxmd.com/read/28212525/ablation-of-ferroptosis-regulator-glutathione-peroxidase-4-in-forebrain-neurons-promotes-cognitive-impairment-and-neurodegeneration
#1
William Sealy Hambright, Rene Solano Fonseca, Liuji Chen, Ren Na, Qitao Ran
Synaptic loss and neuron death are the underlying cause of neurodegenerative diseases such as Alzheimer's disease (AD); however, the modalities of cell death in those diseases remain unclear. Ferroptosis, a newly identified oxidative cell death mechanism triggered by massive lipid peroxidation, is implicated in the degeneration of neurons populations such as spinal motor neurons and midbrain neurons. Here, we investigated whether neurons in forebrain regions (cerebral cortex and hippocampus) that are severely afflicted in AD patients might be vulnerable to ferroptosis...
February 1, 2017: Redox Biology
https://www.readbyqxmd.com/read/28204974/lipid-peroxidation-dependent-cell-death-regulated-by-gpx4-and-ferroptosis
#2
Hirotaka Imai, Masaki Matsuoka, Takeshi Kumagai, Taro Sakamoto, Tomoko Koumura
Glutathione peroxidase 4 (Phospholipid hydroperoxide glutathione peroxidase, PHGPx) can directly reduce phospholipid hydroperoxide. Depletion of GPx4 induces lipid peroxidation-dependent cell death in embryo, testis, brain, liver, heart, and photoreceptor cells of mice. Administration of vitamin E in tissue specific GPx4 KO mice restored tissue damage in testis, liver, and heart. These results indicate that suppression of phospholipid peroxidation is essential for cell survival in normal tissues in mice. Ferroptosis is an iron-dependent non-apoptotic cell death that can elicited by pharmacological inhibiting the cystine/glutamate antiporter, system Xc(-) (type I) or directly binding and loss of activity of GPx4 (Type II) in cancer cells with high level RAS-RAF-MEK pathway activity or p53 expression, but not in normal cells...
February 16, 2017: Current Topics in Microbiology and Immunology
https://www.readbyqxmd.com/read/28203523/glutathione-peroxidase-4-plays-an-important-role-in-oxidative-homeostasis-and-wound-repair-in-corneal-epithelial-cells
#3
Osamu Sakai, Takatoshi Uchida, Hirotaka Imai, Takashi Ueta
Oxidative stress is involved in the pathologies of corneal epithelial cells. However, the importance of specific antioxidant enzymes in corneal epithelial cells is not fully understood. The purpose of this study is to elucidate the role of glutathione peroxidase 4 (GPx4) in corneal epithelial cells. For in vitro experiments, an immortalized human corneal epithelial cell line was used. Cytotoxicity measured through LDH activity, lipid peroxidation immunostained for 4-hydroxynonenal, cell viability, and cell death were compared between cells transfected with either GPx4 siRNA or scrambled control siRNA...
December 2016: FEBS Open Bio
https://www.readbyqxmd.com/read/28195347/characterization-of-ferroptosis-in-murine-models-of-hemochromatosis
#4
Hao Wang, Peng An, Enjun Xie, Qian Wu, Xuexian Fang, Hong Gao, Zhuzhen Zhang, Yuzhu Li, Xudong Wang, Jiaying Zhang, Guoli Li, Lei Yang, Wei Liu, Junxia Min, Fudi Wang
Ferroptosis is a recently identified iron-dependent form of non-apoptotic cell death implicated in brain, kidney, and heart pathology. However, the biological roles of iron and iron metabolism in ferroptosis remain poorly understood. Here, we studied the functional role of iron and iron metabolism in the pathogenesis of ferroptosis. We found that ferric citrate potently induces ferroptosis in murine primary hepatocytes and bone marrow-derived macrophages (BMDMs). Next, we screened for ferroptosis in mice fed a high-iron diet and in mouse models of hereditary hemochromatosis with iron overload...
February 13, 2017: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/28130223/hspa5-regulates-ferroptotic-cell-death-in-cancer-cells
#5
Shan Zhu, Qiuhong Zhang, Xiaofang Sun, Herbert J Zeh, Michael T Lotze, Rui Kang, Daolin Tang
Ferroptosis is a form of regulated cell death driven by oxidative injury promoting lipid peroxidation, although detailed molecular regulators are largely unknown. Here we show that heat shock 70kDa protein 5 (HSPA5) negatively regulates ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cells. Mechanistically, activating transcription factor 4 (ATF4) resulted in the induction of HSPA5, which in turn bound glutathione peroxidase 4 (GPX4) and protected against GPX4 protein degradation and subsequent lipid peroxidation...
January 27, 2017: Cancer Research
https://www.readbyqxmd.com/read/28108525/back-to-the-roots-of-regulated-necrosis
#6
Vladimir Todorov, Andreas Linkermann
In recent years, our knowledge of how cells die by regulated pathways of necrosis has increased tremendously. In this issue, Distéfano et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201605110) provide yet another milestone in our understanding of regulated necrosis as they identify a ferroptosis-like cell death in Arabidopsis thaliana.
February 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28100685/heat-stress-induces-ferroptosis-like-cell-death-in-plants
#7
Ayelén Mariana Distéfano, María Victoria Martin, Juan Pablo Córdoba, Andrés Martín Bellido, Sebastián D'Ippólito, Silvana Lorena Colman, Débora Soto, Juan Alfredo Roldán, Carlos Guillermo Bartoli, Eduardo Julián Zabaleta, Diego Fernando Fiol, Brent R Stockwell, Scott J Dixon, Gabriela Carolina Pagnussat
In plants, regulated cell death (RCD) plays critical roles during development and is essential for plant-specific responses to abiotic and biotic stresses. Ferroptosis is an iron-dependent, oxidative, nonapoptotic form of cell death recently described in animal cells. In animal cells, this process can be triggered by depletion of glutathione (GSH) and accumulation of lipid reactive oxygen species (ROS). We investigated whether a similar process could be relevant to cell death in plants. Remarkably, heat shock (HS)-induced RCD, but not reproductive or vascular development, was found to involve a ferroptosis-like cell death process...
February 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28088622/reactive-oxygen-species-and-cancer-paradox-to-promote-or-to-suppress
#8
REVIEW
Sehamuddin Galadari, Anees Rahman, Siraj Pallichankandy, Faisal Thayyullathil
Reactive oxygen species (ROS), a group of highly reactive ions and molecules, are increasingly being appreciated as powerful signaling molecules involved in the regulation of a variety of biological processes. Indeed, their role is continuously being delineated in a variety of pathophysiological conditions. For instance, cancer cells are shown to have increased ROS levels in comparison to their normal counterparts. This is partly due to an enhanced metabolism and mitochondrial dysfunction in cancer cells. The escalated ROS generation in cancer cells contributes to the biochemical and molecular changes necessary for the tumor initiation, promotion and progression, as well as, tumor resistance to chemotherapy...
January 11, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28027643/switching-apoptosis-to-ferroptosis-metal-organic-network-for-high-efficiency-anticancer-therapy
#9
Di-Wei Zheng, Qi Lei, Jing-Yi Zhu, Jin-Xuan Fan, Chu-Xin Li, Cao Li, Zushun Xu, Si-Xue Cheng, Xian-Zheng Zhang
Discovering advanced materials for regulating cell death is of great importance in the development of anticancer therapy. Herein, by harnessing the recently discovered oxidative stress regulation ability of p53 and the Fenton reaction inducing capability of metal-organic network (MON), MON encapsulated with p53 plasmid (MON-p53) was designed to eradicate cancer cells via ferroptosis/apoptosis hybrid pathway. After confirming the detailed mechanism of MON-p53 in evoking ferroptosis, we further discovered that MON-p53 mediated a "bystander effect" to further sensitize cancer cells toward the MON-p53 induced ferroptosis...
December 29, 2016: Nano Letters
https://www.readbyqxmd.com/read/28012440/nrf2-inhibition-reverses-the-resistance-of-cisplatin-resistant-head-and-neck-cancer-cells-to-artesunate-induced-ferroptosis
#10
Jong-Lyel Roh, Eun Hye Kim, Hyejin Jang, Daiha Shin
: Artesunate, an anti-malarial drug, has been repurposed as an anticancer drug due to its induction of cell death via reactive oxygen species (ROS) production. However, the molecular mechanisms regulating cancer cell death and the resistance of cells to artesunate remain unclear. We investigated the molecular mechanisms behind the antitumor effects of artesunate and an approach to overcome artesunate resistance in head and neck cancer (HNC). The effects of artesunate and trigonelline were tested in different HNC cell lines, including three cisplatin-resistant HNC cell lines...
December 18, 2016: Redox Biology
https://www.readbyqxmd.com/read/27964880/role-of-gpx4-in-human-vascular-endothelial-cells-and-the-compensatory-activity-of-brown-rice-on-gpx4-ablation-condition
#11
Osamu Sakai, Toshinori Yasuzawa, Yoshie Sumikawa, Takashi Ueta, Hirotaka Imai, Akiyoshi Sawabe, Shigeru Ueshima
Oxidative stress is implicated in the pathologies of vascular endothelial cells. However, the importance of specific antioxidant enzymes in vascular endothelial cells is not fully understood. The purpose of this study was to elucidate the importance of Glutathione peroxidase 4 (GPx4), and the involvement of ferroptosis on cell death induced by GPx4 loss in human vascular endothelial cells. In addition, we examined the compensatory activity of brown rice on GPx4 ablation condition. Human umbilical vein endothelial cells were transfected with GPx4 or scramble control siRNA...
December 1, 2016: Pathophysiology: the Official Journal of the International Society for Pathophysiology
https://www.readbyqxmd.com/read/27943621/the-protective-effect-of-human-platelet-lysate-in-models-of-neurodegenerative-disease-involvement-of-the-akt-and-mek-pathways
#12
Flore Gouel, Bruce Do Van, Ming-Li Chou, Aurélie Jonneaux, Caroline Moreau, Régis Bordet, Thierry Burnouf, Jean-Christophe Devedjian, David Devos
Neurodegenerative diseases have huge economic and societal impacts, and place an immense emotional burden on patients and caregivers. Given that platelets have an essential physiological role in wound healing and tissue repair, human platelet lysates (HPLs) are being developed as a novel, effective biotherapy for neurodegenerative diseases. HPLs constitute abundant, readily accessible sources of physiological mixtures of many growth factors (GFs), with demonstrable effects on neuron survival and thus the development, maintenance, function and plasticity of the vertebrate nervous system...
December 12, 2016: Journal of Tissue Engineering and Regenerative Medicine
https://www.readbyqxmd.com/read/27941671/non-canonical-cell-death-induced-by-p53
#13
REVIEW
Atul Ranjan, Tomoo Iwakuma
Programmed cell death is a vital biological process for multicellular organisms to maintain cellular homeostasis, which is regulated in a complex manner. Over the past several years, apart from apoptosis, which is the principal mechanism of caspase-dependent cell death, research on non-apoptotic forms of programmed cell death has gained momentum. p53 is a well characterized tumor suppressor that controls cell proliferation and apoptosis and has also been linked to non-apoptotic, non-canonical cell death mechanisms...
December 9, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27860262/ferroptosis-a-new-form-of-cell-death-and-its-relationships-with-tumourous-diseases
#14
REVIEW
Haitao Yu, Pengyi Guo, Xiaozai Xie, Yi Wang, Gang Chen
Ferroptosis is a newly discovered type of cell death that differs from traditional apoptosis and necrosis and results from iron-dependent lipid peroxide accumulation. Ferroptotic cell death is characterized by cytological changes, including cell volume shrinkage and increased mitochondrial membrane density. Ferroptosis can be induced by two classes of small-molecule substances known as class 1 (system Xc(-) inhibitors) and class 2 ferroptosis inducers [glutathione peroxidase 4 (GPx4) inhibitors]. In addition to these small-molecule substances, a number of drugs (e...
November 10, 2016: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/27850378/740-inhibition-of-ferroptosis-as-a-neuroprotective-strategy-following-traumatic-brain-injury
#15
Elizabeth Kenny, Qin Yang, Emin Fidan, Lee Ann New, Tamil Selvan Anthonymuthu, Patrick Kochanek, Valerian Kagan, Hulya Bayir
No abstract text is available yet for this article.
December 2016: Critical Care Medicine
https://www.readbyqxmd.com/read/27836545/discovery-of-gpx4-inhibitory-peptides-from-random-peptide-t7-phage-display-and-subsequent-structural-analysis
#16
Kotaro Sakamoto, Satoshi Sogabe, Yusuke Kamada, Shin-Ichi Matsumoto, Akito Kadotani, Jun-Ichi Sakamoto, Akiyoshi Tani
The phospholipid hydroperoxidase glutathione peroxidase (GPX4) is an enzyme that reduces lipid hydroperoxides in lipid membranes. Recently, GPX4 has been investigated as a target molecule that induces iron-dependent cell death (ferroptosis) selectively in cancer cells that express mutant Ras. GPX4 inhibitors have the potential to become novel anti-cancer drugs. However, there are no druggable pockets for conventional small molecules on the molecular surface of GPX4. To generate GPX4 inhibitors, we examined the use of peptides as an alternative to small molecules...
January 8, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27793671/antiferroptotic-activity-of-non-oxidative-dopamine
#17
Ding Wang, Yingpeng Peng, Yangchun Xie, Borong Zhou, Xiaofang Sun, Rui Kang, Daolin Tang
Dopamine is a neurotransmitter that has many functions in the nervous and immune systems. Ferroptosis is a non-apoptotic form of regulated cell death that is involved in cancer and neurodegenerative diseases. However, the role of dopamine in ferroptosis remains unidentified. Here, we show that the non-oxidative form of dopamine is a strong inhibitor of ferroptotic cell death. Dopamine dose-dependently blocked ferroptosis in cancer (PANC1 and HEY) and non-cancer (MEF and HEK293) cells following treatment with erastin, a small molecule ferroptosis inducer...
October 25, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27791175/ironing-out-how-p53-regulates-ferroptosis
#18
Maureen E Murphy
No abstract text is available yet for this article.
November 1, 2016: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/27777421/glutathione-peroxidase-4-a-new-player-in-neurodegeneration
#19
B R Cardoso, D J Hare, A I Bush, B R Roberts
Glutathione peroxidase 4 (GPx4) is an antioxidant enzyme reported as an inhibitor of ferroptosis, a recently discovered non-apoptotic form of cell death. This pathway was initially described in cancer cells and has since been identified in hippocampal and renal cells. In this Perspective, we propose that inhibition of ferroptosis by GPx4 provides protective mechanisms against neurodegeneration. In addition, we suggest that selenium deficiency enhances susceptibility to ferroptotic processes, as well as other programmed cell death pathways due to a reduction in GPx4 activity...
October 25, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27773819/fancd2-protects-against-bone-marrow-injury-from-ferroptosis
#20
Xinxin Song, Yangchun Xie, Rui Kang, Wen Hou, Xiaofang Sun, Michael W Epperly, Joel S Greenberger, Daolin Tang
Bone marrow injury remains a serious concern in traditional cancer treatment. Ferroptosis is an iron- and oxidative-dependent form of regulated cell death that has become part of an emerging strategy for chemotherapy. However, the key regulator of ferroptosis in bone marrow injury remains unknown. Here, we show that Fanconi anemia complementation group D2 (FANCD2), a nuclear protein involved in DNA damage repair, protects against ferroptosis-mediated injury in bone marrow stromal cells (BMSCs). The classical ferroptosis inducer erastin remarkably increased the levels of monoubiquitinated FANCD2, which in turn limited DNA damage in BMSCs...
October 20, 2016: Biochemical and Biophysical Research Communications
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