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Antonio Bruni, Andrew R Pepper, Rena L Pawlick, Boris Gala-Lopez, Anissa F Gamble, Tatsuya Kin, Karen Seeberger, Gregory S Korbutt, Stefan R Bornstein, Andreas Linkermann, A M James Shapiro
Human islet transplantation has been hampered by donor cell death associated with the islet preparation procedure before transplantation. Regulated necrosis pathways are biochemically and morphologically distinct from apoptosis. Recently, ferroptosis was identified as a non-apoptotic form of iron-dependent regulated necrosis implicated in various pathological conditions. Mediators of islet oxidative stress, including glutathione peroxidase-4 (GPX4), have been identified as inhibitors of ferroptosis, and mechanisms that affect GPX4 function can impact islet function and viability...
May 22, 2018: Cell Death & Disease
Christian Stoppe, Luisa Averdunk, Andreas Goetzenich, Josefin Soppert, Arnaud Marlier, Sandra Kraemer, Jil Vieten, Mark Coburn, Ana Kowark, Bong-Song Kim, Gernot Marx, Steffen Rex, Akinobu Ochi, Lin Leng, Gilbert Moeckel, Andreas Linkermann, Omar El Bounkari, Alexander Zarbock, Jürgen Bernhagen, Sonja Djudjaj, Richard Bucala, Peter Boor
Acute kidney injury (AKI) represents the most frequent complication after cardiac surgery. Macrophage migration inhibitory factor (MIF) is a stress-regulating cytokine that was shown to protect the heart from myocardial ischemia-reperfusion injury, but its role in the pathogenesis of AKI remains unknown. In an observational study, serum and urinary MIF was quantified in 60 patients scheduled for elective conventional cardiac surgery with the use of cardiopulmonary bypass. Cardiac surgery triggered an increase in MIF serum concentrations, and patients with high circulating MIF (>median) 12 hours after surgery had a significantly reduced risk of developing AKI (relative risk reduction, 72...
May 16, 2018: Science Translational Medicine
Hengli Zhao, Yujie Chen, Hua Feng
Hemorrhagic stroke is a life-threatening disease characterized by a sudden rupture of cerebral blood vessels, and cell death is widely believed to occur after exposure to blood metabolites or subsequently damaged cells. Recently, programmed cell death, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, has been demonstrated to play crucial roles in the pathophysiology of stroke. However, the detailed mechanisms of these novel kinds of cell death are still unclear. The P2X7 receptor, previously known for its cytotoxic activity, is an ATP-gated, non-selective cation channel that belongs to the family of ionotropic P2X receptors...
May 15, 2018: Current Neuropharmacology
Xie-Huang Sheng, Cheng-Cheng Cui, Chao Shan, Yu-Zhen Li, Duo-Hong Sheng, Bin Sun, De-Zhan Chen
Ferroptosis is a non-apoptotic, iron dependent form of regulated cell death that is characterized by the accumulation of lipid hydroperoxides. It has drawn considerable attention owing to its putative involvement in diverse neurodegenerative diseases. Ferrostatins are the first identified inhibitors of ferroptosis and they inhibit ferroptosis by efficiently scavenging free radicals in lipid bilayers. However, their further medicinal application has been limited due to the deficient knowledge of the lipid peroxyl radical-trapping mechanism...
May 11, 2018: Organic & Biomolecular Chemistry
Armelle T Mbaveng, Blanche L Ndontsa, Victor Kuete, Yves M M Nguekeu, İlhami Çelik, Roukayatou Mbouangouere, Pierre Tane, Thomas Efferth
INTRODUCTION: Multidrug resistance of cancer cells constitutes a serious problem in chemotherapy and a challenging issue in the discovery of new cytotoxic drugs. Many saponins are known to display anti-cancer effects. In this study, the cytotoxicity and the modes of action of a naturally occuring oleanane-type tritepene saponin, ardisiacrispin B isolated from the fruit of Ardisia kivuensis Taton (Myrsinaceae) was evaluated on a panel of 9 cancer cell lines including various sensitive and drug-resistant phenotypes...
April 1, 2018: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
Jinbi Zhang, Yang Liu, Wang Yao, Qifa Li, Hong-Lin Liu, Zengxiang Pan
In mammals, more than 99% of ovarian follicles undergo a degenerative process known as atresia. The molecular events involve in atresia initiation remain incompletely understood. The objective of this study was to analyze differential gene expression profiles of medium antral ovarian follicles during early atresia in pig. The transcriptome evaluation was performed on cDNA microarrays using healthy and early atretic follicle samples and was validated by quantitative PCR. Annotation analysis applying current database (sus scrofa 11...
May 9, 2018: Reproduction: the Official Journal of the Society for the Study of Fertility
Jan Lewerenz, Gamze Ates, Axel Methner, Marcus Conrad, Pamela Maher
Although nerve cell death is the hallmark of many neurological diseases, the processes underlying this death are still poorly defined. However, there is a general consensus that neuronal cell death predominantly proceeds by regulated processes. Almost 30 years ago, a cell death pathway eventually named oxytosis was described in neuronal cells that involved glutathione depletion, reactive oxygen species production, lipoxygenase activation, and calcium influx. More recently, a cell death pathway that involved many of the same steps was described in tumor cells and termed ferroptosis due to a dependence on iron...
2018: Frontiers in Neuroscience
Seon Min Woo, Seung Un Seo, Kyoung-Jin Min, Seung-Soon Im, Ju-Ock Nam, Jong-Soo Chang, Shin Kim, Jong-Wook Park, Taeg Kyu Kwon
Corosolic acid is one of the pentacyclic triterpenoids isolated from Lagerstroemia speciose and has been reported to exhibit anti-cancer and anti-proliferative activities in various cancer cells. In the present study, we investigated the molecular mechanisms of corosolic acid in cancer cell death. Corosolic acid induces a decrease of cell viability and an increase of cell cytotoxicity in human renal carcinoma Caki cells. Corosolic acid-induced cell death is not inhibited by apoptosis inhibitor (z-VAD-fmk, a pan-caspase inhibitor), necroptosis inhibitor (necrostatin-1), or ferroptosis inhibitors (ferrostatin-1 and deferoxamine (DFO))...
April 27, 2018: International Journal of Molecular Sciences
Zongqi Wang, Ye Ding, Xuanzhong Wang, Shan Lu, Chongcheng Wang, Chuan He, Lei Wang, Meihua Piao, Guangfan Chi, Yinan Luo, Pengfei Ge
Ferroptosis is a form of programmed cell death decided by iron-dependent lipid peroxidation, but its role in glioma cell death remains unclear. In this study, we found Pseudolaric acid B (PAB) inhibited the viabilities of glioma cells in vitro and in vivo, which was accompanied by abnormal increases of intracellular ferrous iron, H2 O2 and lipid peroxidation, as well as depletion of GSH and cysteine. In vitro studies revealed that the lipid peroxidation and the cell death caused by PAB were both inhibited by iron chelator deferoxamine, but exacerbated by supplement of ferric ammonium citrate...
April 24, 2018: Cancer Letters
Keerthana Gnanapradeepan, Subhasree Basu, Thibaut Barnoud, Anna Budina-Kolomets, Che-Pei Kung, Maureen E Murphy
The p53 tumor suppressor continues to be distinguished as the most frequently mutated gene in human cancer. It is widely believed that the ability of p53 to induce senescence and programmed cell death underlies the tumor suppressor functions of p53. However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53. As reviewed here, the roles of p53 in the control of metabolism and ferroptosis are complex...
2018: Frontiers in Endocrinology
Cong Li, Xiaobing Deng, Weilin Zhang, Xiaowen Xie, Marcus Conrad, Ying Liu, José Pedro Friedmann Angeli, Luhua Lai
Glutathione peroxidase 4 (GPX4) is essential for cell membrane repair, inflammation suppression, and ferroptosis inhibition. GPX4 upregulation provides unique drug discovery opportunities for inflammation and ferroptosis-related diseases. However, rational design of protein activators is challenging. Until now, no compound has been reported to activate the enzyme activity of GPX4. Here, we identified a potential allosteric site in GPX4, and successfully found eight GPX4 activators using a novel computational strategy and experimental studies...
April 24, 2018: Journal of Medicinal Chemistry
Qianghu Tang, LuLu Bai, Zhen Zou, Pan Meng, Yinyin Xia, Shuqun Cheng, Shaoyu Mu, Jianrong Zhou, Xuefeng Wang, Xia Qin, Xianqing Cao, Xuejun Jiang, Chengzhi Chen
Ferroptosis is a novel iron-dependent form of cell death implicated in brain pathology. However, whether arsenite is an inducer of ferroptosis in the neurons remains completely unknown. In this study, the seven-week-old healthy C57BL/6 J male mice were treated with environmental related doses (0.5, 5 and 50 mg/L) of arsenite for 6 months via drinking water, and the ferroptosis-related indicators were further determined. Our results demonstrated for the first time that, arsenite exposure significantly reduced the number of neuron and caused the pathological changes of mitochondria in the cerebral cortex of mice...
April 17, 2018: Neurotoxicology
Lyla A Youssef, Abdelhadi Rebbaa, Sergey Pampou, Stuart P Weisberg, Brent R Stockwell, Eldad A Hod, Steven L Spitalnik
Macrophages play important roles in recycling iron derived from the clearance of red blood cells (RBCs). They are also a critically important component of host defense, protecting against invading pathogens. However, the effects on macrophage biology of acutely ingesting large numbers of RBCs are not completely understood. To investigate this issue, we used a mouse model of RBC transfusion and clearance, which mimics the clinical setting. In this model, transfusions of refrigerator storage-damaged (i.e., "old") RBCs led to increased erythrophagocytosis by splenic red pulp macrophages (RPMs)...
April 17, 2018: Blood
Jennifer Tsoi, Lidia Robert, Kim Paraiso, Carlos Galvan, Katherine M Sheu, Johnson Lay, Deborah J L Wong, Mohammad Atefi, Roksana Shirazi, Xiaoyan Wang, Daniel Braas, Catherine S Grasso, Nicolaos Palaskas, Antoni Ribas, Thomas G Graeber
Malignant transformation can result in melanoma cells that resemble different stages of their embryonic development. Our gene expression analysis of human melanoma cell lines and patient tumors revealed that melanoma follows a two-dimensional differentiation trajectory that can be subclassified into four progressive subtypes. This differentiation model is associated with subtype-specific sensitivity to iron-dependent oxidative stress and cell death known as ferroptosis. Receptor tyrosine kinase-mediated resistance to mitogen-activated protein kinase targeted therapies and activation of the inflammatory signaling associated with immune therapy involves transitions along this differentiation trajectory, which lead to increased sensitivity to ferroptosis...
April 3, 2018: Cancer Cell
Haonan Yu, Zhuang Hou, Ye Tian, Yanhua Mou, Chun Guo
To develop novel agents with anticancer activities, thirty-four new dihydroartemisinin-coumarin hybrids were designed and synthesized in this study. Those compounds were identified that had great anticancer activity against two cancer cell lines (MDA-MB-231 and HT-29). The structure-activity relationships of the derivatives were also discussed, and the results of docking analysis had shown that carbonic anhydrases IX (CA IX) was very likely to be one of the drug targets of the hybrids. Meanwhile, to clarify the mechanism of the anticancer activity of the hybrids molecule, we did further exploration in the bioactivity of the hybrids...
April 3, 2018: European Journal of Medicinal Chemistry
Qiu-Qi Li, Qin-Li, Ji-Ning Jia, Zhao-Qian Liu, Hong-Hao Zhou, Xiao-Yuan Mao
The 12/15-lipoxygenase (12/15-LOX) enzymes react with polyunsaturated fatty acids producing active lipid metabolites that are involved in plethora of human diseases including neurological disorders. A great many of elegant studies over the last decades have contributed to unraveling the mechanism how 12/15-lipoxygenase play a role in these diseases. And the way it works is mainly through apoptosis. However, recent years have found that the way 12/15-lipoxygenase works is also related to autophagy and ferroptosis, a newly defined type of cell death by Stockwell's lab in 2012...
April 5, 2018: Neurochemistry International
Michael M Gaschler, Alexander A Andia, Hengrui Liu, Joleen M Csuka, Brisa Hurlocker, Christopher A Vaiana, Daniel W Heindel, Dylan S Zuckerman, Pieter H Bos, Eduard Reznik, Ling F Ye, Yulia Y Tyurina, Annie J Lin, Mikhail S Shchepinov, Amy Y Chan, Eveliz Peguero-Pereira, Maksim A Fomich, Jacob D Daniels, Andrei V Bekish, Vadim V Shmanai, Valerian E Kagan, Lara K Mahal, K A Woerpel, Brent R Stockwell
Ferroptosis is a non-apoptotic form of regulated cell death caused by the failure of the glutathione-dependent lipid-peroxide-scavenging network. FINO2 is an endoperoxide-containing 1,2-dioxolane that can initiate ferroptosis selectively in engineered cancer cells. We investigated the mechanism and structural features necessary for ferroptosis initiation by FINO2 . We found that FINO2 requires both an endoperoxide moiety and a nearby hydroxyl head group to initiate ferroptosis. In contrast to previously described ferroptosis inducers, FINO2 does not inhibit system xc - or directly target the reducing enzyme GPX4, as do erastin and RSL3, respectively, nor does it deplete GPX4 protein, as does FIN56...
April 2, 2018: Nature Chemical Biology
Young-Sun Lee, Dae-Hee Lee, Haroon A Choudry, David L Bartlett, Yong J Lee
Since its discovery in 2012, ferroptosis has been well-characterized by the accumulation of lipid peroxides due to the failure of glutathione-dependent antioxidant defenses. It is known as an iron-dependent form of programmed cell death, which is distinct from other forms of cell death such as apoptosis and necrosis. Nonetheless, little is known about the ferroptotic agent-induced endoplasmic reticulum (ER) stress response and its role in cell death. Recent studies reveal that the ferroptotic agent-induced ER stress response plays an important role in the crosstalk between ferroptosis and other types of cell death...
March 28, 2018: Molecular Cancer Research: MCR
Chao Mao, Xiang Wang, Yating Liu, Min Wang, Bin Yan, Yiqun Jiang, Ying Shi, Yi Shen, Xiaoli Liu, Weiwei Liai, Rui Yang, Desheng Xiao, Yan Cheng, Shuang Liu, Hu Zhou, Ya Cao, Weishi Yu, Kathrin Muegge, Herbert Yu, Yongguang Tao
Long non-coding RNAs (lncRNA) have been associated with various types of cancer, however, the precise role of many lncRNAs in tumorigenesis remains elusive. Here we demonstrate that the cytosolic lncRNA P53RRA is downregulated in cancers and functions as a tumor suppressor by inhibiting cancer progression. Chromatin remodeling proteins LSH and Cfp1 silenced or increased P53RRA expression respectively. P53RRA bound Ras GTPase-activating protein-binding protein 1 (G3BP1) using nucleotides 1 and 871 of P53RRA and the RRM interaction domain of G3BP1 (aa 177-466)...
March 27, 2018: Cancer Research
Michael J Maroney, Robert J Hondal
This review highlights the contributions of Jean Chaudière to the field of selenium biochemistry. Chaudière was the first to recognize that one of the main reasons that selenium in the form of selenocysteine is used in proteins is due to the fact that it strongly resists permanent oxidation. The foundations for this important concept was laid down by Al Tappel in the 1960's and even before by others. The concept of oxygen tolerance first recognized in the study of glutathione peroxidase was further advanced and refined by those studying [NiFeSe]-hydrogenases, selenosubtilisin, and thioredoxin reductase...
March 24, 2018: Free Radical Biology & Medicine
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