Cell Stress最新文献_第10页

The impact of endothelial cell death in the brain and its role after stroke: A systematic review 脑内皮细胞死亡的影响及其在脑卒中后的作用:一项系统综述

IF 6.4

Cell Stress Pub Date : 2019-09-25 DOI: 10.15698/cst2019.11.203

M. Zille, Maulana Ikhsan, Yun Jiang, J. Lampe, Jan Wenzel, M. Schwaninger

{"title":"The impact of endothelial cell death in the brain and its role after stroke: A systematic review","authors":"M. Zille, Maulana Ikhsan, Yun Jiang, J. Lampe, Jan Wenzel, M. Schwaninger","doi":"10.15698/cst2019.11.203","DOIUrl":"https://doi.org/10.15698/cst2019.11.203","url":null,"abstract":"The supply of oxygen and nutrients to the brain is vital for its function and requires a complex vascular network that, when disturbed, results in profound neurological dysfunction. As part of the pathology in stroke, endothelial cells die. As endothelial cell death affects the surrounding cellular environment and is a potential target for the treatment and prevention of neurological disorders, we have systematically reviewed important aspects of endothelial cell death with a particular focus on stroke. After screening 2876 publications published between January 1, 2010 and August 7, 2019, we identified 154 records to be included. We found that endothelial cell death occurs rapidly as well as later after the onset of stroke conditions. Among the different cell death mechanisms, apoptosis was the most widely investigated (92 records), followed by autophagy (20 records), while other, more recently defined mechanisms received less attention, such as lysosome-dependent cell death (2 records) and necroptosis (2 records). We also discuss the differential vulnerability of brain cells to injury after stroke and the role of endothelial cell death in the no-reflow phenomenon with a special focus on the microvasculature. Further investigation of the different cell death mechanisms using novel tools and biomarkers will greatly enhance our understanding of endothelial cell death. For this task, at least two markers/criteria are desirable to determine cell death subroutines according to the recommendations of the Nomenclature Committee on Cell Death.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2019-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46544959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 44

Acyl-CoA-binding protein (ACBP): the elusive 'hunger factor' linking autophagy to food intake. 酰基辅酶A结合蛋白（ACBP）：将自噬与食物摄入联系起来的难以捉摸的“饥饿因子”

IF 4.1

Cell Stress Pub Date : 2019-09-24 DOI: 10.15698/cst2019.10.200

José Manuel Bravo-San Pedro, Valentina Sica, Frank Madeo, Guido Kroemer

{"title":"Acyl-CoA-binding protein (ACBP): the elusive 'hunger factor' linking autophagy to food intake.","authors":"José Manuel Bravo-San Pedro, Valentina Sica, Frank Madeo, Guido Kroemer","doi":"10.15698/cst2019.10.200","DOIUrl":"10.15698/cst2019.10.200","url":null,"abstract":"The best-known appetite-regulating factors identified in rodents are leptin, an appetite inhibitor, and ghrelin, an appetite stimulator. Rare cases of loss-of-functions mutations affecting leptin and its receptor, as well as polymorphisms concerning ghrelin and its receptor, have been documented in human obesity, apparently validating the relevance of leptin and ghrelin for human physiology. Paradoxically, however, the overwhelming majority of obese individuals manifest high leptin and low ghrelin plasma levels, suggesting that both factors are not directly disease-relevant. We recently discovered that acyl-CoA-binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), acts as an efficient lipogenic and appetite stimulator in mice. Indeed, in response to starvation, ACBP/DBI is released from tissues in an autophagy-dependent fashion and increases in the plasma. Intravenous injection of ACBP/DBI stimulates feeding behavior through a reduction of circulating glucose levels, and consequent activation of orexigenic neurons in the hypothalamus. In contrast, neutralization of ACBP/DBI abolishes the hyperphagia observed after starvation of mice. Of note, ACBP/DBI is increased in the plasma of obese persons and mice, pointing to a convergence (rather than divergence) between its role in appetite stimulation and human obesity. Based on our results, we postulate a novel 'hunger reflex' in which starvation induces a surge in extracellular ACBP/DBI, which in turn stimulates feeding behavior. Thus, ACBP/DBI might be the elusive 'hunger factor' that explains increased food uptake in obesity.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":4.1,"publicationDate":"2019-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6789435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42019532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inflammation induced PD-L1-specific T cells 炎症诱导的PD-L1特异性T细胞

IF 6.4

Cell Stress Pub Date : 2019-09-13 DOI: 10.15698/cst2019.10.201

Shamaila Munir, M. Lundsager, M. Jørgensen, M. Hansen, Trine H Petersen, C. Bonefeld, C. Friese, Ö. Met, P. Straten, M. Andersen

引用次数: 13

Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine. 金纳米粒子使癌症胰腺细胞对吉西他滨敏感。

IF 6.4

Cell Stress Pub Date : 2019-07-31 DOI: 10.15698/cst2019.08.195

Yanyan Huai, Yushan Zhang, Xunhao Xiong, Shamik Das, Resham Bhattacharya, Priyabrata Mukherjee

{"title":"Gold Nanoparticles sensitize pancreatic cancer cells to gemcitabine.","authors":"Yanyan Huai, Yushan Zhang, Xunhao Xiong, Shamik Das, Resham Bhattacharya, Priyabrata Mukherjee","doi":"10.15698/cst2019.08.195","DOIUrl":"10.15698/cst2019.08.195","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest solid cancers with dismal prognosis. Several mechanisms that are mainly responsible for aggressiveness and therapy resistance of PDAC cells include epithelial to mesenchymal transition (EMT), stemness and Mitogen Activated Protein Kinase (MAPK) signaling. Strategies that inhibit these mechanisms are critically important to improve therapeutic outcome in PDAC. In the current study, we wanted to investigate whether gold nanoparticles (AuNPs) could sensitize pancreatic cancer cells to the chemotherapeutic agent gemcitabine. We demonstrated that treatment with AuNPs of 20 nm diameter inhibited migration and colony forming ability of pancreatic cancer cells. Pre-treatment with AuNPs sensitized pancreatic cancer cells to gemcitabine in both viability and colony forming assays. Mechanistically, pre-treatment of pancreatic cancer cells with AuNPs decreased gemcitabine induced EMT, stemness and MAPK activation. Taken together, these findings suggest that AuNPs could be considered as a potential agent to sensitize pancreatic cancer cells to gemcitabine.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2019-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6702449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41180164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unraveling the molecular principles by which ceramides commit cells to death 揭示神经酰胺导致细胞死亡的分子原理

IF 6.4

Cell Stress Pub Date : 2019-07-16 DOI: 10.15698/cst2019.08.196

Shashank Dadsena, Dina G. Hassan, J. Holthuis

引用次数: 12

Immunosurveillance of cancer cell stress. 癌症细胞应激的免疫监测

IF 4.1

Cell Stress Pub Date : 2019-07-03 DOI: 10.15698/cst2019.09.198

Seila Lorenzo-Herrero, Christian Sordo-Bahamonde, Segundo González, Alejandro López-Soto

引用次数: 0

Myelopoiesis, metabolism and therapy: a crucial crossroads in cancer progression 骨髓生成、代谢和治疗:癌症进展的关键十字路口

IF 6.4

Cell Stress Pub Date : 2019-07-01 DOI: 10.15698/cst2019.09.197

A. Sica, V. Guarneri, A. Gennari

引用次数: 32

Impact of prophylactic TNF blockade in the dual PD-1 and CTLA-4 immunotherapy efficacy and toxicity 预防性TNF阻断对PD-1和CTLA-4双重免疫疗法疗效和毒性的影响

IF 6.4

Cell Stress Pub Date : 2019-06-26 DOI: 10.15698/cst2019.07.193

Maite Álvarez, I. Otano, Luna Minute, M. Ochoa, E. Pérez-Ruiz, I. Melero, P. Berraondo

{"title":"Impact of prophylactic TNF blockade in the dual PD-1 and CTLA-4 immunotherapy efficacy and toxicity","authors":"Maite Álvarez, I. Otano, Luna Minute, M. Ochoa, E. Pérez-Ruiz, I. Melero, P. Berraondo","doi":"10.15698/cst2019.07.193","DOIUrl":"https://doi.org/10.15698/cst2019.07.193","url":null,"abstract":"The TNF blockade therapy is currently a well-established treatment option for a variety of autoimmune diseases such as rheumatoid arthritis (RA), psoriasis or Crohn's disease, given the proinflammatory role of TNF in the course of these diseases. Importantly, TNF neutralization is also used for the treatment of corticosteroid-refractory immune-related adverse events (irAEs) induced by the combined anti-PD-1 and anti-CTLA-4 immunotherapy. The manifestation of these toxicities is an important limiting factor for the successful implementation of the inhibitory checkpoint blockade therapy (ICB), restraining its anti-tumor efficacy. In our recent study (Perez-Ruiz et al., Nature 569(7756): 428-432.), we analyzed the potential impact of prophylactic TNF neutralization therapy in the anti-PD1/CTLA-4 efficacy. Through several mouse models, we demonstrated that TNF neutralization ameliorated ICB-exacerbated colitis in addition to improving ICB-dependent anti-tumor efficacy. Similar results were obtained after prophylactic TNF blockade in graft vs host xenografted mouse models with human immune cells, which showed a reduction in colitis and hepatitis. Importantly, there was a preservation of the immunotherapeutic control of xenografted tumors after ICB treatment. Moreover, TNF and TNF-dependent gene expression is upregulated in the colon mucosa from patients affected by colitis as a side effect of ipilimumab and nivolumab. Our results, thus, provide evidence of the successful combination of prophylactic TNF neutralization with ICB therapy strategy to ameliorate toxicities, while keeping or even ameliorating anti-tumor efficacy. The prophylactic TNF blockade strategy is clinically feasible since excellent TNF inhibitors have been approved for the treatment of autoimmunity and are used for the immune-related serious adverse events in immunotherapy.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2019-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46976440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

Immunometabolic cross-talk in the inflamed heart 炎症心脏的免疫代谢串扰

IF 6.4

Cell Stress Pub Date : 2019-06-07 DOI: 10.15698/cst2019.08.194

F. Marelli-Berg, D. Aksentijević

{"title":"Immunometabolic cross-talk in the inflamed heart","authors":"F. Marelli-Berg, D. Aksentijević","doi":"10.15698/cst2019.08.194","DOIUrl":"https://doi.org/10.15698/cst2019.08.194","url":null,"abstract":"Inflammatory processes underlie many diseases associated with injury of the heart muscle, including conditions without an obvious inflammatory pathogenic component such as hypertensive and diabetic cardiomyopathy. Persistence of cardiac inflammation can cause irreversible structural and functional deficits. Some are induced by direct damage of the heart muscle by cellular and soluble mediators but also by metabolic adaptations sustained by the inflammatory microenvironment. It is well established that both cardiomyocytes and immune cells undergo metabolic reprogramming in the site of inflammation, which allow them to deal with decreased availability of nutrients and oxygen. However, like in cancer, competition for nutrients and increased production of signalling metabolites such as lactate initiate a metabolic cross-talk between immune cells and cardiomyocytes which, we propose, might tip the balance between resolution of the inflammation versus adverse cardiac remodeling. Here we review our current understanding of the metabolic reprogramming of both heart tissue and immune cells during inflammation, and we discuss potential key mechanisms by which these metabolic responses intersect and influence each other and ultimately define the prognosis of the inflammatory process in the heart.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2019-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42407725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

The role of epigenetics in hypothalamic energy balance control: implications for obesity 表观遗传学在下丘脑能量平衡控制中的作用:对肥胖的影响

IF 6.4

Cell Stress Pub Date : 2019-06-05 DOI: 10.15698/cst2019.07.191

A. Obri, M. Claret

引用次数: 19