Cell Stress最新文献_第8页

Mitochondria in cancer. 癌症中的线粒体。

IF 6.4

Cell Stress Pub Date : 2020-05-11 DOI: 10.15698/cst2020.06.221

Debora Grasso, Luca X Zampieri, Tânia Capelôa, Justine A Van de Velde, Pierre Sonveaux

引用次数: 94

Copper - a novel stimulator of autophagy. 铜——一种新的自噬刺激剂。

IF 6.4

Cell Stress Pub Date : 2020-04-24 DOI: 10.15698/cst2020.05.218

Hans Zischka, Guido Kroemer

引用次数: 17

Towards understanding the role of Receptor Expression Enhancing Protein 5 (REEP5) in cardiac muscle and beyond. 了解受体表达增强蛋白5 (REEP5)在心肌及其他部位的作用。

IF 6.4

Cell Stress Pub Date : 2020-04-15 DOI: 10.15698/cst2020.06.223

Shin-Haw Lee, Sina Hadipour-Lakmehsari, Anthony O Gramolini

{"title":"Towards understanding the role of Receptor Expression Enhancing Protein 5 (REEP5) in cardiac muscle and beyond.","authors":"Shin-Haw Lee, Sina Hadipour-Lakmehsari, Anthony O Gramolini","doi":"10.15698/cst2020.06.223","DOIUrl":"https://doi.org/10.15698/cst2020.06.223","url":null,"abstract":"The sarco-endoplasmic reticulum (SR/ER) is the largest membrane-bound organelle in eukaryotic cells and plays important roles in essential cellular processes, and in development and progression of many cardiac diseases. However, many aspects of its structural organization remain largely unknown, particularly in cells with a highly differentiated SR/ER network. In a recently published study led by Lee et al. (Nat Commun 11(1):965), we reported a cardiac enriched SR/ER membrane protein REEP5 that is centrally involved in regulating SR/ER organization and cellular stress responses in cardiac myocytes. In vitro REEP5 depletion in mouse cardiac myocytes resulted in SR/ER membrane destabilization and luminal vacuolization along with decreased myocyte contractility and disrupted Ca2+ cycling. Further, in vivo CRISPR/Cas9-mediated REEP5 loss-of-function zebrafish mutants showed sensitized cardiac dysfunction to heart failure induction upon short-term verapamil treatment. Additionally, in vivo adeno-associated viral (AAV9)-induced REEP5 depletion in the mouse demonstrated cardiac dysfunction with dilated cardiac chambers, increased cardiac fibrosis, and reduced ejection fraction. These results demonstrate the critical role of REEP5 in SR/ER organization and function.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38055234","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: 2

Role of RNA Binding Proteins with prion-like domains in muscle and neuromuscular diseases. 带有朊病毒样结构域的RNA结合蛋白在肌肉和神经肌肉疾病中的作用。

IF 6.4

Cell Stress Pub Date : 2020-03-10 DOI: 10.15698/cst2020.04.217

Gina Picchiarelli, Luc Dupuis

引用次数: 33

HIF1α-dependent mitophagy facilitates cardiomyoblast differentiation. 依赖于 HIF1α 的有丝分裂促进了心肌母细胞的分化。

IF 6.4

Cell Stress Pub Date : 2020-03-04 DOI: 10.15698/cst2020.05.220

Jin-Feng Zhao, Catherine E Rodger, George F G Allen, Simone Weidlich, Ian G Ganley

{"title":"HIF1α-dependent mitophagy facilitates cardiomyoblast differentiation.","authors":"Jin-Feng Zhao, Catherine E Rodger, George F G Allen, Simone Weidlich, Ian G Ganley","doi":"10.15698/cst2020.05.220","DOIUrl":"10.15698/cst2020.05.220","url":null,"abstract":"Mitophagy is thought to play a key role in eliminating damaged mitochondria, with diseases such as cancer and neurodegeneration exhibiting defects in this process. Mitophagy is also involved in cell differentiation and maturation, potentially through modulating mitochondrial metabolic reprogramming. Here we examined mitophagy that is induced upon iron chelation and found that the transcriptional activity of HIF1α, in part through upregulation of BNIP3 and NIX, is an essential mediator of this pathway in SH-SY5Y cells. In contrast, HIF1α is dispensable for mitophagy occurring upon mitochondrial depolarisation. To examine the role of this pathway in a metabolic reprogramming and differentiation context, we utilised the H9c2 cell line model of cardiomyocyte maturation. During differentiation of these cardiomyoblasts, mitophagy increased and required HIF1α-dependent upregulation of NIX. Though HIF1α was essential for expression of key cardiomyocyte markers, mitophagy was not directly required. However, enhancing mitophagy through NIX overexpression, accelerated marker gene expression. Taken together, our findings provide a molecular link between mitophagy signalling and cardiomyocyte differentiation and suggest that although mitophagy may not be essential per se, it plays a critical role in maintaining mitochondrial integrity during this energy demanding process.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37947076","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

Coronavirus infections: Epidemiological, clinical and immunological features and hypotheses. 冠状病毒感染:流行病学、临床和免疫学特征及假设。

IF 6.4

Cell Stress Pub Date : 2020-03-02 DOI: 10.15698/cst2020.04.216

Didier Raoult, Alimuddin Zumla, Franco Locatelli, Giuseppe Ippolito, Guido Kroemer

{"title":"Coronavirus infections: Epidemiological, clinical and immunological features and hypotheses.","authors":"Didier Raoult, Alimuddin Zumla, Franco Locatelli, Giuseppe Ippolito, Guido Kroemer","doi":"10.15698/cst2020.04.216","DOIUrl":"https://doi.org/10.15698/cst2020.04.216","url":null,"abstract":"Coronaviruses (CoVs) are a large family of enveloped, positive-strand RNA viruses. Four human CoVs (HCoVs), the non-severe acute respiratory syndrome (SARS)-like HCoVs (namely HCoV 229E, NL63, OC43, and HKU1), are globally endemic and account for a substantial fraction of upper respiratory tract infections. Non-SARS-like CoV can occasionally produce severe diseases in frail subjects but do not cause any major (fatal) epidemics. In contrast, SARS like CoVs (namely SARS-CoV and Middle-East respiratory syndrome coronavirus, MERS-CoV) can cause intense short-lived fatal outbreaks. The current epidemic caused by the highly contagious SARS-CoV-2 and its rapid spread globally is of major concern. There is scanty knowledge on the actual pandemic potential of this new SARS-like virus. It might be speculated that SARS-CoV-2 epidemic is grossly underdiagnosed and that the infection is silently spreading across the globe with two consequences: (i) clusters of severe infections among frail subjects could haphazardly occur linked to unrecognized index cases; (ii) the current epidemic could naturally fall into a low-level endemic phase when a significant number of subjects will have developed immunity. Understanding the role of paucisymptomatic subjects and stratifying patients according to the risk of developing severe clinical presentations is pivotal for implementing reasonable measures to contain the infection and to reduce its mortality. Whilst the future evolution of this epidemic remains unpredictable, classic public health strategies must follow rational patterns. The emergence of yet another global epidemic underscores the permanent challenges that infectious diseases pose and underscores the need for global cooperation and preparedness, even during inter-epidemic periods.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.15698/cst2020.04.216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37836183","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: 298

Biomechanical stress regulates mammalian tooth replacement. 生物力学应力调节哺乳动物牙齿置换。

IF 6.4

Cell Stress Pub Date : 2020-02-18 DOI: 10.15698/cst2020.03.215

Xiaoshan Wu, Songlin Wang

引用次数: 0

Biomechanical stress provides a second hit in the establishment of BMP/TGFβ-related vascular disorders. 生物力学应力在BMP/ tgf β相关血管疾病的建立中提供了第二个打击。

IF 6.4

Cell Stress Pub Date : 2020-01-20 DOI: 10.15698/cst2020.02.213

Christian Hiepen, Jerome Jatzlau, Petra Knaus

{"title":"Biomechanical stress provides a second hit in the establishment of BMP/TGFβ-related vascular disorders.","authors":"Christian Hiepen, Jerome Jatzlau, Petra Knaus","doi":"10.15698/cst2020.02.213","DOIUrl":"https://doi.org/10.15698/cst2020.02.213","url":null,"abstract":"Cardiovascular disorders are still the leading cause for mortality in the western world and challenge economies with steadily increasing healthcare costs. Understanding the precise molecular pathomechanisms behind and identifying players involved in the early onset of cardiovascular diseases remains crucial for the development of new therapeutic strategies. Taking advantage of CRISPR/Cas9 gene editing in human endothelial cells (ECs), we re-investigated the early molecular steps in a genetic vascular disorder termed pulmonary arterial hypertension (PAH) in our recent study (Hiepen C., Jatzlau J. et al.; PLOS Biol, 2019). Here, mutations in the Bone Morphogenetic Protein type II receptor (BMPR2) prime for the hereditary form (HPAH) with downregulated BMPR2 followed by a characteristic change in SMAD signaling, i.e. gain in both SMAD1/5 and SMAD2/3 responses. Remarkably these cells show increased susceptibility to signaling by TGFβ due to remodeling of the extracellular matrix (ECM) and increased biomechanics acting as a secondary stressor for ECs pathobiology. This clearly places BMPR2 not only as a BMP-signaling receptor, but also as a gatekeeper to protect ECs from excess TGFβ signaling.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6997947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37630156","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: 7

ACBP is an appetite stimulator across phylogenetic barriers. ACBP是一种跨越系统发育障碍的食欲刺激物。

IF 6.4

Cell Stress Pub Date : 2020-01-20 DOI: 10.15698/cst2020.02.211

Frank Madeo, Nektarios Tavernarakis, José M Bravo-San Pedro, Guido Kroemer

{"title":"ACBP is an appetite stimulator across phylogenetic barriers.","authors":"Frank Madeo, Nektarios Tavernarakis, José M Bravo-San Pedro, Guido Kroemer","doi":"10.15698/cst2020.02.211","DOIUrl":"https://doi.org/10.15698/cst2020.02.211","url":null,"abstract":"Frank Madeo, Nektarios Tavernarakis, José M. Bravo-San Pedro* and Guido Kroemer* 1 Institute of Molecular Biosciences, NAWI Graz, University of Graz, Humboldtstrasse 50, 8010 Graz, Austria. 2 BioTechMed Graz, Austria. 3 Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Nikolaou Plastira 100, Heraklion 70013, Crete, Greece. 4 Department of Basic Sciences, Faculty of Medicine, University of Crete, Heraklion 71110, Crete, Greece. 5 Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus, Villejuif, France. 6 Inserm U1138, Centre de Recherche des Cordeliers, Sorbonne. Université, Université de Paris, 15 rue de l'école de médecine 75006, Paris, France. 7 Team “Metabolism, Cancer & Immunity”, équipe 11 labellisée par la Ligue contre le Cancer, Paris, France. 8 Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, Paris, France. 9 Suzhou Institute for Systems Medicine, Chinese Academy of Sciences, Suzhou, China. 10 Karolinska Institute, Department of Women's and Children's Health, Karolinska University Hospital, Stockholm, Sweden. # Share senior co-authorship. * Corresponding Authors: Guido Kroemer, E-mail: kroemer@orange.fr; José M. Bravo-San Pedro, E-mail: chemabsp@gmail.com","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6997948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37630155","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: 8

RPA and Pif1 cooperate to remove G-rich structures at both leading and lagging strand. RPA和Pif1共同去除前链和后链上的富g结构。

IF 6.4

Cell Stress Pub Date : 2020-01-17 DOI: 10.15698/cst2020.03.214

Laetitia Maestroni, Julien Audry, Pierre Luciano, Stéphane Coulon, Vincent Géli, Yves Corda

{"title":"RPA and Pif1 cooperate to remove G-rich structures at both leading and lagging strand.","authors":"Laetitia Maestroni, Julien Audry, Pierre Luciano, Stéphane Coulon, Vincent Géli, Yves Corda","doi":"10.15698/cst2020.03.214","DOIUrl":"https://doi.org/10.15698/cst2020.03.214","url":null,"abstract":"In Saccharomyces cerevisiae, the absence of Pif1 helicase induces the instability of G4-containing CEB1 minisatellite during leading strand but not lagging strand replication. We report that RPA and Pif1 cooperate to maintain CEB1 stability when the G4 forming strand is either on the leading or lagging strand templates. At the leading strand, RPA acts in the same pathway as Pif1 to maintain CEB1 stability. Consistent with this result, RPA co-precipitates with Pif1. This association between Pif1 and RPA is affected by the rfa1-D228Y mutation that lowers the affinity of RPA in particular for G-rich single-stranded DNA. At the lagging strand, in contrast to pif1Δ, the rfa1-D228Y mutation strongly increases the frequency of CEB1 rearrangements. We explain that Pif1 is dispensable at the lagging strand DNA by the ability of RPA by itself to prevent formation of stable G-rich secondary structures during lagging strand synthesis. Remarkably, overexpression of Pif1 rescues the instability of CEB1 at the lagging strand in the rfa1-D228Y mutant indicating that Pif1 can also act at the lagging strand. We show that the effects of the rfa1-D228Y (rpa1-D223Y in fission yeast) are conserved in Schizosaccharomyces pombe. Finally, we report that RNase H1 interacts in a DNA-dependent manner with RPA in budding yeast, however overexpression of RNase H1 does not rescue CEB1 instability observed in pif1Δ and rfa1-D228Y mutants. Collectively these results add new insights about the general role of RPA in preventing formation of DNA secondary structures and in coordinating the action of factors aimed at resolving them.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":null,"pages":null},"PeriodicalIF":6.4,"publicationDate":"2020-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7063842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37753929","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: 22