Cell Stress最新文献_第9页

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":"4 5","pages":"99-113"},"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":"4 4","pages":"66-75"},"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":"4 2","pages":"44-47"},"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 4.1

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

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

引用次数: 0

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":"4 3","pages":"48-63"},"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

Fine intercellular connections in development: TNTs, cytonemes, or intercellular bridges? 发育中的精细细胞间连接:tnt，细胞素，还是细胞间桥?

IF 6.4

Cell Stress Pub Date : 2020-01-07 DOI: 10.15698/cst2020.02.212

Olga Korenkova, Anna Pepe, Chiara Zurzolo

引用次数: 50

Kynurenine: an oncometabolite in colon cancer. 犬尿氨酸:结肠癌中的一种肿瘤代谢物。

IF 6.4

Cell Stress Pub Date : 2020-01-03 DOI: 10.15698/cst2020.01.210

Niranjan Venkateswaran, Maralice Conacci-Sorrell

{"title":"Kynurenine: an oncometabolite in colon cancer.","authors":"Niranjan Venkateswaran, Maralice Conacci-Sorrell","doi":"10.15698/cst2020.01.210","DOIUrl":"https://doi.org/10.15698/cst2020.01.210","url":null,"abstract":"Tryptophan is one of the eight essential amino acids that must be obtained from the diet. Interestingly, tryptophan is the least abundant amino acid in most proteins, a large portion of cellular tryptophan is converted into metabolites of the serotonin and kynurenine pathways. In a recent study, (Venkateswaran, Lafita-Navarro et al., 2019, Genes Dev), we discovered that colon cancer cells display greater uptake and processing of tryptophan than normal colonic cells and tissues. This process is mediated by the oncogenic transcription factor MYC that promotes the expression of the tryptophan importers SLC1A5 and SLC7A5 and the tryptophan metabolizing enzyme AFMID. The metabolism of tryptophan in colon cancer cells generates kynurenine, a biologically active metabolite necessary to maintain continuous cell proliferation. Our results indicate that kynurenine functions as an oncometabolite, at least in part, by activating the transcription factor AHR, which then regulates growth promoting genes in cancer cells. We propose that blocking kynurenine production or activity can be an efficient approach to specifically limit the growth of colon cancer cells. Here, we describe our findings and new questions for future studies targeted at understanding AHR-independent function of kynurenine, as well as interfering with the enzyme AFMID as a new strategy to target the kynurenine pathway.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"4 1","pages":"24-26"},"PeriodicalIF":6.4,"publicationDate":"2020-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946015/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37530150","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: 38

Necroptosis, tumor necrosis and tumorigenesis. 坏死下垂、肿瘤坏死和肿瘤发生。

IF 6.4

Cell Stress Pub Date : 2019-12-19 DOI: 10.15698/cst2020.01.208

Zheng-Gang Liu, Delong Jiao

引用次数: 69

Fatty acids - from energy substrates to key regulators of cell survival, proliferation and effector function. 脂肪酸--从能量底物到细胞存活、增殖和效应功能的关键调节因子。

IF 6.4

Cell Stress Pub Date : 2019-12-10 DOI: 10.15698/cst2020.01.209

Danilo Cucchi, Dolores Camacho-Muñoz, Michelangelo Certo, Valentina Pucino, Anna Nicolaou, Claudio Mauro

{"title":"Fatty acids - from energy substrates to key regulators of cell survival, proliferation and effector function.","authors":"Danilo Cucchi, Dolores Camacho-Muñoz, Michelangelo Certo, Valentina Pucino, Anna Nicolaou, Claudio Mauro","doi":"10.15698/cst2020.01.209","DOIUrl":"10.15698/cst2020.01.209","url":null,"abstract":"Recent advances in immunology and cancer research show that fatty acids, their metabolism and their sensing have a crucial role in the biology of many different cell types. Indeed, they are able to affect cellular behaviour with great implications for pathophysiology. Both the catabolic and anabolic pathways of fatty acids present us with a number of enzymes, receptors and agonists/antagonists that are potential therapeutic targets, some of which have already been successfully pursued. Fatty acids can affect the differentiation of immune cells, particularly T cells, as well as their activation and function, with important consequences for the balance between anti- and pro-inflammatory signals in immune diseases, such as rheumatoid arthritis, psoriasis, diabetes, obesity and cardiovascular conditions. In the context of cancer biology, fatty acids mainly provide substrates for energy production, which is of crucial importance to meet the energy demands of these highly proliferating cells. Fatty acids can also be involved in a broader transcriptional programme as they trigger signals necessary for tumorigenesis and can confer to cancer cells the ability to migrate and generate distant metastasis. For these reasons, the study of fatty acids represents a new research direction that can generate detailed insight and provide novel tools for the understanding of immune and cancer cell biology, and, more importantly, support the development of novel, efficient and fine-tuned clinical interventions. Here, we review the recent literature focusing on the involvement of fatty acids in the biology of immune cells, with emphasis on T cells, and cancer cells, from sensing and binding, to metabolism and downstream effects in cell signalling.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"4 1","pages":"9-23"},"PeriodicalIF":6.4,"publicationDate":"2019-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37530151","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