IF 4.1

Cell Stress Pub Date : 2024-12-19 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.12.302

Tatiana P Grazioso, Maria Del Mar Rigual, Cristian Perna, Eduardo J Caleiras, Nabil Djouder

引用次数: 0

Endogenous plasma resuspension of peripheral blood mononuclear cells prevents preparative-associated stress that modifies polyA-enriched RNA responses to subsequent acute stressors. 外周血单核细胞的内源性血浆重悬可防止制备相关应激，这种应激可改变对随后急性应激源的富集多a RNA反应。

IF 4.1

Cell Stress Pub Date : 2024-11-28 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.11.301

Dongyang Li, Karina Al-Dahleh, Daniel A Murphy, Sonya Georgieva, Nik Matthews, Claire L Shovlin

{"title":"Endogenous plasma resuspension of peripheral blood mononuclear cells prevents preparative-associated stress that modifies polyA-enriched RNA responses to subsequent acute stressors.","authors":"Dongyang Li, Karina Al-Dahleh, Daniel A Murphy, Sonya Georgieva, Nik Matthews, Claire L Shovlin","doi":"10.15698/cst2024.11.301","DOIUrl":"10.15698/cst2024.11.301","url":null,"abstract":"Human peripheral blood mononuclear cells (PBMCs) are used to examine biological processes and disease, when basal variability in cellular activation and splicing is described and unexplained. Using isolation systems that maintained buffy coat cells (PBMCs, platelets) in their own plasma, poly-A enriched RNA-sequencing (RNASeq) detected 42,720 Ensembl gene IDs, including >95% of the top 100 Genotype Tissue Expression Project (GTEx)-expressed genes in lung, colon, heart, skeletal muscle and liver, and 10/17 clinically-actionable genes listed by the Pharmacogenomics Knowledgebase. Transcriptome changes were defined after 1h treatment with 32°C hypothermia (hsp70 family member change), 10 μmol/L ferric citrate that had no discernible effect, and 100 μg/mL cycloheximide leading to induction of primary response (immediate early) genes including IL1B and TNF. Same-donor PBMCs prepared conventionally using washes then resuspension in serum-supplemented media demonstrated basal upregulation of stress signalling pathway genes that masked and overlapped differential gene expression profiles after 100 µg/L cycloheximide. Plasma-resuspended PBMCs demonstrated minor transcriptome changes after 40 μmol/L ferric citrate, whereas consistent and greater magnitude changes were observed for washed/media-resuspended PBMCs. We conclude that endogenous plasma-maintained PBMCs provide a more robust platform to interrogate acute cellular perturbations triggering innate immunity, and that varying susceptibility of PBMCs to preparative stresses is an important component of experimental variability.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"11 ","pages":"112-124"},"PeriodicalIF":4.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11613960/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142773126","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

Neuroglobin-enriched secretome provides neuroprotection against hydrogen peroxide and mitochondrial toxin-induced cellular stress. 富含神经胶质蛋白的分泌体可提供针对过氧化氢和线粒体毒素诱导的细胞压力的神经保护。

IF 4.1

Cell Stress Pub Date : 2024-11-20 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.11.300

Giovanna Bastari, Virginia Solar Fernandez, Maurizio Muzzi, Sandra Moreno, Maria Marino, Marco Fiocchetti

{"title":"Neuroglobin-enriched secretome provides neuroprotection against hydrogen peroxide and mitochondrial toxin-induced cellular stress.","authors":"Giovanna Bastari, Virginia Solar Fernandez, Maurizio Muzzi, Sandra Moreno, Maria Marino, Marco Fiocchetti","doi":"10.15698/cst2024.11.300","DOIUrl":"10.15698/cst2024.11.300","url":null,"abstract":"Aberrant response to physiological cell stress is part of the mechanisms underlying the development of diverse human diseases, including neuropathologies. Neuroglobin (NGB), an intracellular monomeric globin, has gained attention for its role in endogenous stress response pathways in neuroprotection. To date, evidence supports the concept of NGB as an inducible protein, triggered by physiological and pathological stimuli via transcriptional and/or post-transcriptional mechanisms, offering cell-autonomous neuroprotective functions under various cellular stresses. Notably, recent evidence suggests the extracellular occurrence of NGB. We aimed to explore whether NGB redistribution in the cell microenvironment may serve in transmitting resilience capability in a model with neuronal characteristics. Results obtained in SH-SY5Y demonstrated that intracellular NGB upregulation is associated with the promotion of the extracellular release of the globin. Additionally, cell secretome from NGB-overexpressing cells, characterized by globin accumulation, exhibits protective effects against oxidative stress and mitochondrial toxicity, as evidenced by reduced apoptosis and preserved mitochondrial structure. These findings shed light on the potential significance of extracellular NGB as part of a common cell response to physiological and stress conditions and as a factor promoting cell resilience. Furthermore, the potential for neuroprotection of extracellular NGB paves the way for future therapeutic opportunities.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"8 ","pages":"99-111"},"PeriodicalIF":4.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11589466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142733169","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

Stress granules formation in HEI-OC1 auditory cells and in H4 human neuroglioma cells secondary to cisplatin exposure. HEI-OC1 听觉细胞和 H4 人类神经胶质瘤细胞继发于顺铂暴露的应激颗粒形成。

IF 4.1

Cell Stress Pub Date : 2024-10-18 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.10.299

Hebatallah Abdelrasol, Avika Chopra, Liana Shvachiy, Dirk Beutner, Tiago F Outeiro, Cristian Setz

{"title":"Stress granules formation in HEI-OC1 auditory cells and in H4 human neuroglioma cells secondary to cisplatin exposure.","authors":"Hebatallah Abdelrasol, Avika Chopra, Liana Shvachiy, Dirk Beutner, Tiago F Outeiro, Cristian Setz","doi":"10.15698/cst2024.10.299","DOIUrl":"10.15698/cst2024.10.299","url":null,"abstract":"Stress granules (SGs) are highly dynamic micromolecular membraneless condensates that generate in cells subjected to stress. Formed from pools of untranslating messenger ribonucleoproteins (RNP), SGs dynamics constitute vital processes essential for cell survival. Here, we investigate whether established cytotoxic agents, such as the platinum-based chemotherapeutic agent cisplatin and the aminoglycoside antibiotic gentamicin, elicit SG formation in the House Ear Institute-Organ of Corti-1 (HEI-OC1) auditory cell line, H4 human neuroglioma cells and HEK-293T human embryonic kidney cells. Cells were treated with cisplatin or gentamicin for specific durations at designated concentrations. SG formation was assessed using immunocytochemistry and live cell imaging. Levels of essential proteins involved in SG assembly were evaluated using immunoblotting. We observed cisplatin-associated SG assembly in HEI-OC1 and H4 cells via confocal microscopy through antibody colabeling of G3BP1 with PABP or Caprin1. While maintaining an unchanged pattern of expression of main constituent SG proteins, cisplatin-related SGs in H4 cells persisted for at least 12 h after drug removal. Cells subjected to gentamicin exposure did not exhibit SGs. Our findings offer insights into subcellular mechanisms related to cisplatin-associated cytotoxicity, highlighting the need for future studies to further investigate this stress-response mechanism.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"8 ","pages":"83-98"},"PeriodicalIF":4.1,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142688997","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

Dynamics of cell membrane lesions and adaptive conductance under the electrical stress. 电应力下细胞膜损伤和适应性传导的动态变化。

IF 4.1

Cell Stress Pub Date : 2024-08-09 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.08.298

Mantas Silkunas, Olga N Pakhomova, Giedre Silkuniene, Andrei G Pakhomov

{"title":"Dynamics of cell membrane lesions and adaptive conductance under the electrical stress.","authors":"Mantas Silkunas, Olga N Pakhomova, Giedre Silkuniene, Andrei G Pakhomov","doi":"10.15698/cst2024.08.298","DOIUrl":"10.15698/cst2024.08.298","url":null,"abstract":"Exceeding physiological limits of the cell membrane potential compromises structural integrity, enabling the passage of normally impermeant solutes and disrupting cell function. Electropermeabilization has been studied extensively at the cellular scale, but not at the individual membrane lesion level. We employed fast total internal reflection fluorescence (TIRF) imaging of Ca2+ entry transients to discern individual lesions in a hyperpolarized cell membrane and characterize their focality, thresholds, electrical conductance, and the lifecycle. A diffuse and momentary membrane permeabilization without a distinct pore formation was observed already at a -100 mV threshold. Polarizing down to -200 mV created focal pores with a low 50- to 300-pS conductance, which disappeared instantly once the hyperpolarization was removed. Charging to -240 mV created high-conductance (> 1 nS) pores which persisted for seconds even at zero membrane potential. With incremental hyperpolarization steps, persistent pores often emerged at locations different from those where the short-lived, low-conductance pores or diffuse permeabilization were previously observed. Attempts to polarize membrane beyond the threshold for the formation of persistent pores increased their conductance adaptively, preventing further potential build-up and \"clamping\" it at a certain limit (-270 ± 6 mV in HEK cells, -284 ± 5 mV in CHO cells, and -243 ± 9 mV in neurons). The data suggest a previously unknown role of electroporative lesions as a protective mechanism against a potentially fatal membrane overcharging and cell disintegration.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"8 ","pages":"69-82"},"PeriodicalIF":4.1,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11318148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141971970","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

Saliva, a molecular reflection of the human body? Implications for diagnosis and treatment. 唾液，人体的分子反映？对诊断和治疗的意义。

IF 6.4

Cell Stress Pub Date : 2024-05-27 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.05.297

Vincent Géli, Norbert Nabet

引用次数: 0

CircRNA regulates the liquid-liquid phase separation of ATG4B, a novel strategy to inhibit cancer metastasis? CircRNA调控ATG4B的液-液相分离，这是一种抑制癌症转移的新策略？

IF 4.1

Cell Stress Pub Date : 2024-05-24 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.05.296

Ziyuan Guo, Yang Chen, Yaran Wu, Jiqin Lian

{"title":"CircRNA regulates the liquid-liquid phase separation of ATG4B, a novel strategy to inhibit cancer metastasis?","authors":"Ziyuan Guo, Yang Chen, Yaran Wu, Jiqin Lian","doi":"10.15698/cst2024.05.296","DOIUrl":"10.15698/cst2024.05.296","url":null,"abstract":"Anoikis is a common programmed death for most of detached cells, but cancer cells can obtain anoikis resistance to facilitate their distant metastasis through the circulation system. Researches have indicated that enhanced autophagic flux accounts for the survival of many cancer cells under detached conditions. Targeting ATG4B, the key factor of autophagy progress, can inhibit cancer metastasis in vitro, but ATG4B-deficient mice are susceptible to many serious diseases, which indicates the potential uncontrolled side effects of direct targeting of ATG4B. In our recent research, we confirmed that ATG4B is a novel RNA binding protein in the gastric cancer (GC) cell. It interacts with circSPECC1 which consequently facilitates the liquid-liquid phase separation and ubiquitination of ATG4B. Additionally, the m6A reader ELAVL1 inhibits the expression of circSPECC1 to enhance the expression of ATG4B and anoikis resistance of GC cells. Further, we screened out an FDA-approved compound, lopinavir, to restore circSPECC1 abundance and suppress GC metastasis. In conclusion, our research identified a novel signal pathway (ELAVL1-circSPECC1-ATG4B-autophagy) to facilitate anoikis resistance and metastasis of GC cells and screened out a compound with clinical application potential to block this pathway, providing a novel strategy for the prevention of GC metastasis.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"8 ","pages":"56-58"},"PeriodicalIF":4.1,"publicationDate":"2024-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11129861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158596","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

Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome. 在哈钦森-吉尔福特早衰综合征中，细胞质 EP300 对 mTORC1 的致病性过度激活。

IF 6.4

Cell Stress Pub Date : 2024-04-30 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.04.295

Lucille Ferret, Guido Kroemer, Mojgan Djavaheri-Mergny

引用次数: 0

The missing hallmark of health: psychosocial adaptation. 缺失的健康标志：社会心理适应。

IF 6.4

Cell Stress Pub Date : 2024-03-12 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.03.294

Carlos López-Otín, Guido Kroemer

引用次数: 0

MiR-200c reprograms fibroblasts to recapitulate the phenotype of CAFs in breast cancer progression. MiR-200c 可重塑成纤维细胞，使其重现乳腺癌进展过程中 CAF 的表型。

IF 4.1

Cell Stress Pub Date : 2024-03-11 eCollection Date: 2024-01-01 DOI: 10.15698/cst2024.03.293

Zhao Lin, Megan E Roche, Víctor Díaz-Barros, Marina Domingo-Vidal, Diana Whitaker-Menezes, Madalina Tuluc, Guldeep Uppal, Jaime Caro, Joseph M Curry, Ubaldo Martinez-Outschoorn

{"title":"MiR-200c reprograms fibroblasts to recapitulate the phenotype of CAFs in breast cancer progression.","authors":"Zhao Lin, Megan E Roche, Víctor Díaz-Barros, Marina Domingo-Vidal, Diana Whitaker-Menezes, Madalina Tuluc, Guldeep Uppal, Jaime Caro, Joseph M Curry, Ubaldo Martinez-Outschoorn","doi":"10.15698/cst2024.03.293","DOIUrl":"10.15698/cst2024.03.293","url":null,"abstract":"Mesenchymal-epithelial plasticity driving cancer progression in cancer-associated fibroblasts (CAFs) is undetermined. This work identifies a subgroup of CAFs in human breast cancer exhibiting mesenchymal-to-epithelial transition (MET) or epithelial-like profile with high miR-200c expression. MiR-200c overexpression in fibroblasts is sufficient to drive breast cancer aggressiveness. Oxidative stress in the tumor microenvironment induces miR-200c by DNA demethylation. Proteomics, RNA-seq and functional analyses reveal that miR-200c is a novel positive regulator of NFκB-HIF signaling via COMMD1 downregulation and stimulates pro-tumorigenic inflammation and glycolysis. Reprogramming fibroblasts toward MET via miR-200c reduces stemness and induces a senescent phenotype. This pro-tumorigenic profile in CAFs fosters carcinoma cell resistance to apoptosis, proliferation and immunosuppression, leading to primary tumor growth, metastases, and resistance to immuno-chemotherapy. Conversely, miR-200c inhibition in fibroblasts restrains tumor growth with abated oxidative stress and an anti-tumorigenic immune environment. This work determines the mechanisms by which MET in CAFs via miR-200c transcriptional enrichment with DNA demethylation triggered by oxidative stress promotes cancer progression. CAFs undergoing MET trans-differentiation and senescence coordinate heterotypic signaling that may be targeted as an anti-cancer strategy.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"8 ","pages":"1-20"},"PeriodicalIF":4.1,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10927306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140111665","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

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