Cell Stress & Chaperones最新文献_第2页

Protective role of short-chain fatty acids on intestinal oxidative stress induced by TNF-α 短链脂肪酸对 TNF-α 诱导的肠道氧化应激的保护作用

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-12-01 DOI: 10.1016/j.cstres.2024.11.002

Miguel Ferrer , Berta Buey , Laura Grasa , Jose Emilio Mesonero , Eva Latorre

{"title":"Protective role of short-chain fatty acids on intestinal oxidative stress induced by TNF-α","authors":"Miguel Ferrer , Berta Buey , Laura Grasa , Jose Emilio Mesonero , Eva Latorre","doi":"10.1016/j.cstres.2024.11.002","DOIUrl":"10.1016/j.cstres.2024.11.002","url":null,"abstract":"<div><div>Inflammatory bowel diseases (IBDs) are driven by an exaggerated inflammatory response, which leads to a marked increase in oxidative stress. This, in turn, exacerbates the inflammatory process and causes significant cellular and tissue damage. Intestinal dysbiosis, a common observation in IBD patients, alters the production of bacterial metabolites, including short-chain fatty acids (SCFAs), which are key by-products of dietary fiber fermentation. While the role of SCFAs in intestinal physiology is still being elucidated, this study aimed to investigate their effects on intestinal oxidative stress, particularly under inflammatory conditions induced by the proinflammatory mediator tumor necrosis factor alpha (TNF-α). The Caco-2/TC7 cell line was employed as an in vitro model of the intestinal epithelium, and the cells were treated with a range of SCFAs, including acetate, propionate, and butyrate. The levels of protein and lipid oxidation were quantified, as well as the activity of antioxidant enzymes. Our findings demonstrate that microbiota-derived SCFAs can effectively mitigate TNF-α-induced oxidative stress by modulating antioxidant enzyme activity. The proinflammatory mediator TNF-α induces lipid peroxidation by inhibiting catalase and glutathione peroxidase activities. SCFAs are able to upregulate antioxidant enzyme activity to restore lipid oxidative levels. These results underscore the critical role of the gut microbiota in maintaining intestinal homeostasis and highlight the therapeutic potential of SCFAs in managing oxidative stress-related pathologies.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 769-776"},"PeriodicalIF":3.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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An outmoded in vitro-inferred mechanism for chaperonin-accelerated protein refolding is confirmed in cells by cryo-electron tomography 低温电子断层扫描技术证实了体外推断的伴侣素加速蛋白质重折叠的过时机制。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-11-15 DOI: 10.1016/j.cstres.2024.11.003

Paolo De Los Rios , Mathieu E. Rebeaud , Pierre Goloubinoff

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Regulation of chondrocyte apoptosis in osteoarthritis by endoplasmic reticulum stress 内质网应激对骨关节炎中软骨细胞凋亡的调节作用

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-11-06 DOI: 10.1016/j.cstres.2024.11.001

Renzhong Li , Kui Sun

引用次数: 0

Corrigendum to “The mechanism and therapeutic strategies in doxorubicin induced cardiotoxicity: Role of programmed cell death” [Cell Stress Chaperones. 2024;29:666-680] 多柔比星诱发心脏毒性的机制和治疗策略：细胞应激合子的作用》[Cell Stress Chaperones.］

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-24 DOI: 10.1016/j.cstres.2024.10.005

Yanzhao Li , Jing Yan , Pingzhen Yang

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The heat shock factor code: Specifying a diversity of transcriptional regulatory programs broadly promoting stress resilience 热休克因子代码：明确转录调控程序的多样性，广泛促进应激恢复能力。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-23 DOI: 10.1016/j.cstres.2024.10.006

Milad J. Alasady , Marc L. Mendillo

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IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-18 DOI: 10.1016/j.cstres.2024.10.004

Brenda A. Schilke , Thomas Ziegelhoffer , Przemyslaw Domanski , Jaroslaw Marszalek , Bartlomiej Tomiczek , Elizabeth A. Craig

{"title":"Functional similarities and differences among subunits of the nascent polypeptide-associated complex (NAC) of Saccharomyces cerevisiae","authors":"Brenda A. Schilke , Thomas Ziegelhoffer , Przemyslaw Domanski , Jaroslaw Marszalek , Bartlomiej Tomiczek , Elizabeth A. Craig","doi":"10.1016/j.cstres.2024.10.004","DOIUrl":"10.1016/j.cstres.2024.10.004","url":null,"abstract":"<div><div>Protein factors bind ribosomes near the tunnel exit, facilitating protein trafficking and folding. In eukaryotes, the heterodimeric nascent polypeptide-associated complex (NAC) is the most abundant—equimolar to ribosomes. <em>Saccharomyces cerevisiae</em> has a minor β-type subunit (Nacβ2) in addition to abundant Nacβ1, and therefore two NAC heterodimers, α/β1 and α/β12. The additional beta NAC gene arose at the time of the whole genome duplication that occurred in the <em>S. cerevisiae</em> lineage. Nacβ2 has been implicated in regulating the fate of messenger RNA encoding ribosomal protein Rpl4 during translation <em>via</em> its interaction with the Caf130 subunit of the regulatory CCR4-Not complex. We found that Nacβ2 residues just C-terminal to the globular domain are required for its interaction with Caf130 and its negative effect on the growth of cells lacking Acl4, the specialized chaperone for Rpl4. Substitution of these Nacβ2 residues at homologous positions in Nacβ1 results in a chimeric protein that interacts with Caf130 and slows the growth of ∆<em>acl4</em> cells lacking Nacβ2. Furthermore, alteration of residues in the N-terminus of Nacβ2 or chimeric Nacβ1 previously shown to affect ribosome binding overcomes the growth defect of ∆<em>acl4</em>. Our results are consistent with a model in which Nacβ2’s ribosome association <em>per se</em> or its precise positioning is necessary for productive recruitment of CCR4-Not <em>via</em> its interaction with the Caf130 subunit to drive Rpl4 messenger RNA degradation.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 721-734"},"PeriodicalIF":3.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

In memoriam James S. Clegg (1933–2024) 纪念詹姆斯-克莱格（James S. Clegg，1933-2024 年）。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-11 DOI: 10.1016/j.cstres.2024.10.003

Lawrence E. Hightower

引用次数: 0

Flow cytometry FRET reveals post-translational modifications drive Protein Phosphatase-5 conformational changes in mammalian cells 流式细胞仪 FRET 揭示翻译后修饰驱动蛋白磷酸酶-5 在哺乳动物细胞中的构象变化

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-10 DOI: 10.1016/j.cstres.2024.10.002

Rebecca A. Sager , Sarah J. Backe , Jennifer Heritz , Mark R. Woodford , Dimitra Bourboulia , Mehdi Mollapour

{"title":"Flow cytometry FRET reveals post-translational modifications drive Protein Phosphatase-5 conformational changes in mammalian cells","authors":"Rebecca A. Sager , Sarah J. Backe , Jennifer Heritz , Mark R. Woodford , Dimitra Bourboulia , Mehdi Mollapour","doi":"10.1016/j.cstres.2024.10.002","DOIUrl":"10.1016/j.cstres.2024.10.002","url":null,"abstract":"<div><div>The serine/threonine Protein Phosphatase-5 (PP5) plays an essential role in regulating hormone and stress-induced signaling networks as well as extrinsic apoptotic pathways in cells. Unlike other Protein Phosphatases, PP5 possesses both regulatory and catalytic domains, and its function is further modulated through post-translational modifications (PTMs). PP5 contains a tetratricopeptide repeat (TPR) domain, which usually inhibits its phosphatase activity by blocking the active site (closed conformation). Certain activators bind to the PP5–TPR domain, alleviating this inhibition and allowing the catalytic domain to adopt an active (open) conformation. While this mechanism has been proposed based on structural and biophysical studies, PP5 conformational changes and activity have yet to be observed in cells. Here, we designed and developed a flow cytometry-based fluorescence resonance energy transfer (FC-FRET) method, enabling real-time observation of PP5 autoinhibition and activation within live mammalian cells. By quantifying FRET efficiency using sensitized emission, we established a standardized and adaptable data acquisition workflow. Our findings revealed that, in a cellular context, PP5 exists in multiple conformational states, none of which alone fully predicts its activity. Additionally, we have demonstrated that PTMs such as phosphorylation and SUMOylation impact PP5 conformational changes, representing a significant advancement in our understanding of its regulatory mechanisms.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 709-717"},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells 依贝地农和peimisine可抑制香烟烟雾提取物诱导的BEAS-2B细胞氧化应激损伤和凋亡。

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-04 DOI: 10.1016/j.cstres.2024.10.001

Chuanlan Liu , Xiaomu Zhu , Erbu Aga , Wai Ming Tse , Kathy Wai Gaun Tse , Yanyong Liu , Bengui Ye

{"title":"Ebeiedinone and peimisine inhibit cigarette smoke extract-induced oxidative stress injury and apoptosis in BEAS-2B cells","authors":"Chuanlan Liu , Xiaomu Zhu , Erbu Aga , Wai Ming Tse , Kathy Wai Gaun Tse , Yanyong Liu , Bengui Ye","doi":"10.1016/j.cstres.2024.10.001","DOIUrl":"10.1016/j.cstres.2024.10.001","url":null,"abstract":"<div><div>Ebeiedinone and peimisine are the major active ingredients of Fritillariae Cirrhosae Bulbus. In this study, we looked at how these two forms of isosteroidal alkaloids protect human bronchial epithelial BEAS-2B cells from oxidative stress and apoptosis caused by cigarette smoke extract (CSE). First, the cytotoxicity was determined using the CCK8 assay, and an oxidative stress model was established. Then the antioxidative stress activity and mechanism were investigated by ELISA, flow cytometry, and Western blotting. By the CCK-8 assay, exposure to CSE (20%, 40%, and 100%) reduced the viability of BEAB-2S cells. The flow cytometry findings indicated that CSE-induced production of ROS (0.5% to maximum) and treatments with 10 μM ebeiedinone and 20 μM peimisine attenuated the production of ROS. The western blot assay results indicate that ebeiedinone and peimisine reduce CSE-induced oxidative stress, DNA damage, apoptosis, and autophagy dysregulation by inhibiting ROS, upregulating SOD and GSH/GSSG, and downregulating MDA, 4-HNE, and 8-OHdG through the NRF2/KEAP1 and JNK/MAPK-dependent pathways, thereby delaying the pathological progression of COPD caused by CS.Our data suggest that CSE causes oxidative stress, DNA damage, and apoptosis in BEAS-2B cells, as well as the progression of COPD. Ebeiedinone and peimisine fight CS-induced COPD by suppressing autophagy deregulation and apoptosis.</div></div>","PeriodicalId":9684,"journal":{"name":"Cell Stress & Chaperones","volume":"29 6","pages":"Pages 697-708"},"PeriodicalIF":3.3,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Editorial Board Members/Copyright 编委会成员/版权

IF 3.3 3区生物学

Cell Stress & Chaperones Pub Date : 2024-10-01 DOI: 10.1016/S1355-8145(24)00122-6

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