Archives of biochemistry and biophysics最新文献_第8页

TET3 inhibits the decidualization of human endometrial stromal cells by regulating ITGA10 transcription through recruiting HDAC1/2 TET3通过募集HDAC1/2调控ITGA10转录抑制人子宫内膜间质细胞去细胞化

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-15 DOI: 10.1016/j.abb.2025.110552

Ying Zhou , Shuyue Zheng , Yahui Xie , Mengyu Jing , Meiyan Jiang , Dan Li , Aixia Liu

{"title":"TET3 inhibits the decidualization of human endometrial stromal cells by regulating ITGA10 transcription through recruiting HDAC1/2","authors":"Ying Zhou , Shuyue Zheng , Yahui Xie , Mengyu Jing , Meiyan Jiang , Dan Li , Aixia Liu","doi":"10.1016/j.abb.2025.110552","DOIUrl":"10.1016/j.abb.2025.110552","url":null,"abstract":"<div><div>Decidualization is a critical physiological process necessary for successful embryo implantation and pregnancy maintenance. Disruptions in this process can result in infertility and various pregnancy complications. Ten-eleven translocation protein 3 (TET3) is a key molecule in the dedifferentiation process, but its pathogenic mechanism remains unclear. In this study, we aimed to uncover the molecular mechanisms by which TET3 modulates decidualization through utilizing an <em>in vitro</em> ESC model overexpressing TET3. TET3 overexpression was found to inhibit the transcription of <em>ITGA10</em> (integrin subunit alpha 10), a novel downstream target, thereby suppressing the proliferation and migration of endometrial stromal cells. This repression of <em>ITGA10</em> is independent of TET3's catalytic activity and instead relies on its non-catalytic function. Mechanistically, TET3 recruits histone deacetylases 1 and 2 (HDAC1/2) to the <em>ITGA10</em> promoter to repress its transcription. Silencing <em>HDAC1</em> or <em>HDAC2</em> individually had little effect on the repressive action of TET3. However, simultaneous knockdown of <em>HDAC1</em> and <em>HDAC2</em> via siRNA, or pharmacological inhibition using the <em>HDAC1/2</em> inhibitor romidepsin, effectively reversed TET3-mediated repression of <em>ITGA10</em>. These findings uncover a non-catalytic role for TET3 in regulating decidualization and provide insights into potential therapeutic targets for pregnancy-related disorders.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110552"},"PeriodicalIF":3.8,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The immunological and prognostic landscape of TFAP4 in cancer: A single-cell RNA sequencing perspective 肿瘤中TFAP4的免疫学和预后：单细胞RNA测序的观点。

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-11 DOI: 10.1016/j.abb.2025.110551

Linghui Zhong , Zidong Feng , Feng Li , Honghui Zhao , Ziyu Zhang , Wenyang Zhang , Heiko Hermeking , Lei Shi

{"title":"The immunological and prognostic landscape of TFAP4 in cancer: A single-cell RNA sequencing perspective","authors":"Linghui Zhong , Zidong Feng , Feng Li , Honghui Zhao , Ziyu Zhang , Wenyang Zhang , Heiko Hermeking , Lei Shi","doi":"10.1016/j.abb.2025.110551","DOIUrl":"10.1016/j.abb.2025.110551","url":null,"abstract":"<div><div>Transcription factor activating enhancer-binding protein 4 (TFAP4) has been implicated in tumorigenesis, yet its precise role in the tumor microenvironment remains inadequately characterized. In this study, we employed single-cell RNA sequencing and multi-omics analysis to investigate the immunological and prognostic significance of TFAP4 across various cancer types. Our analysis reveals that TFAP4 is upregulated in malignant epithelial cells across multiple cancer types and correlated with advanced tumor stages and poor patient survival. High TFAP4 expression is associated with activation of oncogenic signaling pathways, including MAPK, JAK-STAT, and TGF-β signaling. TFAP4-high expressing tumors exhibit reduced CD8<sup>+</sup> and CD4<sup>+</sup> T cell infiltration and increased T cell exhaustion. Cell-cell communication analysis reveals that TFAP4-high cells orchestrate immunosuppressive signaling in the tumor microenvironment. Notably, TFAP4 knockdown enhances the efficacy of chemotherapy and is downregulated following anti-PD-1 treatment, indicating its role in modulating therapeutic response. Collectively, our findings provide novel insights into the immunological functions of TFAP4, highlighting its potential as a prognostic biomarker and therapeutic target in cancer.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110551"},"PeriodicalIF":3.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bim and Mcl-1 coordinate NVP-BEZ235-induced renal cell carcinoma cell apoptosis Bim与Mcl-1协同nvp - bez235诱导肾癌细胞凋亡

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-09 DOI: 10.1016/j.abb.2025.110549

Yen-Chuan Ou , Jian-Ri Li , Tung-Min Yu , Chih-Cheng Wu , Su-Lan Liao , Wen-Ying Chen , Yu-Hsiang Kuan , Chun-Jung Chen

{"title":"Bim and Mcl-1 coordinate NVP-BEZ235-induced renal cell carcinoma cell apoptosis","authors":"Yen-Chuan Ou , Jian-Ri Li , Tung-Min Yu , Chih-Cheng Wu , Su-Lan Liao , Wen-Ying Chen , Yu-Hsiang Kuan , Chun-Jung Chen","doi":"10.1016/j.abb.2025.110549","DOIUrl":"10.1016/j.abb.2025.110549","url":null,"abstract":"<div><div>Dysregulation of the PI3K/Akt/mTOR pathway has been reported in renal cell carcinoma (RCC) and is associated with an aggressive phenotype and a poor prognosis. To obtain insights into the action mechanisms of PI3K/mTOR dual inhibitors, the anti-tumor actions of NVP-BEZ235 were investigated in human 786-O and ACHN RCC cells. NVP-BEZ235 decreased cell proliferation and migration, and induced autophagic cell death. Inactivation of the Akt by NVP-BEZ235 was accompanied by forkhead box O1 (FOXO1) and extracellular signal-regulated kinase (ERK) activation as well as signal transducer and activator of transcription 3 (Stat3) inactivation. Despite the reduction of Mcl-1 and accumulation of Bim seen in NVP-BEZ235-treated cells, evidence of apoptosis was rare. Bcl-2 inhibitor ABT-737 and Mcl-1 inhibitor AZD5991 predisposed NVP-BEZ235-treated cells to transform into the apoptotic phenotype. PI3K inhibitor LY294002 and Stat3 inhibitor AG490 duplicated the sensitized actions towards NVP-BEZ235. FoxO1 had roles in NVP-BEZ235-induced Bim expression. Data on pharmacological approaches with ubiquitin proteasome inhibitor together with genetic silencing highlight a role of Bim in NVP-BEZ235-directed RCC cell apoptosis. However, the pro-apoptotic actions of Bim were limited by a compensatory activation of ERK, resulting in decreased Bim protein stability. Data of <em>in vivo</em> tumor-bearing studies further revealed a better anti-tumor potential in the combination treatment of NVP-BEZ235 and MEK/ERK inhibitors without obvious toxicity. Our findings suggest that the feedback activation of pro-survival machinery is likely to be the main cause of cancer cells being refractory to NVP-BEZ235, and a combination treatment is a feasible strategy to sensitize cancer cell responses.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110549"},"PeriodicalIF":3.8,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144605373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The lncRNA MIR503HG/miR-16-5p/FOSL1 pathway mediates autophagy to promote esophageal epithelial cells proliferation and EMT in esophageal restenosis lncRNA MIR503HG/miR-16-5p/FOSL1通路介导自噬，促进食管再狭窄中食管上皮细胞增殖和EMT

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-08 DOI: 10.1016/j.abb.2025.110536

Ning Xia , Peng Zhang , Ling Yang , Xiang Yin , Shao-Qiu Wu , Ying Yao , Ming-Yi Shang , Li Weng

{"title":"The lncRNA MIR503HG/miR-16-5p/FOSL1 pathway mediates autophagy to promote esophageal epithelial cells proliferation and EMT in esophageal restenosis","authors":"Ning Xia , Peng Zhang , Ling Yang , Xiang Yin , Shao-Qiu Wu , Ying Yao , Ming-Yi Shang , Li Weng","doi":"10.1016/j.abb.2025.110536","DOIUrl":"10.1016/j.abb.2025.110536","url":null,"abstract":"<div><div>Esophageal stents have been used increasingly to relieve malignant dysphagia and are widely employed in the treatment of esophageal stenosis. However, the clinical application of esophageal stents has been limited by esophageal restenosis. Our preliminary studies have indicated that long non-coding RNAs (lncRNAs) may be involved in the development of esophageal restenosis. The aim of this study was to investigate the role of the lncRNA MIR503HG (MIR503HG)/miR-16–5p/Fos-like antigen-1 (FOSL1) pathway in esophageal restenosis. We demonstrate that MIR503HG and FOSL1 expression levels were significantly upregulated, while miR-16–5p was decreased in hyperplastic esophageal tissues compared to normal controls. Knockdown of MIR503HG significantly repressed proliferation, extracellular matrix deposition, migration, epithelial-mesenchymal transition, autophagy, and promoted apoptosis in Het-1A cells, while MIR503HG overexpression had the opposite effect. Mechanistically, MIR503HG was found to competitively interact with miR-16–5p leading to increased FOSL1 expression. Taken together, our findings indicate that MIR503HG is involved in the development of esophageal restenosis through miR-16-5p-dependent regulation of FOSL1. Thus, targeting MIR503HG could be beneficial in the development of a novel targeted therapeutic strategy for esophageal restenosis.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110536"},"PeriodicalIF":3.8,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144587444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SERS and Contemporary selenium research SERS与当代硒研究。

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-08 DOI: 10.1016/j.abb.2025.110533

Pheeranat Punyamung , Lucy M. Kyung , Jongkeol An , David G. Churchill

{"title":"SERS and Contemporary selenium research","authors":"Pheeranat Punyamung , Lucy M. Kyung , Jongkeol An , David G. Churchill","doi":"10.1016/j.abb.2025.110533","DOIUrl":"10.1016/j.abb.2025.110533","url":null,"abstract":"<div><div>The ongoing efforts in the synthesis of selenium (Se) containing molecules have led to the emergence of various potential applications and have spurred additional investigative studies, especially those using spectroscopic techniques. With the use of ultra-sensitive techniques such as Surface Enhanced Raman Spectroscopy (SERS), a new dimension of Se research has emerged, providing prospective opportunities for the development of Se-containing materials. This advancement also extends to related main group elements materials, especially those which are sulfur and tellurium-containing. <em>Selenium</em> compounds of many different designs can be interrogated, as has been done with sulfur, often using a chosen (roughened) substrate. The substrate itself may also contain Se center. This review article presents the recent developments in Se and SERS chemistry, highlingthing key advances in enhancement factors, since the 2020 review by Langer et al. (Nano, 2019, 14(1), 28–117). The types of materials mentioned in this paper include nanosheets, surface coatings, nanoshell cores, graphene derivatives, and thin films. Finally, we provide a future outlook on the direction of Se and SERS-based research.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110533"},"PeriodicalIF":3.8,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “Thymidine and 2′-deoxyuridine reduce microglial activation and improve oxidative stress damage by modulating glycolytic metabolism on the Aβ25-35-induced brain injury” [Archiv. Biochem. Biophys. 729 (2022) 109377] 胸苷嘧啶和2 ' -脱氧尿苷通过调节a β25-35诱导的脑损伤的糖酵解代谢，减少小胶质细胞的激活，改善氧化应激损伤。物化学。生物物理学报。729 (2022)109377 [j]

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-08 DOI: 10.1016/j.abb.2025.110528

Meng Liu , Mengnan Zeng , Shengchao Wang , Bing Cao , Pengli Guo , Yuhan Zhang , Jufang Jia , Qinqin Zhang , Beibei Zhang , Ru Wang , Jinyue Li , Xiaoke Zheng , Weisheng Feng

引用次数: 0

Proteomic analysis reveals the potential mechanism of ergothioneine in preventing acute kidney injury to chronic kidney disease transition 蛋白质组学分析揭示麦角硫因预防急性肾损伤向慢性肾病过渡的潜在机制

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-07 DOI: 10.1016/j.abb.2025.110534

Jiaxin Peng , Jing Chen , Mengran Wu , Tao He , Xiaojuan Guo , Qiangguo Ao , Ling Chen

{"title":"Proteomic analysis reveals the potential mechanism of ergothioneine in preventing acute kidney injury to chronic kidney disease transition","authors":"Jiaxin Peng , Jing Chen , Mengran Wu , Tao He , Xiaojuan Guo , Qiangguo Ao , Ling Chen","doi":"10.1016/j.abb.2025.110534","DOIUrl":"10.1016/j.abb.2025.110534","url":null,"abstract":"<div><div>Acute kidney injury (AKI) is widely recognized as an important risk factor for chronic kidney disease (CKD), and preventing or delaying the AKI-CKD transition represents a critical therapeutic priority. Ergothioneine (EGT), a natural antioxidant, has demonstrated renal protective potential, but its role in attenuating the AKI-CKD transition remains unclear. To investigate this, an AKI-CKD mouse model was constructed by administering multiple small-dose injections of cisplatin. Mice were divided into control, AKI-CKD, and AKI-CKD + EGT groups. The protective function of EGT was assessed using biochemical indexes and histopathology. Proteomic analysis and network pharmacology were applied to identify potential EGT targets, which were further verified by molecular docking and Western blot. Results showed that EGT significantly mitigated renal damage in AKI-CKD mice. Proteomic analysis identified 35 differentially expressed proteins (DEPs) potentially associated with EGT treatment, with GO and KEGG enrichment implicating complement activation as a key pathway. Protein-protein interaction (PPI) network analysis, topology analyses, and molecular docking identified C4B and PON1 as potential core EGT targets. In conclusion, EGT attenuates AKI-CKD progression by targeting C4B and PON1, modulating complement activation and oxidative stress. These findings highlight the therapeutic potential of EGT and provide novel insights for drug development targeting the AKI-CKD transition.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110534"},"PeriodicalIF":3.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144587443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AAV-mediated inhibition of endothelial IL-1β/IL-1R1 signaling alleviates the development of sepsis-associated encephalopathy aav介导的内皮细胞IL-1β/IL-1R1信号的抑制可减轻败血症相关脑病的发展。

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-07 DOI: 10.1016/j.abb.2025.110535

Dan Xiao , Lingling Liu , Wanting Liang , Xiao Wang , Yuting Du , Chunmao Liu , Yanghe Liu , Weifeng Zhang , Guodong Yang

{"title":"AAV-mediated inhibition of endothelial IL-1β/IL-1R1 signaling alleviates the development of sepsis-associated encephalopathy","authors":"Dan Xiao , Lingling Liu , Wanting Liang , Xiao Wang , Yuting Du , Chunmao Liu , Yanghe Liu , Weifeng Zhang , Guodong Yang","doi":"10.1016/j.abb.2025.110535","DOIUrl":"10.1016/j.abb.2025.110535","url":null,"abstract":"<div><div>Sepsis-Associated Encephalopathy (SAE), a disorder affecting the central nervous system (CNS), is highly prevalent, occurring in approximately 70 % of sepsis patients in intensive care units (ICU). Although numerous studies have highlighted the critical role of IL-1β in the pathogenesis of SAE, the specific downstream mechanisms remain poorly understood. Moreover, the Phase III clinical trial of IL-1R1 antagonists for SAE therapy ended in failure. In this study, we found that IL-1R1, the receptor for IL-1β, is exclusively and highly expressed on CNS endothelial cells during early sepsis. Specifically inhibiting IL-1R1 expression in endothelial cells during the early stage of sepsis can significantly suppress the onset of SAE. Mechanistically, elevated levels of LPS, IL-1α, or IL-1β in the serum during sepsis induce IL-1R1 expression on endothelial cells, leading to the activation of IL-1β signaling. Activation of the IL-1β/IL-1R1 signaling pathway in endothelial cells triggers the expression of adhesion molecules, pro-inflammatory cytokines, and chemokines, which in turn exacerbate neuroinflammation and contribute to cognitive impairments. This research not only elucidates the pathogenic mechanisms underlying SAE but also introduces an advanced approach for targeted gene intervention in CNS endothelial cells, potentially offering a new strategy for the treatment of SAE and other neurodegenerative disease induced by systemic inflammation.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110535"},"PeriodicalIF":3.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genesis of additional open state zones in the extended polyQ tract of the ATXN2 gene depends on its length and interruptions localization ATXN2基因扩展多q通道中额外开放状态区的发生取决于其长度和中断定位

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-07 DOI: 10.1016/j.abb.2025.110531

Mikhail I. Drobotenko , Luis Velázquez-Pérez , Аnna A. Dorohova , Oksana M. Lyasota , Jose Luis Hernandez-Caceres , Roberto Rodriguez-Labrada , Alexandr A. Svidlov , Olga A. Leontyeva , Mikhail G. Baryshev , Yury D. Nechipurenko , Stepan S. Dzhimak

{"title":"Genesis of additional open state zones in the extended polyQ tract of the ATXN2 gene depends on its length and interruptions localization","authors":"Mikhail I. Drobotenko , Luis Velázquez-Pérez , Аnna A. Dorohova , Oksana M. Lyasota , Jose Luis Hernandez-Caceres , Roberto Rodriguez-Labrada , Alexandr A. Svidlov , Olga A. Leontyeva , Mikhail G. Baryshev , Yury D. Nechipurenko , Stepan S. Dzhimak","doi":"10.1016/j.abb.2025.110531","DOIUrl":"10.1016/j.abb.2025.110531","url":null,"abstract":"<div><div>The <em>ATXN2</em> gene is located on chromosome 12q24.1 and encodes the ataxin-2 protein, which is involved in the regulation of RNA metabolism, protein synthesis, and intracellular signaling. The polyQ tract encoding glutamine can expand, which leads to the development of various neurodegenerative diseases. CAA interruptions play an important role in stabilizing the polyQ tract in the <em>ATXN2</em> gene. However, CAA interruptions may be associated with other neurodegenerative conditions such as parkinsonism. In this paper, the stability of the polyQ tract in the presence of CAA interruptions depending on their localization was studied using mathematical modeling methods. It was found that interruptions located near the center of the polyQ tract significantly reduce its stability, and those located near its borders can both reduce and increase the stability of the polyQ tract. In this case, a certain asymmetry is observed: CAA interruptions located near the left border of the polyQ tract have a more stabilizing effect than CAA interruptions located near the right border.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110531"},"PeriodicalIF":3.8,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144579377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Prolonged oleic acid exposure impairs Caco-2 cell differentiation and tight junction integrity 长时间的油酸暴露会损害Caco-2细胞分化和紧密连接的完整性。

IF 3.8 3区生物学

Archives of biochemistry and biophysics Pub Date : 2025-07-05 DOI: 10.1016/j.abb.2025.110532

Alexandra Receveur , Wei Zhu , Patricia I. Oteiza

{"title":"Prolonged oleic acid exposure impairs Caco-2 cell differentiation and tight junction integrity","authors":"Alexandra Receveur , Wei Zhu , Patricia I. Oteiza","doi":"10.1016/j.abb.2025.110532","DOIUrl":"10.1016/j.abb.2025.110532","url":null,"abstract":"<div><div>Proliferation to differentiation transition (PDT) of the intestinal epithelium is a critical step in intestinal homeostasis. Disruption of PDT balance can contribute to the onset and progression of systemic diseases. Consumption of high-fat diet (HFD) is known to promote systemic inflammation, in part due to the associated intestinal barrier permeabilization. This could be due to alterations in tight junction (TJ) formation and/or altered function during the process of stem cell differentiation into mature enterocytes. To investigate this potential mechanism, this study investigated the effects of exposure to oleic acid (OA), a fatty acid abundant in HFD, on Caco-2 cell differentiation. Caco-2 cells were incubated with 0.2–1.6 mM OA for 6 h/day, during the 10–21 days period involved in the transition of undifferentiated Caco-2 cells into mature enterocytes. We assessed time-dependent changes in markers of cell differentiation, monolayer permeability, and parameters of TJ structure and dynamics. We observed that OA: (1) altered barrier formation, as assessed by measuring the monolayer transepithelial electrical resistance; (2) decreased levels of the TJ proteins ZO-1 and claudin-1; and (3) activated signaling cascades/events leading to TJ opening, i.e. ERK1/2, NF-κB, and myosin light chain (MLC) phosphorylation, and (4) caused alterations in redox homeostasis. These findings suggest that prolonged exposure to OA has a disruptive effect on the transition of Caco-2 cells into fully differentiated enterocytes. This can in part explain the permeabilization of the intestinal barrier and systemic inflammation associated with regular HFD consumption.</div></div>","PeriodicalId":8174,"journal":{"name":"Archives of biochemistry and biophysics","volume":"772 ","pages":"Article 110532"},"PeriodicalIF":3.8,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144582880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0