Journal of cellular biochemistry最新文献

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RETRACTION: Fibronectin Promotes Cervical Cancer Tumorigenesis Through Activating FAK Signaling Pathway
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-04-03 DOI: 10.1002/jcb.70022
{"title":"RETRACTION: Fibronectin Promotes Cervical Cancer Tumorigenesis Through Activating FAK Signaling Pathway","authors":"","doi":"10.1002/jcb.70022","DOIUrl":"https://doi.org/10.1002/jcb.70022","url":null,"abstract":"<p><b>RETRACTION:</b> Y. Zhou, C. Shu, and Y. Huang, “Fibronectin Promotes Cervical Cancer Tumorigenesis Through Activating FAK Signaling Pathway,” <i>Journal of Cellular Biochemistry</i> 120, no. 7 (2019): 10988–10997, https://doi.org/10.1002/jcb.28282.</p><p>The above article, published online on 11 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Multiple image elements in Figures 2B and 3C were found to have been previously published by different author groups in different scientific contexts. Additionally, Figure 3C contains duplication, with the same panel being used to depict different scientific contexts. Accordingly, the article is retracted as the editors consider its conclusions to be invalid.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761849","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
RETRACTION: LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-04-03 DOI: 10.1002/jcb.70017
{"title":"RETRACTION: LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke","authors":"","doi":"10.1002/jcb.70017","DOIUrl":"https://doi.org/10.1002/jcb.70017","url":null,"abstract":"<p><b>RETRACTION:</b> L. Zhang, X. Luo, F. Chen, W. Yuan, X. Xiao, X. Zhang, Y. Dong, Y. Zhang, and Y. Liu, “LncRNA SNHG1 Regulates Cerebrovascular Pathologies as a Competing Endogenous RNA Through HIF-1α/VEGF Signaling in Ischemic Stroke, ” <i>Journal of Cellular Biochemistry</i> 119, no. 7 (2018): 5460-5472, https://doi.org/10.1002/jcb.26705.</p><p>The above article, published online on 27 January 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Image elements within Figures 3 C and 6 F were found to have been published previously by different authors in different scientific contexts. The authors were invited to comment on these concerns but did not respond. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761848","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
RETRACTION: Lycopene Protects Keratinocytes Against UVB Radiation-Induced Carcinogenesis via Negative Regulation of FOXO3a Through the mTORC2/AKT Signaling Pathway
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-04-03 DOI: 10.1002/jcb.70016
{"title":"RETRACTION: Lycopene Protects Keratinocytes Against UVB Radiation-Induced Carcinogenesis via Negative Regulation of FOXO3a Through the mTORC2/AKT Signaling Pathway","authors":"","doi":"10.1002/jcb.70016","DOIUrl":"https://doi.org/10.1002/jcb.70016","url":null,"abstract":"<p><b>RETRACTION:</b> P. Chen, S. Xu, and J. Qu, “Lycopene Protects Keratinocytes Against UVB Radiation-Induced Carcinogenesis via Negative Regulation of FOXO3a Through the mTORC2/AKT Signaling Pathway,” <i>Journal of Cellular Biochemistry</i> 119, no. 1 (2018): 366-377, https://doi.org/10.1002/jcb.26189.</p><p>The above article, published online on 6 June 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Multiple image elements within Figures 2 A and 4 A were found to have been published previously and/or subsequently by different authors in different scientific contexts. Furthermore, evidence of inappropriate image editing/manipulation were found within Figure 3 C. The authors were invited to comment on these concerns but did not respond. Accordingly, the article is retracted as the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider its conclusions invalid. The authors were informed of the retraction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70016","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143761847","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
RETRACTION: Characterization of the Kynurenine Pathway in Skin-Derived Fibroblasts and Keratinocytes
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-31 DOI: 10.1002/jcb.70013
{"title":"RETRACTION: Characterization of the Kynurenine Pathway in Skin-Derived Fibroblasts and Keratinocytes","authors":"","doi":"10.1002/jcb.70013","DOIUrl":"https://doi.org/10.1002/jcb.70013","url":null,"abstract":"<p><b>RETRACTION</b>: D. Sheipouri, R. Grant, S. Bustamante, D. Lovejoy, G. J. Guillemin, and N. Braidy, “Characterization of the Kynurenine Pathway in Skin-Derived Fibroblasts and Keratinocytes,” <i>Journal of Cellular Biochemistry</i> 116, no. 6 (2015): 903-922. https://doi.org/10.1002/jcb.25019.</p><p>The above article, published online on January 12, 2015, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The journal received notice from a third party regarding evidence of duplication and image manipulation between the QPRT and KMO panels in Figure 5D as well as the QPRT and KAT-II panels in Figure 5B. The publisher confirmed these duplications. Some authors responded to an inquiry by the publisher but were not able to provide an explanation for the duplicated panels and were not able to provide original data for verification. An initial investigation by the University of New South Wales Conduct &amp; Integrity Office concluded that the immunochemistry data presented in this article had been misrepresented, fabricated and/or falsified and warranted further investigation by an independent research misconduct inquiry panel. The retraction has been agreed to because the evidence of image duplication and manipulation compromises the integrity of the study and the conclusions presented in the article. S.B. and D.L. agree with the retraction. All other authors did not respond to our notice regarding the retraction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741691","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
Cross-Kingdom Genomic Conservation of Putative Human Sleep-Related Genes: Phylogenomic Evidence From Chlamydomonas reinhardtii
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-31 DOI: 10.1002/jcb.70030
Seithikurippu R. Pandi-Perumal, Konda Mani Saravanan, Sayan Paul, George C. Abraham, David Warren Spence, Saravana Babu Chidambaram
{"title":"Cross-Kingdom Genomic Conservation of Putative Human Sleep-Related Genes: Phylogenomic Evidence From Chlamydomonas reinhardtii","authors":"Seithikurippu R. Pandi-Perumal,&nbsp;Konda Mani Saravanan,&nbsp;Sayan Paul,&nbsp;George C. Abraham,&nbsp;David Warren Spence,&nbsp;Saravana Babu Chidambaram","doi":"10.1002/jcb.70030","DOIUrl":"https://doi.org/10.1002/jcb.70030","url":null,"abstract":"<div>\u0000 \u0000 <p>Sleep is a widespread and evolutionarily conserved process observed in diverse organisms, from jellyfish to mammals, hinting at its origin as a life-supporting mechanism over 500 million years ago. Although its fundamental purpose and mechanisms remain unclear, sleep's evolution and adaptive significance continue to be debated. This study explores the evolutionary origins of sleep using <i>Chlamydomonas reinhardtii</i> as a model organism, identifying 112 putative sleep-related genes across species and highlighting the evolutionary conservation of sleep-regulatory pathways. Additionally, discovering uncharacterized proteins with high sequence similarity and significant e-values suggests unexplored roles in sleep regulation, underscoring the potential of <i>C. reinhardtii</i> to reveal new insights into the molecular basis of sleep. This study provides a foundation for identifying previously unknown sleep-associated proteins, particularly within single-celled organisms, which may offer novel perspectives on the biological role of sleep. The study demonstrates that phylogenomic analysis of diverse model organisms can expand our understanding of the evolutionary trajectory of sleep and its fundamental function, paving the way for further research in sleep biology and its health implications. Overall, the fundamental functions of sleep observed in higher animal phyla originated from its primordial activities, demonstrating an evolutionary continuum wherein more specialized tasks were integrated with sleep's essential restorative properties.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741651","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
RETRACTION: MiR-125a-3p Suppresses the Growth and Progression of Papillary Thyroid Carcinoma Cell by Targeting MMP11
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-30 DOI: 10.1002/jcb.70014
{"title":"RETRACTION: MiR-125a-3p Suppresses the Growth and Progression of Papillary Thyroid Carcinoma Cell by Targeting MMP11","authors":"","doi":"10.1002/jcb.70014","DOIUrl":"https://doi.org/10.1002/jcb.70014","url":null,"abstract":"<p><b>RETRACTION</b>: M. Song, N. Wang, Z. Li, Y. Zhang, Y. Zheng, P. Yi, and J. Chen, “MiR-125a-3p Suppresses the Growth and Progression of Papillary Thyroid Carcinoma Cell by Targeting MMP11,” <i>Journal of Cellular Biochemistry</i> 121, no. 2 (2020): 984-995, https://doi.org/10.1002/jcb.29333.</p><p>The above article, published online on September 6, 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed upon at the authors' request. The authors informed the journal of methodological flaws that affect the reliability of the study's conclusions. Accordingly, the article is retracted as the editors acknowledge the reported issues and their impact on the validity of the study's findings.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741216","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
The Expression Profile of the RANK/RANKL/OPG Pathway in Breast Cancer Stem Cells Isolated From Breast Cancer Cell Lines
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-30 DOI: 10.1002/jcb.70028
Hassnaa H. Elgohary, Mohamed M. Kamal, Sherine Maher Rizk, Nadine W. Maurice
{"title":"The Expression Profile of the RANK/RANKL/OPG Pathway in Breast Cancer Stem Cells Isolated From Breast Cancer Cell Lines","authors":"Hassnaa H. Elgohary,&nbsp;Mohamed M. Kamal,&nbsp;Sherine Maher Rizk,&nbsp;Nadine W. Maurice","doi":"10.1002/jcb.70028","DOIUrl":"https://doi.org/10.1002/jcb.70028","url":null,"abstract":"<div>\u0000 \u0000 <p>The RANK/RANKL/OPG signaling pathway plays a crucial role in breast cancer progression and metastasis. However, its expression patterns and potential implications in breast cancer stem cells remain poorly understood. This study aimed to characterize the expression profile of this pathway in breast cancer stem cells isolated from two distinct breast cancer cell lines: MDA-MB-231 and MCF-7. Mammospheres (MS), representing breast cancer stem cells, were generated using agar-coated 6 well tissue culture plates in suitable mammospheres culture conditions. Flow cytometric analysis showed enrichment of the CD44<sup>+</sup>/CD24<sup>−</sup> subpopulations in the mammospheres cultures, with MDA-MB-231 exhibiting a higher percentage compared to MCF-7. The isolated MS from both cell lines showed upregulation of stemness markers OCT4 and SOX2, with MS. MDA-MB-231 demonstrating higher expression levels. Analysis of the RANK/RANKL/OPG axis revealed differential expression patterns between the two cell lines. RANK expression was significantly upregulated in MS. MDA-MB-231 but not in MS. MCF-7. Interestingly, while OPG mRNA levels were elevated in mammospheres from both cell lines, secreted OPG protein levels were paradoxically reduced in the mammospheres conditioned media. Additionally, RUNX2, an osteoblastic marker, and a downstream target of RANK signaling, showed a decreased expression in both mammospheres compared to adherent cells. These findings suggest a complex, context-dependent regulation of the RANK/RANKL/OPG pathway in breast cancer stem cells, potentially contributing to the aggressive nature and metastatic propensity of triple-negative breast cancer. This study provides novel insights into the molecular characteristics of breast cancer stem cells and underscores the complexity of OPG/RANK/RANKL axis expression in them; a role yet to be fully elucidated.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741220","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 Molecular Mechanisms of Bergapten Against Abdominal Aortic Aneurysm: Evidence From Network Pharmacology, Molecular Docking/Dynamics, and Experimental Validation
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-30 DOI: 10.1002/jcb.70029
Fujia Xu, Sihan Luo, Zhenhua Huang, Junfen Wang, Tian Li, Lintao Zhong, Xiaoyun Si
{"title":"The Molecular Mechanisms of Bergapten Against Abdominal Aortic Aneurysm: Evidence From Network Pharmacology, Molecular Docking/Dynamics, and Experimental Validation","authors":"Fujia Xu,&nbsp;Sihan Luo,&nbsp;Zhenhua Huang,&nbsp;Junfen Wang,&nbsp;Tian Li,&nbsp;Lintao Zhong,&nbsp;Xiaoyun Si","doi":"10.1002/jcb.70029","DOIUrl":"https://doi.org/10.1002/jcb.70029","url":null,"abstract":"<div>\u0000 \u0000 <p>This study endeavors to assess the potential protective role of bergapten (BP) in mitigating abdominal aortic aneurysm (AAA) and to decipher the underlying mechanisms and molecular targets. Network pharmacology was utilized to search for potential targets of BP against AAA. Molecular docking and molecular dynamics simulations were utilized to validate the interaction of BP with core targets, and then the therapeutic effect and mechanism of BP on AAA were verified by using an elastase-induced AAA model. Network pharmacology analysis identified five pharmacological targets for BP, including EGFR, SRC, PIK3CA, PIK3CB, and JAK2. Molecular docking and molecular dynamics simulations further prioritized JAK2 as the most promising candidate for the potential treatment of AAA. The results of animal experiments demonstrated that BP significantly reduced the expression of inflammatory cytokines IL-6, TNF-α, and IL-1β in the aortic tissue of AAA mouse model, and inhibited the phosphorylation of JAK2 and STAT3. BP plays an important role in the treatment of AAA, and it may become a promising drug to combat AAA progression. The inhibitory effect of BP on AAA vascular progression and the attenuation of inflammatory cell infiltration may be related to the regulation of JAK2/STAT3 signaling pathway.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 4","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143741217","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
“Exploration of Novel Anticancerous Agents Targeting Human Aurora Kinase C”
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-24 DOI: 10.1002/jcb.70025
Deepali Gupta, Prakash Kumar Shukla, Subarnarekha Chowdhury, Supriya Kumari, Punit Kaur, Mukesh Kumar
{"title":"“Exploration of Novel Anticancerous Agents Targeting Human Aurora Kinase C”","authors":"Deepali Gupta,&nbsp;Prakash Kumar Shukla,&nbsp;Subarnarekha Chowdhury,&nbsp;Supriya Kumari,&nbsp;Punit Kaur,&nbsp;Mukesh Kumar","doi":"10.1002/jcb.70025","DOIUrl":"https://doi.org/10.1002/jcb.70025","url":null,"abstract":"<div>\u0000 \u0000 <p>Aurora kinases (AKs), a family of serine/threonine kinases, play a vital role in chromosome segregation during the cell cycle (Mountzios et al., 2008). This family includes Aurora Kinase A (AKA), Aurora Kinase B (AKB), and Aurora Kinase C (AKC). AKA and AKB are active during mitosis, while AKC is involved mostly in germ cell as well as somatic cells. Elevated levels of AKC have been found in several cancer cell lines including breast, cervical, thyroid, colorectal, and liver cancers, making it a significant target for cancer therapy (Tang et al., 2017). In cancers such as glioblastoma and prostate cancer, for example, AKC up regulation has been associated with increased tumor aggressiveness, highlighting its potential role in tumor progression and poor prognosis. Our study employs computational methods, including molecular docking and structure-based virtual screening, to explore a data set of 2 65 241 compounds from the National Cancer Institute (NCI) database, focusing on AKC as a potential target for drug discovery. Through docking studies, several promising compounds that interact with the enzyme's ATP binding pocket, particularly with residues Phe54, Lys72, Ala123, Glu121 and Glu127 of AKC, were identified. The stability of these interactions was assessed through 200-ns molecular dynamics (MD) simulations, revealing that the majority of compounds exhibited stable interactions, while a few displayed fluctuations in their trajectories. Most compounds adhered to favorable pharmacokinetic properties. Comprehensive MD simulations and free energy calculations identified three top candidates (90 729, 37 623, and 134 546) with strong potential as potent inhibitors of AKC. Additional in vitro and in vivo studies are required to confirm the therapeutic potential of these candidates.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 3","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143689760","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
Sirtuin-2 Is Involved in the Regulation of Claudin-4 Expression and Paracellular Barrier Function in Keratinocytes
IF 3 3区 生物学
Journal of cellular biochemistry Pub Date : 2025-03-20 DOI: 10.1002/jcb.70027
Shunsuke Matsuda, Maika Miwa, Miki Tanabe, Mao Kobayashi, Shokoku Shu, Yuta Yoshino, Norihiro Tada, Akichika Itoh, Akira Ikari
{"title":"Sirtuin-2 Is Involved in the Regulation of Claudin-4 Expression and Paracellular Barrier Function in Keratinocytes","authors":"Shunsuke Matsuda,&nbsp;Maika Miwa,&nbsp;Miki Tanabe,&nbsp;Mao Kobayashi,&nbsp;Shokoku Shu,&nbsp;Yuta Yoshino,&nbsp;Norihiro Tada,&nbsp;Akichika Itoh,&nbsp;Akira Ikari","doi":"10.1002/jcb.70027","DOIUrl":"10.1002/jcb.70027","url":null,"abstract":"<div>\u0000 \u0000 <p>Claudin-1 (CLDN1) and CLDN4 are highly expressed in keratinocytes and may function as a paracellular barrier to water and small molecules. The physiological function of CLDN4 has not been fully understood, whereas dysfunction of CLDN1 is involved in the pathophysiology of allergy and inflammatory diseases. Here, we found that the protein level of CLDN4 in the skin tissues of 36-week-old mice was lower than that in 6-week-old mice. In contrast, there was not much difference in the mRNA levels of <i>CLDN4</i>. Tenovin-1 (Ten-1), a sirtuin-1/2 inhibitor, decreased the protein level of CLDN4 without affecting that of CLDN1 in human keratinocyte-derived HaCaT cells. The decrease in <i>CLDN4</i> mRNA by Ten-1 was much less than that in protein. Cycloheximide-chase assay showed that the protein stability of CLDN4 was attenuated by Ten-1. The Ten-1-induced decrease in CLDN4 protein was inhibited by clathrin-dependent endocytosis and proteasome inhibitors. The Ten-1 treatment or SIRT2 silencing induced the elevation of acetylated CLDN4 protein, leading to the reduction of CLDN4 protein. In addition, the paracellular barrier function was reduced by Ten-1 treatment or SIRT2 silencing. These results indicate that Ten-1 may enhance the clathrin-dependent endocytosis and proteasome-dependent degradation of CLDN4 protein, resulting in the dysfunction of paracellular barrier. The Ten-1-induced reduction of CLDN4 protein and paracellular barrier function were inhibited by curcumin, a polyphenol contained in <i>Curcuma longa</i> plant. We suggest that the reduction of CLDN4 protein in keratinocytes may be involved in the age-related dysfunction of the skin barrier, which may be rescued by curcumin.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 3","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670013","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
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