Journal of Cellular Physiology最新文献

{"title":"Maternal Obesity Programs Adipogenic Commitment in Neonatal Mesenchymal Stem Cells: A Link to Redox-Dependent FOXO1 Signaling.","authors":"Sofía Bellalta, Erika Pinheiro-Machado, Theo Borghuis, Jelmer Prins, Torsten Plösch, Paola Casanello, Marijke Faas","doi":"10.1002/jcp.70178","DOIUrl":"https://doi.org/10.1002/jcp.70178","url":null,"abstract":"<p><p>Maternal obesity increases the risk of obesity and metabolic disease in the offspring, yet the cellular mechanisms that program adipose tissue development remain poorly understood. Mesenchymal stem cells (MSCs), the precursors of adipocytes, may represent an early target of metabolic programming during fetal development. In this study, we investigated whether maternal obesity alters stemness, redox homeostasis and adipogenic signaling through FOXO1 in neonatal MSCs. MSCs were isolated from Wharton's jelly of umbilical cords from neonates born to mothers with normal weight (NW-MSCs, n = 15) or obesity (OB-MSCs, n = 15). OB-MSCs exhibited reduced stemness characteristics, including lower OCT3/4 expression and decreased clonogenic capacity. These cells also displayed increased mitochondrial superoxide levels and reduced SOD2 expression, indicating mitochondrial oxidative stress. In addition, OB-MSCs showed increased GSH levels and decreased antioxidant enzyme response, compared to NW-MSCs. Further, OB-MSCs exhibited higher FOXO1 expression levels, reduced acetyl-FOXO1 levels, and altered subcellular localization during early adipogenesis, consistent with reduced repression of the adipogenic regulator PPARγ. Finally, OB-MSC-derived adipocytes exhibited increased PPARγ expression at later stages of differentiation. These findings suggest that maternal obesity disrupts redox balance and FOXO1 dynamics in neonatal MSCs, thereby shifting early adipogenic signaling toward enhanced adipocyte commitment. This early programming mechanism may expand the adipocyte precursor pool, potentially predisposing the progeny to higher adiposity and metabolic disorders later in life.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70178"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Chitinase 3-like-1 in Myelofibrosis via Fibroblast-Produced Extracellular Matrix Enhancement.","authors":"Shoichiro Kato, Toshikuni Kawamura, Takaaki Maekawa, Hiraku Ogata, Noriaki Tachi, Yukiko Osawa, Shinichi Kobayashi","doi":"10.1002/jcp.70166","DOIUrl":"10.1002/jcp.70166","url":null,"abstract":"<p><p>Cluster of differentiation 14⁺ monocytes produced spindle-shaped fibrocytes, similar to fibroblasts. Recent studies have reported that fibrocytes are crucial for the development and progression of primary myelofibrosis (MF); however, their functional role remains unclear. We compared monocytes and fibrocytes using RNA sequencing for gene expression profiles. We focused on chitinase 3-like-1 (CHI3L1), which causes inflammation, organ fibrosis, and extracellular tissue remodeling. We found higher CHI3L1 levels in patients with myeloproliferative neoplasm with MF than in those without MF. Further, serum CHI3L1 levels were significantly associated with the presence of MF and splenomegaly in patients with lymphoid tumors. Romiplostim-induced MF in a mouse model demonstrated extensive bone marrow (BM) CHI3L1 mRNA expression, which was reversed by clodronate treatment. Two MF induction experiments on CHI3L1^-/- mice, based on romiplostim or Janus kinase 2 mutations, revealed fewer reticular fibers in silver-stained BM slices than in wild-type mice. A culture assay revealed that high CHI3L1 concentrations promoted extracellular matrix production by fibroblast cell lines, and that a CHI3L1-neutralizing antibody abrogated this effect. These results indicate the importance of CHI3L1 in the association between fibrocytes and fibroblasts in MF and could be a focus for future treatment.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70166"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13051415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: MicroRNA-6869-5p Acts as a Tumor Suppressor via Targeting TLR4/NF-κB Signaling Pathway in Colorectal Cancer.","authors":"","doi":"10.1002/jcp.70169","DOIUrl":"https://doi.org/10.1002/jcp.70169","url":null,"abstract":"<p><p>RETRACTION: \"MicroRNA-6869-5p Acts as a Tumor Suppressor via Targeting TLR4/NF-κB Signaling Pathway in Colorectal Cancer,\" by S. Yan, G. Liu, C. Jin, Z. Wang, Q. Duan, J. Xu, and D. Xu, Journal of Cellular Physiology 233, no. 9 (2018): 6660-6668, https://doi.org/10.1002/jcp.26316. The above article, published online on December 5, 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Specifically, Figure 5A presents panels previously published by the author group in a different scientific context. Furthermore, scientific inconsistencies have been identified related to the patient data. The authors did not respond to our request for comments. Accordingly, the article has been retracted as the editors have lost confidence in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors were informed of the retraction decision but were unavailable for final confirmation.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70169"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Ang II-AT1R Increases Cell Migration Through PI3K/AKT and NF-κB Pathways in Breast Cancer.","authors":"","doi":"10.1002/jcp.70162","DOIUrl":"https://doi.org/10.1002/jcp.70162","url":null,"abstract":"<p><strong>Retraction: </strong>Y. Zhao, H. Wang, X. Li, M. Cao, H. Lu, Q. Meng, H. Pang, H. Li, C. Nadolny, X. Dong, and L. Cai, \"Ang II-AT1R Increases Cell Migration Through PI3K/AKT and NF-κB Pathways in Breast Cancer,\" Journal of Cellular Physiology 229, no. 11 (2014): 1855-1862, https://doi.org/10.1002/jcp.24639. The above article, published online on 01 April 2014 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties. Image duplications have been identified within Figure 1a and across Figures 1a, 1b, 2 f, 3a, 3c, 3 d, 4a, and 4e. The scope of the corrections proposed by the authors extended beyond the panels implicated in the identified issues, thereby further undermining the editors' confidence in the accuracy and integrity of the whole body of work presented in the article. Accordingly, the article has been retracted, as the editors consider the conclusions to be invalid.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70162"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147673665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"PIEZO1 Channels Modulate the Small Extracellular Vesicle Release in C2C12 Cells\".","authors":"","doi":"10.1002/jcp.70167","DOIUrl":"https://doi.org/10.1002/jcp.70167","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70167"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clock Modulation by Naringenin Suppresses Lipogenesis and Promotes Adipose Tissue Browning.","authors":"Xuekai Xiong, Jemima Pangemanan, Tali Kiperman, Zuoming Sun, Antoni Paul, Vijay Yechoor, Ke Ma","doi":"10.1002/jcp.70175","DOIUrl":"10.1002/jcp.70175","url":null,"abstract":"<p><p>The circadian clock orchestrates adipocyte development and lipid remodeling, with its disruption leading to the development of obesity and insulin resistance. Here we demonstrate that the flavonoid compound naringenin displays clock modulatory activity that suppresses adipocyte lipid storage while promoting browning. In adipogenic progenitors, naringenin activates RORα with induction of clock gene expression to promote circadian clock oscillation with protective effect against cytokine-induced dampening. The clock-enhancing properties of naringenin suppressed lipogenesis in mature adipocytes together with induction of browning characteristics. The inhibitory effect of naringenin on lipogenesis was dependent on clock modulation as it was abolished in RORα-deficient adipocytes. We further show that naringenin administration in vivo up-regulated RORα expression with clock gene induction together with browning of subcutaneous beige fat depot, resulting reduced fat mass and body weight. Naringenin treatment in vivo also lowered plasma glucose and free fatty acid levels, with markedly enhanced insulin signaling in adipose depots and skeletal muscle. Collectively, our findings uncover a new clock-activating mechanism of action in mediating the metabolic benefits of naringenin, suggesting its potential as a natural supplement for anti-obesity and metabolic disease interventions.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70175"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tooth Decay Promotes Senescence in Dental Pulp Stem Cells, Modifying Their Biological and Proteomic Profiles.","authors":"Sebahat Melike Durukan, Mustafa Burak Acar, Banu Çiçek Tez, Ahmet Şimşek, Sura Hilal Ahmed Al-Sammarrie, Zeynep Günaydın, Melis Güzel, Başak Bilge Süer, Şerife Ayaz Güner, Hüseyin Güner, Nicola Alessio, Kemal Erdem Başaran, Zeynep Burçin Gönen, Servet Özcan","doi":"10.1002/jcp.70172","DOIUrl":"10.1002/jcp.70172","url":null,"abstract":"<p><p>Dental caries is a prevalent oral health problem that significantly reduces an individual's quality of life; although, it can be effectively managed through restorative treatments. Even in cases where the caries does not reach the pulp, released microbial products from the lesion can still penetrate the pulp chamber, potentially inducing stress on pulp cells. In this study, we conducted a comparative analysis of the biological and proteomic profiles of dental pulp stem cells (DPSCs) isolated from clinically asymptomatic teeth with dentinal caries that had not reached the pulp and isolated from healthy teeth. Following biological evaluations, we examined proteomes of these DPSCs by conducting a shotgun proteomics approach. Our findings show that DPSCs from decayed teeth exhibit a significantly higher proportion of senescent cells. Proteomic profiling revealed upregulation of inflammatory signaling, extracellular matrix remodeling, and senescence-associated secretory phenotype (SASP) related proteins. Additionally, we observed an upregulation in the expression of proteins associated with extracellular matrix (ECM) remodeling and components of the SASP, which are hallmarks of the senescence process. The study reveals that DPSCs can be affected by stress from carious lesions, even when the pulp appears clinically intact. Senescence and inflammatory response in these affected cells may have deleterious effects on other tissues within the organism. Consequently, restorative treatments should consider targeting not only the decayed tissue but also the senescent cells within the pulp that may have been affected by the stress induced by caries.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70172"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innate Immune Receptor NLRX1: Potential Modulator of Glioblastoma Pathophysiology","authors":"Durgesh Meena,&nbsp;Divya Shivakumar,&nbsp;Sushmita Rajkhowa,&nbsp;Priya Solanki,&nbsp;Shalini Chhipa,&nbsp;Neermita Bhattacharya,&nbsp;M S Revanth,&nbsp;Deepak Kumar,&nbsp;Vikas Janu,&nbsp;Mayank Garg,&nbsp;Jaskaran Singh Gosal,&nbsp;Sushmita Jha","doi":"10.1002/jcp.70163","DOIUrl":"10.1002/jcp.70163","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Gliomas</i> are primary brain tumors that develop from glial cells within the central nervous system and are among the deadliest human cancers. Glioblastoma (GBM) is the most malignant form of glioma. NLRX1 is an innate immune pattern recognition receptor that exhibits tumor-suppressive or tumor-promoting effects that may be cancer type- and context-dependent, aided by differences in the microenvironment. Here, we report that NLRX1 is differentially expressed in microglia, astrocytes, GBM cell lines, and glioma patient tissues. siRNA-mediated silencing of <i>NLRX1</i> induces metabolic stress in GBM cells, as observed by an increased number of tunneling nanotubes (TNTs) formation between GBM cells and decreased expression of autophagy markers. Moreover, silencing of <i>NLRX1</i> decreases the ability of the GBM cell lines, LN-229 and LN-18, to proliferate and migrate. si-NLRX1 GBM cells exhibit attenuated ability to generate 3D spheroids. In summary, our findings indicate that NLRX1 positively regulates GBM pathophysiology by supporting GBM cell metabolism, proliferation, migration, and anchorage-independent growth. We believe our understanding of NLRX1 in GBM pathophysiology paves the way for potential development of GBM-targeting therapeutics that may delay disease progression and/or improve survival.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Laminin-Derived Peptide C16 Interacts With β1 Integrin, and Is Internalized by Vesicles Through Endocytic Pathway","authors":"Maria Raquel Unterkircher Galheigo,&nbsp;Raquel Sarmento Mateus,&nbsp;Mario Costa Cruz,&nbsp;Olga Aldana Nora,&nbsp;Basilio Smuczek,&nbsp;Nicolas Jones Villarinho,&nbsp;Julia Moura Bernardi,&nbsp;Maria Aparecida Juliano,&nbsp;Joao Jesus Viana Pinheiro,&nbsp;Vanessa Morais Freitas,&nbsp;Ruy Gastaldoni Jaeger","doi":"10.1002/jcp.70157","DOIUrl":"10.1002/jcp.70157","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer is one of the leading causes of mortality worldwide. The tumor microenvironment plays a critical role in cancer progression. This microenvironment is composed of various cells embedded in the extracellular matrix (ECM). Laminin-111, a major ECM glycoprotein, produces bioactive peptides that influence tumor biology. We have shown that the laminin-derived peptide C16 (KAFDITYVRLKF), located in the short arm of the γ1 chain, regulates migration, invasion, and invadopodia formation in different cancer cells. Our findings suggest that the regulatory mechanisms underlying the effects of C16 are associated with β1 integrin. This prompted us to investigate the interaction between the C16 peptide and β1 integrin in breast cancer cells. We found that breast cancer cells bind to C16 peptide, and this attachment is inhibited by β1 integrin depletion via siRNA. Cellular localization of the C16 peptide was analyzed using transmission electron microscopy (TEM) and time-lapse fluorescence microscopy. TEM revealed that nanogold-conjugated C16 decorated the cell membrane and was localized in intracellular vesicles, indicating peptide endocytosis. Time-lapse confocal microscopy showed that C16 was internalized by breast cancer cells within 2 h of incubation, with this process increasing over time. Based on these observations, we hypothesized that the peptide is endocytosed and directed to the endosome-lysosome pathway for degradation. Time-lapse imaging demonstrated that part of the internalized peptide colocalized with lysosomes in breast cancer cells. This suggests that C16 may be involved in integrin recycling. Furthermore, rhodamine-labeled C16 colocalized with activated β1 integrins. Flow cytometry analysis showed that C16 increased β1 integrin activation starting at 1 h of treatment. In summary, our results suggest that after interacting with the cell membrane and activating β1 integrins, breast cancer cells internalize peptide C16, which plays a role in β1 integrin turnover.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Long Noncoding Ribonucleic Acid NKILA Induces the Endoplasmic Reticulum Stress/Autophagy Pathway and Inhibits the Nuclear Factor-k-Gene Binding Pathway in Rats After Intracerebral Hemorrhage","authors":"","doi":"10.1002/jcp.70139","DOIUrl":"10.1002/jcp.70139","url":null,"abstract":"<p><b>RETRACTION:</b> J. Jia, M. Zhang, Q. Li, Q. Zhou, and Y. Jiang, “Long Noncoding Ribonucleic Acid NKILA Induces the Endoplasmic Reticulum Stress/Autophagy Pathway and Inhibits the Nuclear Factor-k-Gene Binding Pathway in Rats After Intracerebral Hemorrhage” <i>Journal of Cellular Physiology</i> 233, no. 1 (2018): 8839-8849. https://doi.org/10.1002/jcp.26798.</p><p>The above article, published online on 12 June 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. A third party reported that all images in Figure 11 were duplicated within the same figure and that all images in Figure 3 were duplicated from other articles by different authors [Yu et al. 2016 (https://doi.org/10.18632/oncotarget.7492) and Cheng et al. 2018 (https://doi.org/10.1002/cam4.1276)]. An investigation by the publisher confirmed these duplications and also found that the beta-actin band in Figure 5B had been duplicated in a later article by different authors [Liu et al. 2019 (https://doi.org/10.1080/15384101.2020.1717041)].</p><p>The authors did not respond to an inquiry by the publisher. The retraction has been agreed to because the evidence of multiple image duplications both within the article and with other articles by different authors fundamentally compromises the editors' confidence in the results presented in this article.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 3","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}