Journal of Cellular Physiology最新文献_第9页

RETRACTION: Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint 回放：环境对昼夜节律的干扰易使小鼠膝关节发生骨关节炎样改变。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31457

{"title":"RETRACTION: Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint","authors":"","doi":"10.1002/jcp.31457","DOIUrl":"10.1002/jcp.31457","url":null,"abstract":"RETRACTION: R. Kc, X. Li, R. M. Voigt, M. B. Ellman, K. C. Summa, M. H. Vitaterna, A. Keshavarizian, F. W. Turek, Q.-J. Meng, G. S. Stein, A. J. van Wijnen, D. Chen, C. B. Forsyth, and H.-J. Im, “Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint,” Journal of Cellular Physiology 230, no. 9 (2015): 2174-2183, https://doi.org/10.1002/jcp.24946.The above article, published online on 5 February 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.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 occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figure 4 A were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390826","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}

引用次数: 0

Emerging understandings of the role of exosomes in atherosclerosis 对外泌体在动脉粥样硬化中作用的新认识。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-06 DOI: 10.1002/jcp.31454

Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H. Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H. Eid

{"title":"Emerging understandings of the role of exosomes in atherosclerosis","authors":"Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H. Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H. Eid","doi":"10.1002/jcp.31454","DOIUrl":"10.1002/jcp.31454","url":null,"abstract":"Atherosclerosis remains a major contributor to cardiovascular disease, the leading cause of global morbidity and mortality. Despite the elucidation of several molecular, biochemical, and cellular aspects that contribute to the etio-pathogenesis of atherosclerosis, much remains to be understood about the onset and progression of this disease. Emerging evidence supports a role for exosomes in the cellular basis of atherosclerosis. Indeed, exosomes of activated monocytes seem to accentuate a positive feedback loop that promotes recruitment of pro-inflammatory leukocytes. Moreover, in addition to their role in promoting proliferation and invasion of vascular smooth muscle cells, exosomes can also induce neovascularization within lesions and increase endothelial permeability, two important features of fibrous plaques. Depending on their sources and cargo, exosomes can also induce clot formation and contribute to other hallmarks of atherosclerosis. Taken together, it is becoming increasingly evident that a better understanding of exosome biology is integral to elucidating the pathogenesis of atherosclerosis, and may thus provide insight into a potentially new therapeutic target for this disease.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380941","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}

引用次数: 0

Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice 乙硫宁诱导的 S-腺苷蛋氨酸缺乏会抑制小鼠神经管发育过程中的 H3K27me3 和细胞分化。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-06 DOI: 10.1002/jcp.31452

Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang

{"title":"Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice","authors":"Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang","doi":"10.1002/jcp.31452","DOIUrl":"10.1002/jcp.31452","url":null,"abstract":"S-adenosylmethionine (SAM) as a major methyl donor plays a key role in methylation modification in vivo, and its disorder was closely related to neural tube defects (NTDs). However, the exact mechanism between SAM deficiency and NTDs remained unclearly. Hence, we investigated the association between histone methylation modification and cell differentiation in NTDs mice induced by SAM deficiency. The levels of SAM and SAH (S-adenosylhomocysteine) were determined by enzyme linked immunosorbent assay (ELISA). The level of histone methylation, β-catenin were analyzed by Western blot, reversing transcription and quantitative PCR (RT-qPCR) and immunofluorescence. The results showed that the incidence rate of NTDs induced by ethionine were 46.2%. Post treatment of ethionine combined with SAM, the incidence rate of NTDs was reduced to 26.2%. The level of SAM was significantly decreased (p < 0.05) and a reduction in the SAM/SAH ratio was observed after entionine treatment. The SAM deficiency caused the reduction of H3K27me3 modifications and the elevated UTX activity (p < 0.05), and inhibited the expressions of β-catenin. The differentiations of NSCs into neurons and oligodendrocytes were inhibited under SAM deficiency (p < 0.05). These results indicated that the SAM deficiency led to reduce H3K27me3 modifications, prevented the β-catenin signaling pathway and NSCs differentiation, which provided an understanding of the novel function of epigenetic regulation in NTDs.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380942","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}

引用次数: 0

RETRACTION: Circular RNA Circ_0001946 Acts As a Competing Endogenous RNA to Inhibit Glioblastoma Progression by Modulating miR-671-5p and CDR1 返回：环状 RNA Circ_0001946 通过调节 miR-671-5p 和 CDR1 作为竞争性内源性 RNA 抑制胶质母细胞瘤的进展。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-02 DOI: 10.1002/jcp.31408

引用次数: 0

Feedback modulation of Orai1α and Orai1β protein content mediated by STIM proteins 由 STIM 蛋白介导的对 Orai1α 和 Orai1β 蛋白含量的反馈调节。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-02 DOI: 10.1002/jcp.31450

Joel Nieto-Felipe, Alvaro Macias-Díaz, Vanesa Jimenez-Velarde, Jose J. Lopez, Gines M. Salido, Tarik Smani, Isaac Jardin, Juan A. Rosado

{"title":"Feedback modulation of Orai1α and Orai1β protein content mediated by STIM proteins","authors":"Joel Nieto-Felipe, Alvaro Macias-Díaz, Vanesa Jimenez-Velarde, Jose J. Lopez, Gines M. Salido, Tarik Smani, Isaac Jardin, Juan A. Rosado","doi":"10.1002/jcp.31450","DOIUrl":"10.1002/jcp.31450","url":null,"abstract":"Store-operated Ca2+ entry is a mechanism controlled by the filling state of the intracellular Ca2+ stores, predominantly the endoplasmic reticulum (ER), where ER-resident proteins STIM1 and STIM2 orchestrate the activation of Orai channels in the plasma membrane, and Orai1 playing a predominant role. Two forms of Orai1, Orai1α and Orai1β, have been identified, which arises the question whether they are equally regulated by STIM proteins. We demonstrate that STIM1 preferentially activates Orai1α over STIM2, yet both STIM proteins similarly activate Orai1β. Under resting conditions, there is a pronounced association between STIM2 and Orai1α. STIM1 and STIM2 are also shown to influence the protein levels of the Orai1 variants, independently of Ca2+ influx, via lysosomal degradation. Interestingly, Orai1α and Orai1β appear to selectively regulate the protein level of STIM1, but not STIM2. These observations offer crucial insights into the regulatory dynamics between STIM proteins and Orai1 variants, enhancing our understanding of the intricate processes that fine-tune intracellular Ca2+ signaling.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365368","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}

引用次数: 0

Pressure loading regulates the stemness of liver cancer stem cells via YAP/BMF signaling axis 压力负荷通过YAP/BMF信号轴调节肝癌干细胞的干性。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-02 DOI: 10.1002/jcp.31451

Di Ma, Rui Liang, Qing Luo, Guanbin Song

{"title":"Pressure loading regulates the stemness of liver cancer stem cells via YAP/BMF signaling axis","authors":"Di Ma, Rui Liang, Qing Luo, Guanbin Song","doi":"10.1002/jcp.31451","DOIUrl":"10.1002/jcp.31451","url":null,"abstract":"Cancer stem cells (CSCs) are considered the major cause of the occurrence, progression, chemoresistance/radioresistance, recurrence, and metastasis of cancer. Increased interstitial fluid pressure (IFP) is a key feature of solid tumors. Our previous study showed that the distribution of liver cancer stem cells (LCSCs) correlated with the mechanical heterogeneity within liver cancer tissues. However, the regulation of liver cancer's mechanical microenvironment on the LCSC stemness is not fully understood. Here, we employed a cellular pressure-loading device to investigate the effects of normal IFP (5 mmHg), as well as increased IFP (40 and 200 mmHg) on the stemness of LCSCs. Compared to the control LCSCs (exposure to 5 mmHg pressure loading), the LCSCs exposed to 40 mmHg pressure loading exhibited significantly upregulated expression of CSC markers (CD44, EpCAM, Nanog), enhanced sphere and colony formation capacities, and tumorigenic potential, whereas continuously increased pressure to 200 mmHg suppressed the LCSC characteristics. Mechanistically, pressure loading regulated Yes-associated protein (YAP) activity and Bcl-2 modifying factor (BMF) expression. YAP transcriptionally regulated BMF expression to affect the stemness of LCSCs. Knockdown of YAP and overexpression of BMF attenuated pressure-mediated stemness and tumorgenicity, while YAP-deficient and BMF-deletion recused pressure-dependent stemness on LCSCs, suggesting the involvement of YAP/BMF signaling axis in this process. Together, our findings provide a potential target for overcoming the stemness of CSCs and elucidate the significance of increased IFP in cancer progression.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365369","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}

引用次数: 0

An in vitro cell model for exploring inflammatory and amyloidogenic events in alkaptonuria 探索碱蛋白尿中炎症和淀粉样蛋白生成事件的体外细胞模型。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-01 DOI: 10.1002/jcp.31449

Pierfrancesco Mastroeni, Michela Geminiani, Tommaso Olmastroni, Luisa Frusciante, Alfonso Trezza, Anna Visibelli, Annalisa Santucci

{"title":"An in vitro cell model for exploring inflammatory and amyloidogenic events in alkaptonuria","authors":"Pierfrancesco Mastroeni, Michela Geminiani, Tommaso Olmastroni, Luisa Frusciante, Alfonso Trezza, Anna Visibelli, Annalisa Santucci","doi":"10.1002/jcp.31449","DOIUrl":"10.1002/jcp.31449","url":null,"abstract":"Alkaptonuria (AKU) is a progressive systemic inherited metabolic disorder primarily affecting the osteoarticular system, characterized by the degeneration of cartilage induced by ochronosis, ultimately leading to early osteoarthritis (OA). However, investigating AKU pathology in human chondrocytes, which is crucial for understanding the disease, encounters challenges due to limited availability and donor variability. To overcome this obstacle, an in vitro model has been established using homogentisic acid (HGA) to simulate AKU conditions. This model employed immortalized C20/A4 human chondrocytes and serves as a dependable platform for studying AKU pathogenesis. Significantly, the model demonstrates the accumulation of ochronotic pigment in HGA-treated cells, consistent with findings from previous studies. Furthermore, investigations into inflammatory processes during HGA exposure revealed notable oxidative stress, as indicated by elevated levels of reactive oxygen species and lipid peroxidation. Additionally, the model demonstrated HGA-induced inflammatory responses, evidenced by increased production of nitric oxide, overexpression of inducible nitric oxide synthase, and cyclooxygenase-2. These findings underscore the model's utility in studying inflammation associated with AKU. Moreover, analysis of serum amyloid A and serum amyloid P proteins revealed a potential interaction, corroborating evidence of amyloid fibril formation. This hypothesis was further supported by Congo red staining, which showed fibril formation exclusively in HGA-treated cells. Overall, the C20/A4 cell model provided valuable insights into AKU pathogenesis, emphasizing its potential for facilitating drug development and therapeutic interventions.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347414","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}

引用次数: 0

Research advances in protein lysine 2-hydroxyisobutyrylation: From mechanistic regulation to disease relevance 蛋白质赖氨酸 2-羟基异丁酰化的研究进展：从机理调控到疾病相关性。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-01 DOI: 10.1002/jcp.31435

Jinglei Huang, Hui Peng, Diqi Yang

引用次数: 0

RETRACTION: LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p 返回：LINC00339 通过抑制 miR-377-3p 提高 DCP1A 的表达，从而促进胃癌的进展。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-09-30 DOI: 10.1002/jcp.31375

{"title":"RETRACTION: LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p","authors":"","doi":"10.1002/jcp.31375","DOIUrl":"10.1002/jcp.31375","url":null,"abstract":"RETRACTION: C. Shi, T. Liu, J. Chi, H. Luo, Z. Wu, B. Xiong, S. Liu, Y. Zeng, “LINC00339 promotes gastric cancer progression by elevating DCP1A expression via inhibiting miR-377-3p,” Journal of Cellular Physiology 234, no. 12 (2019): 23667-23674, https://doi.org/10.1002/jcp.28934.The above article, published online on 12 June 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC.The retraction has been agreed upon the authors' request due to concerns related to the data presented in the article. In the following investigation performed by the journal, several inconsistencies between results presented and experimental methods described were found. Specifically, the experimental methods were found to lack or have unavailable supporting data, making the experiments not comprehensible to readers. Additionally, the raw data provided do not entirely support the results presented. Accordingly, the conclusions of this article are considered invalid by the editors.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 11","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31375","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142347425","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}

引用次数: 0

Correction: MitoNEET prevents iron overload-induced insulin resistance in H9c2 cells through regulation of mitochondrial iron 更正：MitoNEET通过调节线粒体铁防止铁超载诱导的H9c2细胞胰岛素抵抗。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-09-30 DOI: 10.1002/jcp.31456

引用次数: 0