Journal of Cellular Physiology最新文献

{"title":"Unraveling pH Regulation of TMEM175, an Endolysosomal Cation Channel With a Role in Parkinson's Disease","authors":"Tobias Schulze,&nbsp;Oliver Rauh,&nbsp;Gerhard Thiel,&nbsp;Niels Fertig,&nbsp;Andre Bazzone,&nbsp;Christian Grimm","doi":"10.1002/jcp.70008","DOIUrl":"https://doi.org/10.1002/jcp.70008","url":null,"abstract":"<p>Transmembrane protein 175 (TMEM175) is an endolysosomal cation channel, which has attracted much attention recently from academics and the pharmaceutical industry alike since human mutations in TMEM175 were found to be associated with the development of Parkinson's disease (PD). Thus, gain-of-function mutations were identified, which reduce and loss-of-function mutations, which increase the risk of developing PD. After having been characterized as an endolysosomal potassium channel initially, soon after TMEM175 was claimed to act as a proton channel. In fact, recent evidence suggests that depending on the conditions, TMEM175 can act as either a potassium or proton channel, without acting as an antiporter or exchanger. A recent work has now identified amino acid H57 to be directly involved in gating, increasing proton conductance of the channel while leaving the potassium conductance unaffected. We review here the current knowledge of TMEM175 function, pharmacology, physiology, and pathophysiology. We discuss the potential of this ion channel as a novel drug target for the treatment of neurodegenerative diseases such as PD, and we discuss the discovery of H57 as proton sensor.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111716","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: Promotion of Cell Autophagy and Apoptosis in Cervical Cancer by Inhibition of Long Noncoding RNA LINC00511 via Transcription Factor RXRA-regulated PLD1","authors":"","doi":"10.1002/jcp.31527","DOIUrl":"10.1002/jcp.31527","url":null,"abstract":"<p><b>RETRACTION:</b> Y. Shi, M. Liu, Y. Huang, J. Zhang, and L. Yin, “Promotion of Cell Autophagy and Apoptosis in Cervical Cancer by Inhibition of Long Noncoding RNA LINC00511 via Transcription Factor RXRA-regulated PLD1,” <i>Journal of Cellular Physiology</i> 235, no. 10 (2020): 6592-6604. https://doi.org/10.1002/jcp.29529.</p><p>The above article, published online on 17 February 2020 in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. A third party reported that images shared overlapping sections in Figure 5D in this article, and this duplication was confirmed by the publisher. The third party also reported that the tumor measurement ruler used in Figure 5 A is identical to the ruler used in the figures of previously published articles from different authors, each of which describes a different scientific context (Chen, et al. 2019 [https://doi.org/10.1002/jcp.28911]) and (Feng, et al. 2019 [https://doi.org/10.1186/s13287-022-02841-z]). The use of the identical ruler in the figures of different articles from unrelated research groups at different institutions puts in doubt the veracity of the data reported. The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication within this article, as well as unexplained duplication of image elements and equipment with other experiments by different authors, fundamentally compromises the conclusions reported in this article. The authors did not respond to our notice regarding the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31527","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065872","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: Role of Mirnas in Lung Cancer","authors":"","doi":"10.1002/jcp.31519","DOIUrl":"10.1002/jcp.31519","url":null,"abstract":"<p><b>RETRACTION</b>: A. Uddin and S. Chakraborty, “Role of miRNAs in Lung Cancer,” <i>Journal of Cellular Physiology</i> (Early View), https://doi.org/10.1002/jcp.26607.</p><p>The above article, published online on 20 April 2018 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 upon following an investigation into concerns raised by a third party, which revealed major textual overlap between this article and two previously published articles by different groups of authors elsewhere (Guz et al. 2014; Hubaux 2012).</p><p>The authors noted the major textual overlap and revised their manuscript during the proofing stage, yet the wrong version of the manuscript was published in Early View by mistake. The editors and the publisher apologize for this oversight. During the investigation, the authors were able to provide their revised article, however, also the revised version shows high textual and conceptual similarity to the two previously published review articles (Guz et al. 2014; Hubaux 2012). The authors disagree with the retraction.</p><p><b>References</b></p><p>Guz, M., A. Rivero-Müller, E. Okoń, et al. 2014. “Micrornas-Role in Lung Cancer.” Disease Markers 2014, no. 1: 1–13. https://doi.org/10.1155/2014/218169.</p><p>Hubaux, R. 2012. “Micrornas as Biomarkers for Clinical Features of Lung Cancer.” Journal of Postgenomics: Drug &amp; Biomarker Development 2, no. 3: 1000108. https://doi.org/10.4172/2153-0769.1000108.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065959","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":"Carboxyl Terminal Modulator Protein Induces Cell Senescence and Is Upregulated With Aging by Zic2 in Rats","authors":"Weiran Shan,&nbsp;Jun Li,&nbsp;Zachary Philpot,&nbsp;Zhiyi Zuo","doi":"10.1002/jcp.70007","DOIUrl":"10.1002/jcp.70007","url":null,"abstract":"<p>Carboxyl terminal modulator protein (CTMP) may be involved in various physiological and pathological processes, such as inflammation, tumor growth, and cardiac hypertrophy. Our recent study has shown that CTMP is increased with aging and plays a role in determining brain ischemic tolerance. However, it is not known how CTMP expression with aging is regulated and whether the changed CTMP expression has an effect on cell senescence. Here, cells that stably overexpressed CTMP were generated and cell senescence biomarkers were determined. The brains of Fischer 344 male rats were harvested for Western blot analysis and immunostaining to detect CTMP and the Zinc finger protein Zic2. The regulations of CTMP expression by Zic2 were examined by promoter activity assays. Increasing CTMP enhanced cells expressing senescence-associated β-galactosidase staining but without expression of Ki67, decreased cell proliferation and colony formation, and increased cells with condensed DNA of more than one pair of homologous chromosomes caused by senescence. Zic2 was decreased with aging in rats. Zic2 and CTMP were mainly expressed in the neurons in rats. Similarly, CTMP protein was expressed in the neurons of human brain. An anti-Zic2 antibody immunoprecipitated DNA fragments of <i>ctmp</i> gene. Zic2 inhibited the activity of presumptive <i>ctmp</i> promoter. Overexpressing Zic2 decreased CTMP in cells. These results suggest that CTMP induces cell senescence and that Zic2 is a suppressor of CTMP expression. The decrease of Zic2 contributes to CTMP increase with aging.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065870","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":"Rho GTPase Signaling: A Molecular Switchboard for Regulating the Actin Cytoskeleton in Axon Guidance","authors":"Madhavi Gorla,&nbsp;Digvijay Singh Guleria","doi":"10.1002/jcp.70005","DOIUrl":"10.1002/jcp.70005","url":null,"abstract":"<div>\u0000 \u0000 <p>Axon pathfinding is a highly dynamic process regulated by the interactions between cell-surface guidance receptors and guidance cues present in the extracellular environment. During development, precise axon pathfinding is crucial for the formation of functional neural circuits. The spatiotemporal expression of axon guidance receptors helps the navigating axon make correct decisions in a complex environment comprising both attractive and repulsive guidance cues. Axon guidance receptors initiate distinct signaling cascades that eventually influence the cytoskeleton at the growing tip of an axon, called the growth cone. The actin cytoskeleton is the primary target of these guidance signals and plays a key role in growth cone motility, exploration, and behavior. Of the many regulatory molecules that modulate the actin cytoskeleton in response to distinct guidance signals, Rho GTPases play central roles. Rho GTPases are molecular switchboards; their ON (GTP-bound) and OFF (GDP-bound) switches are controlled by their interactions with proteins that regulate the exchange of GDP for GTP or with the proteins that promote GTP hydrolysis. Various upstream signals, including axon guidance signals, regulate the activity of these Rho GTPase switch regulators. As cycling molecular switches, Rho GTPases interact with and control the activities of downstream effectors, which directly influence actin reorganization in a context-dependent manner. A deeper exploration of the spatiotemporal dynamics of Rho GTPase signaling and the molecular basis of their involvement in regulating growth cone actin cytoskeleton can unlock promising therapeutic strategies for neurodevelopmental disorders linked to dysregulated Rho GTPase signaling. This review not only provides a comprehensive overview of the field but also highlights recent discoveries that have considerably advanced our understanding of the complex regulatory roles of Rho GTPases in modulating actin cytoskeleton arrangement at the growth cone during axon guidance.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065960","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":"Corrigendum to “Defining Early Hematopoietic-Fated Primitive Streak Specification of Human Pluripotent Stem Cells by the Orchestrated Balance of Wnt, Activin, and BMP Signaling”","authors":"","doi":"10.1002/jcp.70003","DOIUrl":"10.1002/jcp.70003","url":null,"abstract":"<p><b>This article corrects the following:</b></p><p>Defining Early Hematopoietic-Fated Primitive Streak Specification of Human Pluripotent Stem Cells by the Orchestrated Balance of Wnt, Activin, and BMP Signaling</p><p>Jun Shen, Cuicui Lyu, Yaoyao Zhu, Zicen Feng, Shuo Zhang, Dixie L. Hoyle, Guangzhen Ji, Robert A. Brodsky, Tao Cheng, Zack Z. Wang.</p><p>Journal of Cell Physiology</p><p>https://doi.org/10.1002/jcp.28272</p><p>First published: 10 February 2019</p><p><b>Correction text:</b></p><p>The authors made two inadvertent mistakes in the original figures, as follows:</p><p>1. The flow cytometry image in the left panel of the original Figure 2e was inadvertently duplicated from the far-right panel of the original Figure 3d.</p><p>2. In the original Figure 1d, a duplication of flow figures, for +BMP4 (B) and +BC, occurred. The +BMP4 (B) panel of Figure 1d was incorrectly selected.</p><p>The corrected Figure 1 and Figure 2 are as follows:</p><p>This correction does not alter the interpretation of the data or the conclusions presented in the paper. The figure legends remain unchanged.</p><p>The authors sincerely apologize for any confusion this error may have caused.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046850","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":"Corrigendum to “Immortalized Hertwig's Epithelial Root Sheath Cell Line Works as a Model for Epithelial-Mesenchymal Interaction During Tooth Root Formation”","authors":"","doi":"10.1002/jcp.70002","DOIUrl":"10.1002/jcp.70002","url":null,"abstract":"<p><b>This article corrects the following:</b></p><p>Immortalized Hertwig's epithelial root sheath cell line works as a model for epithelial-mesenchymal interaction during tooth root formation</p><p>Sicheng Zhang, Xuebing Li, Shikai Wang, Yan Yang, Weihua Guo, Guoqing Chen, Weidong Tian</p><p><b>Journal of Cellular Physiology</b></p><p>https://doi.org/10.1002/jcp.29174</p><p>First Published Online: 12 September 2019</p><p><b>Correction text:</b></p><p>During manuscript preparation the authors inadvertently presented a duplicated version of the H&amp;E staining image for the DPC group in Figure 6a as the anti-DMP1 staining group image. The corrected Figure 1 is presented below:</p><p>The authors apologize for this oversight and any confusion that may have arisen as a result.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046859","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":"Single-Cell Transcriptomic Analysis Reveals Biomechanical Loading-Induced Imbalance in Bone and Fat, Leading to Ossification in Lumbar Intervertebral Disc Nucleus Pulposus Degeneration","authors":"Ping Zhang,&nbsp;Yuan Wang,&nbsp;Jianqi Bai,&nbsp;Jingru Zhang,&nbsp;Shimin Zhang,&nbsp;Xiaofei Guo,&nbsp;Jiawen Zhan,&nbsp;Liguo Zhu","doi":"10.1002/jcp.31506","DOIUrl":"10.1002/jcp.31506","url":null,"abstract":"<div>\u0000 \u0000 <p>In this study, we explored the impact of different biomechanical loadings on lumbar spine motion segments, particularly concerning intervertebral disc degeneration (IVDD). We aimed to uncover the cellular milieu and mechanisms driving ossification in the nucleus pulposus (NP) during IVDD, a process whose underlying mechanisms have remained elusive. The study involved the examination of fresh NP tissue from the L3-S1 segment of five individuals, either with IVDD or healthy. The analysis consisted of histopathological evaluation and single-cell RNA sequencing. To further validate the impact of biomechanical loading on IVDD, particularly on the CITED4 + METRN + NP chondrocytes and the bone-fat balance mechanism, a retrospective analysis was conducted using paraffin-embedded NP samples from patients. A distinct subset of CITED4 + METRN+ chondrocytes in the degenerated NP that were influenced by biomechanical loading was identified. These cells were evaluated for their potential as diagnostic biomarkers. Pseudotemporal analysis indicated that inflammation and repair processes were integral to NP ossification. Notably, the L4/5 and L5/S1 segments with severe IVDD showed pronounced ossification and heightened lipogenic metabolism. Cell communication analysis sheds light on the roles of bone-fat balance proteins and various ossification genes. Additionally, immunohistochemistry and immunofluorescence confirmed that biomechanical loading intensified IVDD by fostering osteogenic differentiation, mediated by macrophage migration inhibitory factor (MIF)-regulated bone-fat balance. This research reveals the microenvironmental factors of IVDD NP ossification under biomechanical loading, highlighting the role of bone-fat imbalance. These insights significantly enhance the understanding of IVDD pathogenesis and pave the way for innovative therapeutic approaches.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033306","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":"CD44/Integrin β1 Association Drives Fast Motility on Hyaluronic Acid Substrates","authors":"Tanusri Roy,&nbsp;Sarbajeet Dutta,&nbsp;Swetlana Ghosh,&nbsp;Lakshmi Kavitha Sthanam,&nbsp;Shamik Sen","doi":"10.1002/jcp.70001","DOIUrl":"10.1002/jcp.70001","url":null,"abstract":"<div>\u0000 \u0000 <p>In addition to proteins such as collagen (Col) and fibronectin, the extracellular matrix (ECM) is enriched with bulky proteoglycan molecules such as hyaluronic acid (HA). However, how ECM proteins and proteoglycans collectively regulate cellular processes has not been adequately explored. Here, we address this question by studying cytoskeletal and focal adhesion organization and dynamics on cells cultured on polyacrylamide hydrogels functionalized with Col, HA and a combination of Col and HA (Col/HA). We show that fastest migration on HA substrates is attributed to the presence of smaller and weaker focal adhesions. Integrin <span></span><math>\u0000 <semantics>\u0000 <mrow>\u0000 \u0000 <mrow>\u0000 <mi>β</mi>\u0000 </mrow>\u0000 </mrow>\u0000 <annotation> $beta $</annotation>\u0000 </semantics></math>1 co-localization and its association with CD44—which is the receptor for HA, and insensitivity of cell spreading to RGD on HA substrates suggests that focal adhesions on HA substrates are formed via integrin association with HA bound CD44. Consistent with this, adhesion formation and cell motility were inhibited when CD44 was knocked out. Collectively, our results suggest that association of integrin <span></span><math>\u0000 <semantics>\u0000 <mrow>\u0000 \u0000 <mrow>\u0000 <mi>β</mi>\u0000 </mrow>\u0000 </mrow>\u0000 <annotation> $beta $</annotation>\u0000 </semantics></math>1 with CD44 drives fast motility on HA substrates.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006141","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":"Reprogramming of Fatty Acid Metabolism in Acute Leukemia","authors":"Judith Sokei,&nbsp;Joice Kanefsky,&nbsp;Stephen M. Sykes","doi":"10.1002/jcp.70000","DOIUrl":"10.1002/jcp.70000","url":null,"abstract":"<div>\u0000 \u0000 <p>Fatty acids are essential biomolecules that support several cellular processes, such as membrane structures, energy storage and production, as well as signal transduction. Accordingly, changes in fatty acid metabolism can have a significant impact on cell behavior, such as growth, survival, proliferation, differentiation, and motility. Therefore, it is not surprising that many aspects of fatty acid metabolism are frequently dysregulated in human cancer, including in highly aggressive blood cancers such as acute leukemia. The aims of this review are to summarize the aspects of fatty acid metabolism that are specifically coopted in acute leukemia as well as current preclinical strategies for targeting fatty acid metabolism in these cancers.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006142","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}