Journal of Cellular Physiology最新文献_第2页

Glucose Transporter 1 Deficiency Impairs Glucose Metabolism and Barrier Induction in Human Induced Pluripotent Stem Cell-Derived Astrocytes

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-14 DOI: 10.1002/jcp.31523

Iqra Pervaiz, Yash Mehta, Abraham Jacob Al-Ahmad

{"title":"Glucose Transporter 1 Deficiency Impairs Glucose Metabolism and Barrier Induction in Human Induced Pluripotent Stem Cell-Derived Astrocytes","authors":"Iqra Pervaiz, Yash Mehta, Abraham Jacob Al-Ahmad","doi":"10.1002/jcp.31523","DOIUrl":"10.1002/jcp.31523","url":null,"abstract":"<div>\u0000 \u0000 Glucose is a major source of energy for the brain. At the blood–brain barrier (BBB), glucose uptake is facilitated by glucose transporter 1 (GLUT1). GLUT1 Deficiency Syndrome (GLUT1DS), a haploinsufficiency affecting SLC2A1, reduces glucose brain uptake. A lot of effort has been made to characterize GLUT1DS at the BBB, but the impact on astrocytes remains unclear. In this study, we investigated the impact of GLUT1DS on astrocyte differentiation and function in vitro, using human induced pluripotent stem cells GLUT1DS (GLUT1DS-iPSCs) differentiated into astrocyte-like cells (iAstros). GLUT1 expression is decreased during the differentiation of iPSCs into astrocytes, with neural progenitor cells showing the lowest expression. The presence of a truncated GLUT1 did not compromise the differentiation of iPSCs into iAstros, as these cells could express several key markers representative of the astrocyte lineage. GLUT1DS-iAstros failed to express full-length GLUT1 at protein levels while showing no signs of impaired GLUT4 expression. However, GLUT1DS-iAstros showed decreased glucose uptake and lactate production compared to control-iAstros, reduced glycolysis, and mitochondrial activity as well as ATP deficit. In addition to reduced energy production, astrocytes displayed a reduced extracellular glutamate release. As previously observed, one iAstros clone (C7) showed the most severe phenotype from all groups. Our study provides an insightful view of the contribution of GLUT1 in astrocytes' energetic metabolism and raises the possible contribution of these cells in the astrocyte–neuron metabolic coupling. Our future direction is to understand better how GLUT1DS impacts astrocytes and neurons within their metabolic coupling.</div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056029","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: Long Noncoding RNA LINC00958 Regulates Cell Sensitivity to Radiotherapy Through RRM2 by Binding to microRNA-5095 in Cervical Cancer 回归：长非编码 RNA LINC00958 通过与宫颈癌中的 microRNA-5095 结合，通过 RRM2 调节细胞对放疗的敏感性。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-13 DOI: 10.1002/jcp.31525

{"title":"RETRACTION: Long Noncoding RNA LINC00958 Regulates Cell Sensitivity to Radiotherapy Through RRM2 by Binding to microRNA-5095 in Cervical Cancer","authors":"","doi":"10.1002/jcp.31525","DOIUrl":"10.1002/jcp.31525","url":null,"abstract":"RETRACTION: H. Zhao, G.-H. Zheng, G.-C. Li, L. Xin, Y.-S. Wang, Y. Chen, and X.-M. Zheng, “Long Noncoding RNA LINC00958 Regulates Cell Sensitivity to Radiotherapy Through RRM2 by Binding to microRNA-5095 in Cervical Cancer,” Journal of Cellular Physiology 234, no. 12 (2019): 23349-23359. https://doi.org/10.1002/jcp.28902.The above article, published online on 06 June 2019 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 the same tumor image was detected between Figure 6 A in this article and Figure 7B in another article (Guo, et al. 2019 [https://doi.org/10.18632/aging.102271]. The third party reported additional image duplications between Figure 2B in this article and other articles by different authors (Guo, et al. 2018 [https://doi.org/10.1186/s12964-018-0290-6]; (Liu, et al. 2019 [https://doi.org/10.1002/jcp.27893]; (Wen, et al. 2019 [https://doi.org/10.1096/fj.201900310 R]; and (Ou, et al. 2020 [https://doi.org/10.1016/j.ebiom.2020.102694]. Each mentioned article describes a different scientific context. The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication with other articles fundamentally compromises the conclusions reported in this article. The authors did not respond to our notice regarding the retraction.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31525","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970955","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

RETRACTION: MiR-145 Promotes MiR-133b Expression Through c-myc and DNMT3A-mediated Methylation in Ovarian Cancer Cells 回归：MiR-145 通过 c-myc 和 DNMT3A 介导的甲基化促进卵巢癌细胞中 MiR-133b 的表达

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-13 DOI: 10.1002/jcp.31507

引用次数: 0

RETRACTION: Long Noncoding RNA LEF1-AS1 Silencing Suppresses the Initiation and Development of Prostate Cancer by Acting as a Molecular Sponge of miR-330-5p via LEF1 Repression RETRACTION：长非编码 RNA LEF1-AS1 沉默通过 LEF1 抑制作用作为 miR-330-5p 的分子海绵，抑制前列腺癌的发生和发展。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-13 DOI: 10.1002/jcp.31526

{"title":"RETRACTION: Long Noncoding RNA LEF1-AS1 Silencing Suppresses the Initiation and Development of Prostate Cancer by Acting as a Molecular Sponge of miR-330-5p via LEF1 Repression","authors":"","doi":"10.1002/jcp.31526","DOIUrl":"10.1002/jcp.31526","url":null,"abstract":"RETRACTION: D.-C. Liu, L.-L. Song, Q. Liang, L. Hao, Z.-G. Zhang, and C.-H. Han, “Long Noncoding RNA LEF1-AS1 Silencing Suppresses the Initiation and Development of Prostate Cancer by Acting as a Molecular Sponge of miR-330-5p via LEF1 Repression,” Journal of Cellular Physiology 234, no. 8 (2019): 12727-12744. https://doi.org/10.1002/jcp.27893.The above article, published online on 05 January 2019 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 3B in this article, and this duplication was confirmed by the publisher. The third party also reported that duplicated images in this article had been detected in subsequent articles by different authors, each of which describes different experimental conditions (Zhao, et al. 2019 [https://doi.org/10.1002/jcp.28902]); (Ou, et al. 2020 [https://doi.org/10.1016/j.ebiom.2020.102694]; and (Sha, et al. 2021 [https://doi.org/10.18632/aging.203088]). 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 subsequent unexplained duplications with other articles, fundamentally compromises the conclusions reported in this article. The authors responded to our notice regarding the retraction but did not state their agreement nor their disagreement with the retraction.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31526","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970954","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

High Glucose Inhibits O-GlcNAc Transferase Translocation in Early Osteoblast Differentiation by Altering Protein Phosphatase 2A Activity 高糖通过改变蛋白磷酸酶2A活性抑制O-GlcNAc转移酶易位在成骨细胞早期分化中的作用

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-12 DOI: 10.1002/jcp.31524

Heriati Sitosari, Yoko Fukuhara, Yao Weng, Yilin Zheng, Yuhan He, Xinyu Zheng, Mika Ikegame, Hirohiko Okamura

引用次数: 0

Point of No Return—What Is the Threshold of Mitochondria With Permeability Transition in Cells to Trigger Cell Death 不归之点——细胞中通透性转变的线粒体触发细胞死亡的阈值是什么？

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-06 DOI: 10.1002/jcp.31521

Kristina A. Kritskaya, Olga A. Stelmashchuk, Andrey Y. Abramov

{"title":"Point of No Return—What Is the Threshold of Mitochondria With Permeability Transition in Cells to Trigger Cell Death","authors":"Kristina A. Kritskaya, Olga A. Stelmashchuk, Andrey Y. Abramov","doi":"10.1002/jcp.31521","DOIUrl":"10.1002/jcp.31521","url":null,"abstract":"Programmed cell death (apoptosis) is essential part of the process of tissue regeneration that also plays role in the mechanism of pathology. The phenomenon of fast and transient permeability of mitochondrial membranes by various triggers, known as permeability transition pore (mPTP) leads to the release of proapoptotic proteins and acts as an initial step in initiation of apoptosis. However, a role for mPTP was also suggested for physiology and it is unclear if there is a threshold in number of mitochondria with mPTP which induces cell death and how this mechanism is regulated in different tissues. Using simultaneous measurements of mitochondrial membrane potential and a fluorescent marker for caspase-3 activation we studied the number of mitochondria with calcium-induced mPTP opening necessary for induction of apoptosis in rat primary cortical neurons, astrocytes, fibroblasts, and cancer (BT-474) cells. The induction of apoptosis was correlated with 80%–90% mitochondrial signal loss in neural cells but only 35% in fibroblasts, and in BT-474 cancer cells over 90% of mitochondria opens mPTP before apoptosis becomes obvious. The number of mitochondria with mPTP which induce cell death did not correlate with total expression levels of proapoptotic proteins but was consistent with the Bax/Bcl-2 ratio in these cells. Calcium-induced mPTP opening increased levels of necrosis which was higher in fibroblasts compared to neurons, astrocytes and BT-474 cells. Thus, different tissues require specific numbers of mitochondria with PTP opening to induce apoptosis and it correlates to the proapoptotic/antiapoptotic proteins expression ratio in them.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31521","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142931713","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

SMAD4 Regulates the Expression of LCK Affecting Chimeric Antigen Receptor-T Cells Proliferation Through PI3K/Akt Signaling Pathway SMAD4通过PI3K/Akt信号通路调控LCK表达影响嵌合抗原受体- t细胞增殖

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-06 DOI: 10.1002/jcp.31520

Rongxue Wan, Bowen Fu, Xiaokang Fu, Zengping Liu, Nafeisha Simayi, Yongshui Fu, Huaqin Liang, Chengyao Li, Wenhua Huang

{"title":"SMAD4 Regulates the Expression of LCK Affecting Chimeric Antigen Receptor-T Cells Proliferation Through PI3K/Akt Signaling Pathway","authors":"Rongxue Wan, Bowen Fu, Xiaokang Fu, Zengping Liu, Nafeisha Simayi, Yongshui Fu, Huaqin Liang, Chengyao Li, Wenhua Huang","doi":"10.1002/jcp.31520","DOIUrl":"10.1002/jcp.31520","url":null,"abstract":"The proliferation of CAR-T cells was hindered and cannot play its killing function well in solid tumors. And yet the regulatory mechanism of CAR-T cell proliferation is not fully understood. Here, we showed that recombinant expression of CD19CAR in T cells significantly increased the basal activation level of CAR-T cells and LCK activation. Both LCK and SMAD4 were essential for CAR-T cells proliferation since over-express LCK or SMAD4 significantly promotes CAR-T cells proliferation, while knock-down LCK or SMAD4 expression inhibited the proliferation of CAR-T cells seriously. More cells go into apoptosis when knock-down LCK or SMAD4 expression, and the cell cycle was arrested in G2/M or S phase, respectively. Over-express LCK or SMAD4 significantly promotes phosphorylation of PI3K and Akt, while it was inhibited when cells were treated with PI3K and Akt inhibitors (LY294002 or MK2206). Further mechanism exploration experiments showed that SMAD4 bound on the promoter region of LCK regulating its expression. Taken together, we reported that the transcription factor SMAD4 regulated the expression of LCK and further involved in the PI3K/Akt signaling pathway to affect the proliferation of CAR-T cells.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11704455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949520","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

Physiological Insights Into the Role of Pericytes in Spinal Cord Injury 从生理学角度揭示脊髓损伤中周皮细胞的作用

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-06 DOI: 10.1002/jcp.31500

Haiming Jin, Jessica Rawlins, Yiqi Chen, Xiaohang Zheng, Oscar Charlesworth, Junchun Chen, Gang Wang, Huoling Luo, Wenxiang Cheng, Zhong Alan Li, Sipin Zhu, Jiake Xu

引用次数: 0

Advances in Aggrephagy: Mechanisms, Disease Implications, and Therapeutic Strategies 聚合性疾病的研究进展：机制、疾病意义和治疗策略。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-03 DOI: 10.1002/jcp.31512

Haixia Zhuang, Xinyu Ma

引用次数: 0

KIF18A Is a Novel Target of JNK1/c-Jun Signaling Pathway Involved in Cervical Tumorigenesis KIF18A是JNK1/c-Jun信号通路参与宫颈肿瘤发生的新靶点

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2025-01-03 DOI: 10.1002/jcp.31516

Yajie Wang, Bowen Zhou, Xiaoying Lian, Siqi Yu, Baihai Huang, Xinyue Wu, Lianpu Wen, Changjun Zhu

{"title":"KIF18A Is a Novel Target of JNK1/c-Jun Signaling Pathway Involved in Cervical Tumorigenesis","authors":"Yajie Wang, Bowen Zhou, Xiaoying Lian, Siqi Yu, Baihai Huang, Xinyue Wu, Lianpu Wen, Changjun Zhu","doi":"10.1002/jcp.31516","DOIUrl":"10.1002/jcp.31516","url":null,"abstract":"<div>\u0000 \u0000 Cervical cancer remains a significant global health concern. KIF18A, a kinesin motor protein regulating microtubule dynamics during mitosis, is frequently overexpressed in various cancers, but its regulatory mechanisms are poorly understood. This study investigates KIF18A's role in cervical cancer and its regulation by the JNK1/c-Jun signaling pathway. Cell growth was assessed in vitro using MTT and colony formation assays, and in vivo using a nude mouse xenograft model with KIF18A knockdown HeLa cells. The Genomic Data Commons (GDC) data portal was used to identify KIF18A-related protein kinases in cervical cancer. Western blot analysis was employed to analyze phosphor-c-Jun, c-Jun, and KIF18A expression levels following JNK1 inhibition, c-Jun knockdown/overexpression, and KIF18A knockdown in cervical cancer cells. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to assess c-Jun binding and transcriptional activity of the KIF18A promoter. KIF18A knockdown significantly impaired cervical cancer cell growth both in vitro and in vivo. A strong positive correlation was observed between JNK1 and KIF18A expression in cervical and other cancers. JNK1 inhibition decreased both KIF18A expression and c-Jun phosphorylation. c-Jun was found to directly bind to and activate the KIF18A promoter. Furthermore, c-Jun knockdown inhibited cervical cancer cell growth, and this effect was partially rescued by KIF18A overexpression. This study demonstrates that the JNK1/c-Jun pathway activates KIF18A expression, which is essential for cervical cancer cell growth. Targeting the JNK/c-Jun/KIF18A axis may represent a promising novel therapeutic strategy for cancer treatment.\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921836","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