Journal of Cellular Physiology最新文献

{"title":"Loss of UCHL1 Leads to Enhanced Mouse Osteoclast Formation","authors":"Mitsuki Chiba,&nbsp;Seira Hoshikawa,&nbsp;Kouhei Shimizu,&nbsp;Hiromi Fujita,&nbsp;Keiji Wada,&nbsp;Aya Yamada,&nbsp;Kan Saito,&nbsp;Hiroyuki Inuzuka,&nbsp;Satoshi Fukumoto","doi":"10.1002/jcp.70032","DOIUrl":"https://doi.org/10.1002/jcp.70032","url":null,"abstract":"<div>\u0000 \u0000 <p>Enhanced osteoclastogenesis causes bone fragility, osteoporosis, and an increased risk of fractures. Recent studies have suggested a possible correlation between osteoporosis and the pathological features of Parkinson's disease (PD). To establish a molecular link between these conditions, we focused on the physiological function of the PD-related protein ubiquitin carboxy-terminal hydrolase L1 (UCHL1) in bone remodeling. To this end, we investigated the role of UCHL1 in regulating osteoclast differentiation in <i>Uchl1</i> spontaneous mutant <i>gad</i> mice. We found that <i>gad-</i>mouse-derived osteoclast progenitors exhibit enhanced osteoclast differentiation. Likewise, CRISPR-mediated <i>Uchl1</i> knockout in mouse macrophage-derived preosteoclast RAW-D cells increased RANKL-dependent osteoclastogenesis. Supporting this observation, these <i>Uchl1</i>-depleted cells showed elevated expression of osteoclast marker genes. To uncover the molecular mechanisms by which the loss of <i>Uchl1</i> enhances osteoclast differentiation, we screened for UCHL1-interacting proteins in RAW-D preosteoclast cells and identified AKT1 as a potential UCHL1-regulated protein. UCHL1 depletion in preosteoclasts led to increased Thr308/Ser473 phosphorylation of AKT1. Furthermore, ectopic expression of UCHL1 decreased the K63-linked polyubiquitination of AKT1. These findings suggest that UCHL1 is critical in partially suppressing osteoclastogenesis through modulating AKT signaling.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831117","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":"Mesenchymal Stem Cell Treatment for Peripheral Nerve Injuries","authors":"Yue Wu,&nbsp;Ruijie Lu,&nbsp;Hongtao Yin,&nbsp;Deqing Peng,&nbsp;Ruolang Pan,&nbsp;Liangzhong Lv","doi":"10.1002/jcp.70031","DOIUrl":"https://doi.org/10.1002/jcp.70031","url":null,"abstract":"<div>\u0000 \u0000 <p>Peripheral nerve injuries (PNI) affect hundreds of thousands of patients annually, often leading to life-altering consequences such as significant impairments in motor function and sensory perception. In recent years, a growing body of evidence indicates that mesenchymal stem cell (MSC) treatment could complement traditional treatment and improve therapeutic outcomes for these injuries. This paper reviews emerging insights into the potential benefits of MSC treatment for PNI and summarizes selected examples of the interactions between MSCs, peripheral nerves, and their microenvironment, which have advanced our understanding of the pathophysiology of MSC-based therapy. We believe that this rapidly moving field holds great promise for future advancements, guiding the rational design of safe and effective treatments for patients with PNI.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818419","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 “Beta-Arrestin 2 Mediates Cardiac Hypertrophy Induced by Thyroid Hormones via AT1R”","authors":"","doi":"10.1002/jcp.70030","DOIUrl":"https://doi.org/10.1002/jcp.70030","url":null,"abstract":"<p>Caroline A. L., L. de Bortoli Teixeira, S. C. Simões, et al. 2021. <i>Journal of Cellular Physiology</i> 236, no. 6: 4640–4654.</p><p>In Figure 4B of “Results” section, the images representing GAPDH protein expression in the nucleus and Histone expression in the cytoplasm were inadvertently omitted. The correct images representative Western Blotting images are presented below.</p><p>The authors apologize for this error.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143818418","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: Porphyromonas Gingivalis and Dental Stem Cells Crosstalk Amplify Inflammation and Bone Loss in the Periodontitis Niche","authors":"","doi":"10.1002/jcp.70021","DOIUrl":"https://doi.org/10.1002/jcp.70021","url":null,"abstract":"<p><b>RETRACTION:</b> D. Ezhilarasan, and S. S. Varghese, “Porphyromonas Gingivalis and Dental Stem Cells Crosstalk Amplify Inflammation and Bone Loss in the Periodontitis Niche,” <i>Journal of Cellular Physiology</i> 237, no. 10 (2022): 3768-3777, https://doi.org/10.1002/jcp.30848.</p><p>The above article, published online on 4 August 2022 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. Following publication, it has come to the attention of the journal that the article was accepted solely on the basis of compromised peer review processes. Therefore, the decision to retract this article was taken. The authors have been informed of the decision of retraction and disagree with it.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762223","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":"Pleiotropic Role of TNIK in Sepsis-Induced Cardiomyopathy","authors":"Wenwen Yang,&nbsp;Aizhen Zhao,&nbsp;Wangrui Lei,&nbsp;Junmin Chen,&nbsp;Huanle Yan,&nbsp;Jiawen Li,&nbsp;Yang Yang,&nbsp;Ying Chen","doi":"10.1002/jcp.70027","DOIUrl":"https://doi.org/10.1002/jcp.70027","url":null,"abstract":"<div>\u0000 \u0000 <p>Heart failure induced by sepsis is considered one of the foremost contributors to mortality in intensive care unit (ICU) patients. However, the molecular mechanism of myocardial damage in sepsis has not been fully elucidated at present. TNF receptor-associated factor-2 and Nck-interacting protein kinase (TNIK) are members of the germinal center kinase superfamily. TNIK exhibits a pivotal role as a conserved modulator of glucose and lipid homeostasis. Here, we aimed to investigate the potential direct roles of TNIK and whether TNIK exerts anti-septic myocardial damage by regulating the NLRP3 pathway. We initially revealed that TNIK was the crucial involvement of septic myocardial injury. Subsequently, we constructed a cecal ligation and puncture (CLP) mouse model and employed LPS-induced injury in HL-1 cardiomyocytes. Our observations revealed an upregulation of TNIK levels in both CLP-injured mice and LPS-treated HL-1 cells. However, TNIK inhibitor TNIK-IN-7 or siRNA attenuated cardiomyocyte LPS injury. Especially, TNIK siRNA can significantly downregulate TNIK as well as decrease NLRP3 and IL-1β mRNA and protein levels, though the explicit molecular mechanisms of TNIK-NLRP3 in septic myocardial require further investigation. Together, our investigation presents novel evidence suggesting TNIK as a potential therapeutic target for the prevention and therapeutic intervention in sepsis-induced cardiomyopathy.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762222","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: Phytosomal Curcumin Inhibits Tumor Growth in Colitis-Associated Colorectal Cancer","authors":"","doi":"10.1002/jcp.70018","DOIUrl":"https://doi.org/10.1002/jcp.70018","url":null,"abstract":"<p><b>RETRACTION:</b> R. M. Marjaneh, F. Rahmani, S. M. Hassanian, N. Rezaei, M. Hashemzehi, A. Bahrami, F. Ariakia, H. Fiuji, A. Sahebkar, A. Avan, and M. Khazaei, “Phytosomal Curcumin Inhibits Tumor Growth in Colitis-Associated Colorectal Cancer,” <i>Journal of Cellular Physiology</i> 233, no. 10 (2018): 6785-6798, https://doi.org/10.1002/jcp.26538.</p><p>The above article, published online on 8 May 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.</p><p>The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, evidence of inappropriate post-acquisition image editing, including splicing sites have been detected in Figure 6a. Furthermore, no correspondence between sections at lower and higher magnification was found for the “AOM”, “5-FU”, and “Curcumin” groups in Figure 4e and f. The authors were unable to retrieve the original data underlying the Western Blot experiments presented in Figure 6a due to the time elapsed since performing the experiments. Additionally, original data provided for Figure 4 was insufficient to resolve the issues. Accordingly, the article is retracted as the editors have lost confidence in the accuracy and integrity of the whole body of data presented in the article and consider its conclusions invalid. The authors have been informed of the decision of retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749860","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":"The Thromboxane Levels in Ovarian Follicular Fluid Are Inversely Correlated With Oocyte Maturation: Implications of PAR-2/-3 Cooperation and Thromboxane Participation in Follicle Development","authors":"Hsuan-Ting Chen,&nbsp;Tsung-Hsuan Lai,&nbsp;Jun-Jie Lin,&nbsp;Chao-Chi Chen,&nbsp;Wen-Bin Wu","doi":"10.1002/jcp.70025","DOIUrl":"https://doi.org/10.1002/jcp.70025","url":null,"abstract":"<div>\u0000 \u0000 <p>It has been reported the presence of components from the coagulation thrombin-generating pathway and prostaglandins (PGs) in human ovarian follicular fluid (FF) but with unclear functions. Moreover, thrombin can induce COX-2 expression linking to PG synthesis in several cell types. Therefore, this study sought to explore the thromboxane (TX) generation in FF and the correlation between FF TX levels and oocyte maturation. The FF TXB₂ (a stable metabolite of TXA₂) levels exhibited a negative correlation between large preovulatory leading and small mid-antral follicles from in vitro fertilization (IVF) patients, indicating a requirement of TX for a small follicle/oocyte to grow/mature. Further receiver operating characteristic curve analysis identified that intrafollicular TXB₂ level could predict oocyte maturity. Thrombin was found expressed in a similar pattern/trend to TXB₂ in intrafolliclar FF, where it could induce TXB₂ production/secretion in human ovarian follicular GCs via proteinase-activated receptor-2 (PAR-2) and PAR-3 cooperation/transactivation and Erk/p38 MAPK/JNK signaling to cause COX-2/TXB₂ induction. Accordingly, PAR-2 and -3 were present in human ovarian follicular GCs and thrombin, PAR-2 agonist, and TXA₂ analog caused a substantial enhancement in follicle development, which could be blocked by the PAR-2, COX-2, and TXA₂ prostanoid (TP) receptor inhibitors in an ex vivo cultured murine ovary model. Collectively, we first demonstrated that FF thrombin regulates PAR-2/-3 cooperation and MAPK signaling pathways to induce COX-2 expression and TX production in follicular GCs, possibly supporting intrafollicular TX levels and triggering TP-related pathways to enhance follicle development. The FF TX levels also can be a predictor for oocyte maturation during IVF.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749439","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":"SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy","authors":"Juan J. Ferreira,&nbsp;Lindsey N. Kent,&nbsp;Ronald McCarthy,&nbsp;Alice Butler,&nbsp;Xiaofeng Ma,&nbsp;Nikita Peramsetty,&nbsp;Chinwendu Amazu,&nbsp;Alexander Zhang,&nbsp;Grace C. Whitter,&nbsp;Ethan Li,&nbsp;Sarah K. England,&nbsp;Celia M. Santi","doi":"10.1002/jcp.70024","DOIUrl":"https://doi.org/10.1002/jcp.70024","url":null,"abstract":"<p>At the end of pregnancy, the uterus transitions from a quiescent to a highly contractile state. This is partly due to the depolarization of the resting membrane potential in uterine (myometrial) smooth muscle cells (MSMCs). In human MSMCs, the membrane potential is regulated by a functional complex between the sodium (Na⁺)-activated potassium (K⁺) channel SLO2.1 and the Na⁺ leak channel nonselective (NALCN). Na⁺ entering through NALCN activates SLO2.1, leading to K⁺ efflux, membrane hyperpolarization (cells become more negative inside), and reduced contractility. Decreased SLO2.1/NALCN activity results in reduced K⁺ efflux, leading to membrane depolarization, Ca²⁺ influx via voltage-dependent calcium channels, and increased MSMC contractility. However, all of these data are from MSMCs isolated from women at term, so the role of the SLO2.1/NALCN complex early in pregnancy was speculative. To address this question here, we examined the role of the SLO2.1/NALCN complex in regulating mouse MSMC membrane potential across pregnancy. We report that <i>Slo2.1</i> and <i>Nalcn</i> are more highly expressed in MSMCs from nonpregnant and early pregnant mice than in those from late-pregnant mice. Functional studies revealed that SLO2.1 channels mediate a significant portion of the K⁺ current in mouse MSMCs, particularly in cells from nonpregnant and early pregnant mice. Activation of SLO2.1 by Na⁺ influx through NALCN led to membrane hyperpolarization in MSMCs from early pregnancy but not in MSMCs from later pregnancy. Moreover, the NALCN/SLO2.1 complex regulates intracellular Ca²⁺ responses more in MSMCs from nonpregnant and early pregnancy mice than in MSMCs from late pregnancy. Together, these findings reveal that the SLO2.1/NALCN functional complex is conserved between mice and humans and functions throughout pregnancy. This study could open avenues for targeted pharmacological interventions for pregnancy-related complications.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143749440","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: DUSP1 Recuses Diabetic Nephropathy via Repressing JNK-Mff-Mitochondrial Fission Pathways","authors":"","doi":"10.1002/jcp.70017","DOIUrl":"https://doi.org/10.1002/jcp.70017","url":null,"abstract":"<p><b>RETRACTION:</b> Sheng, J., H. Li, Q. Dai, C. Lu, M. Xu, J. Zhang, and J. Feng, “DUSP1 Recuses Diabetic Nephropathy via Repressing JNK-Mff-Mitochondrial Fission Pathways.” <i>Journal of Cellular Physiology</i> 234, no. 3 (2019): 3043-3057. https://doi.org/10.1002/jcp.27124.</p><p>The above article, published online on September 7, 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 due to concerns raised by third parties. Several irregularities were found, including, but not limited to, multiple image elements being published in later articles by different author groups and in distinct scientific contexts, indicating inappropriate data sharing. The authors were invited to comment on these concerns but did not respond. Further investigation by the publisher revealed that the article was accepted solely on the basis of a compromised peer review process. 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":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707363","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":"SMC2 and Condensin II Subunits Are Essential for the Development of Hematopoietic Stem and Progenitor Cells in Zebrafish","authors":"Chang-Kyu Oh,&nbsp;Man S. Kim,&nbsp;Unbeom Shin,&nbsp;Ji Wan Kang,&nbsp;Yun Hak Kim,&nbsp;Hwa Soo Ko,&nbsp;Jae Sun Ra,&nbsp;Soyul Ahn,&nbsp;Eun Young Choi,&nbsp;Sanghyeon Yu,&nbsp;Uijeong Nam,&nbsp;Taesoo Choi,&nbsp;Kyungjae Myung,&nbsp;Yoonsung Lee","doi":"10.1002/jcp.70023","DOIUrl":"https://doi.org/10.1002/jcp.70023","url":null,"abstract":"<p>Hematopoietic stem and progenitor cells (HSPCs) play a pivotal role in blood cell production, maintaining the health and homeostasis of individuals. Dysregulation of HSPC function can lead to blood-related diseases, including cancer. Despite its importance, our understanding of the genes and pathways underlying HSPC development and the associated pathological mechanisms remains limited. To elucidate these unknown mechanisms, we analyzed databases of patients with blood disorders and performed functional gene studies using zebrafish. We employed bioinformatics tools to explore three public databases focusing on patients with myelodysplastic syndrome (MDS) and related model studies. This analysis identified significant alterations in several genes, especially <i>SMC2</i> and other condensin-related genes, in patients with MDS. To further investigate the role of Smc2 in hematopoiesis, we generated <i>smc2</i> loss-of-function zebrafish mutants using CRISPR mutagenesis. Further analyses of the mutants revealed that <i>smc2</i> depletion induced G2/M cell cycle arrest in HSPCs, leading to their maintenance and expansion failure. Notably, although the condensin II subunits (<i>ncaph2</i>, <i>ncapg2</i>, and <i>ncapd3</i>) were essential for HSPC maintenance, the condensin I subunits did not affect HSPC development. These findings emphasize the crucial role of condensin II in ensuring healthy hematopoiesis via promoting HSPC proliferation.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 3","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143698726","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}