Cell Biochemistry and Function最新文献

{"title":"Correction to “Exosomes Derived From BMMSCs Promote B10 Cell Differentiation but Not IL-10 Production”","authors":"","doi":"10.1002/cbf.70084","DOIUrl":"https://doi.org/10.1002/cbf.70084","url":null,"abstract":"<p>J. Wang, Y. Gu, J. Wang, N. Zhang, X. Han, and Y. Bai, “Exosomes Derived From BMMSCs Promote B10 Cell Differentiation but Not IL-10 Production,” <i>Cell Biochemistry and Function</i>, 43 (2025): e70083, https://doi.org/10.1002/cbf.70083.</p><p>In the author byline “Jiran Wang¹ | Yingzhi Gu¹ | Jing Wang¹ | Ning Zhang¹ | Xiaozhe Han² | Yuxing Bai¹”, co-authors are not marked. This should be “Jiran Wang^1# | Yingzhi Gu^1# | Jing Wang¹ | Ning Zhang¹ | Xiaozhe Han² | Yuxing Bai¹”. Also, the following footnote is missing: “^#These authors contributed equally to this work.”</p><p>In the Funding section, “the Young Scientist Program of Beijing Stomatological Hospital Capital Medical University (No. YSP202001)” should not be present.</p><p>In Figure 4A, cocultured group, the annotated number “36.9” is incorrect. It should should be “38.9” instead. The correct figure should be,</p><p>We apologize for these errors.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 6","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZIP14 Deletion Disrupts Divalent Metal Homeostasis in Mouse Cerebrospinal Fluid","authors":"Shannon M. McCabe,&nbsp;Ningning Zhao","doi":"10.1002/cbf.70086","DOIUrl":"https://doi.org/10.1002/cbf.70086","url":null,"abstract":"<div>\u0000 \u0000 <p>ZIP14 is a member of the SLC39A (ZIP) family of metal transporters, primarily facilitating the cellular influx of divalent metals including manganese (Mn), zinc (Zn), and iron (Fe). Previous studies have demonstrated that <i>Zip14</i> knockout (<i>Zip14</i>^-/-) mice exhibit significant increases in whole blood and brain Mn levels. However, the impact of ZIP14 deletion on metal homeostasis within the cerebrospinal fluid (CSF) remained unexplored. In this study, we comprehensively assessed Mn, Zn, Fe, sodium (Na), potassium (K), and calcium (Ca) levels in whole blood, serum, and CSF of male and female <i>Zip14</i>^-/- mice to elucidate both systemic and central nervous system (CNS)-specific alterations in metal homeostasis. Our findings reveal that <i>Zip14</i>^-/- mice exhibit pronounced Mn accumulation, with CSF Mn levels increasing by approximately 15-fold in males and 46-fold in females compared to wild-type controls. Correspondingly, blood Mn levels rose 23-fold in males and 17-fold in females, while serum Mn levels increased 10-fold and 15-fold, respectively. In contrast, Zn and Fe levels in whole blood and serum remained comparable between <i>Zip14</i>^-/- and wild-type mice. However, significant elevations in CSF Zn were observed, with a sevenfold increase in males and a 16-fold increase in females, alongside a threefold rise in CSF Fe levels in females. The CSF to serum ratios of Zn and Fe remained below 1 but were increased in the knockout mice, suggesting the activation of alternative metal transporters in the absence of ZIP14, which may contribute to the increased Mn accumulation in the CSF as well. Importantly, Na⁺ and K⁺ levels in whole blood, serum, and CSF were unaltered in <i>Zip14</i>^-/- mice, indicating that ZIP14 deletion does not broadly disrupt systemic electrolyte balance or compromise blood—CSF barrier integrity. Conversely, CSF Ca²⁺ levels were significantly reduced by 33% in male and 23% in female <i>Zip14</i>^-/- mice, suggesting a specific effect of ZIP14 on calcium homeostasis within the CNS.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 6","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144244123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphorylation State of RB Modulates Ferroptotic Sensitivity","authors":"Nishanth Kuganesan,&nbsp;Samkeliso Dlamini,&nbsp;L. M. Viranga Tillekeratne,&nbsp;William R. Taylor","doi":"10.1002/cbf.70085","DOIUrl":"https://doi.org/10.1002/cbf.70085","url":null,"abstract":"<p>Tumor suppressor RB is a central regulator of cell cycle progression. By binding to E2F transcription factors, RB can inhibit transcription of E2F target genes to cause cell cycle arrest. Cyclin dependent kinases (CDK) regulate the interaction of RB/E2F by phosphorylating RB at multiple sites. Previously, we observed that CDK2, RB and E2F inhibit ferroptosis. Ferroptosis is a non-apoptotic, iron-dependent form of cell death characterized by toxic lipid peroxidation. Here, we investigate whether RB is a downstream target of CDK activity in the regulation of ferroptosis. We approach this question by overexpressing wild-type (WT) RB or a mutant RB that cannot be phosphorylated by CDKs (RBΔCDK) followed by analysis of ferroptosis. Overexpressing WT-RB reduced sensitivity to ferroptosis while the RBΔCDK mutant increased sensitivity. As we previously found, increasing CDK2 expression reduced ferroptotic sensitivity. This reduction persisted in cells expressing RBΔCDK. However, WT-RB blocked the ability of CDK2 to inhibit ferroptosis. These observations suggest that at least part of the mechanism by which CDK2 inhibits ferroptosis is by phosphorylating RB.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 6","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144213760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of p53 on the Regulation of Carbonic Anhydrase 8 in Human Colorectal Cancer Cells: Interaction Between p53 and Sp1","authors":"Jia-Yo Yu,&nbsp;Benjamin Y. Hsieh,&nbsp;Shang-Feng Tsai,&nbsp;Mingli Hsieh","doi":"10.1002/cbf.70081","DOIUrl":"https://doi.org/10.1002/cbf.70081","url":null,"abstract":"<div>\u0000 \u0000 <p>Colorectal cancer ranks among the most common malignancies worldwide. Our previous study indicated Carbonic anhydrase 8 (CA8) is linked to cell proliferation and mobility in colon cancer cells. In the present study, we observed a significant increase in the expression of mutant p53 R273H/P309S in colon cancer cell lines (SW480 and SW620) with stably downregulated CA8. P53, a well-known tumor suppressor gene, is frequently mutated in cancer cells, leading to poor prognosis and drug resistance. Although p53 acts as a transcription factor, the increased mutant p53 did not activate downstream target molecules, suggesting activation defects of mutant p53 R273H/P309S. Furthermore, transient downregulation of CA8 did not alter p53 expression, indicating that the observed increase in mutant p53 in stable cells may be a compensatory effect for cell survival. Given that p53 shares similar consensus sequences at GC-boxes with specific protein 1 (Sp1), a predominant transcription factor for CA8 regulation, we examined the relationship between CA8, p53 and Sp1 in HCT116 and SW620 cells harboring wild-type (WT) or mutant p53, respectively. Notably, transient downregulation of p53 or Sp1 led to a significant decrease in CA8 at both mRNA and protein levels in HCT116 and SW620 cells. Additionally, immunoprecipitation results revealed a protein-protein interaction between Sp1 and p53, suggesting that their interaction may be involved in the regulation of CA8 expression. Although the precise mechanism by which Sp1 and p53 regulate CA8 expression remains unclear, we are the first to report that both Sp1 and p53 are involved in the regulation of the novel <i>hCA8</i> gene. By further unraveling the interplay among CA8, p53, and Sp1, we hope to pave the way for new therapeutic approaches in colon cancer treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes Derived From BMMSCs Promote B10 Cell Differentiation but Not IL-10 Production","authors":"Jiran Wang,&nbsp;Yingzhi Gu,&nbsp;Jing Wang,&nbsp;Ning Zhang,&nbsp;Xiaozhe Han,&nbsp;Yuxing Bai","doi":"10.1002/cbf.70083","DOIUrl":"https://doi.org/10.1002/cbf.70083","url":null,"abstract":"<div>\u0000 \u0000 <p>The role of IL-10-producing regulatory B cells in inflammatory diseases has recently gained substantial attention. Here, we evaluated the function of mouse bone marrow mesenchymal stem cell-derived exosomes (BMMSC-Exos) and their effect on B-cell differentiation. This study aimed to establish an association between BMMSC-Exos and purified B cells and further explored the anti-inflammatory effect of B10 cells. The expression of inflammatory factors, such as IL-1β, TNF-α, and bone metabolism-related factors, including RANKL, OPG, and secreted IL-10, was investigated by RT-qPCR and ELISA. Populations of CD1d^highCD5⁺ B cells were analyzed by flow cytometry and immunofluorescence. Cell viability was assessed by CCK8 assay. The results showed that when B cells were separated from BMMSCs by Transwell, IL-1β, TNF-α, and RANKL were downregulated, whereas IL-10, OPG/RANKL, and CD1d^highCD5⁺ Breg proportion were upregulated in the cocultured groups. Conversely, when B cells were cultured with BMMSC-Exos, increasing concentrations of exosomes increased the proportion of CD1d^highCD5⁺ and IL-10⁺CD45⁺ Bregs; however, the secretion of both pro-inflammatory cytokines and IL-10 were decreased. We found that BMMSC-Exos induce the differentiation of B cells toward the CD1d^highCD5⁺ and IL-10⁺CD45⁺ Breg phenotype but cannot increase the secretion of IL-10 in vitro.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormonal Dynamics of Cervical Cancer: Role of Estrogen and Progesterone","authors":"Jyoti Rani,&nbsp;Seema Yadav,&nbsp;Ritu Yadav,&nbsp;Ravindresh Chhabra","doi":"10.1002/cbf.70082","DOIUrl":"https://doi.org/10.1002/cbf.70082","url":null,"abstract":"<div>\u0000 \u0000 <p>Cervical cancer remains a significant global health burden, with its etiology intricately linked to hormonal influences such as estrogen and progesterone. The effect of estrogen on cervical cancer is dependent upon factors like estrogen receptor subtype and microenvironmental context. Conversely, progesterone has a more complex role, acting as an inducer as well as inhibitor, by coordinating with tumor suppressor genes and cell proliferation markers. Understanding the interplay among these hormones, HPV infection, and cervical carcinogenesis is crucial for improving current preventive strategies and therapeutic interventions. This review outlines the latest insights on how hormones influence cervical cancer development, highlighting their protective and inhibitory effects. It explores the interaction between HPV oncogenes and hormones in cervical cancer progression. Additionally, it consolidates existing knowledge and identifies future research directions, underscoring the potential of hormone modulation as a therapeutic strategy for cervical cancer.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143950217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disulfidoptosis: A New Key to Unlocking Cancer Treatment","authors":"Xue Li,&nbsp;Shujun Xu,&nbsp;Liwei Jia,&nbsp;Yuan Tian,&nbsp;Xin Meng","doi":"10.1002/cbf.70079","DOIUrl":"https://doi.org/10.1002/cbf.70079","url":null,"abstract":"<div>\u0000 \u0000 <p>The metabolic properties of disulfidoptosis targeting cancer cells have become a new key to unlocking cancer treatment's lock. Conventional cancer therapies aim to kill tumor cells through apoptosis, but cell death is carried out by a network of cascading enzymes. Malignant cells can evade the death process by downregulating key enzymes or inhibiting death-inducing triggers, leading to cancer persistence and recurrence of cancer cells that are resistant to conventional therapies and immune escape, which has compelled researchers to explore new therapeutic avenues. Disulfidoptosis is triggered by the accumulation of excessive intracellular disulfides in cells with high expression of solute carrier family 7 member 11 (SLC7A11) under glucose starvation conditions, which simultaneously induces the breakage of intracellular disulfide bonds and leads to protein malfunction, thereby triggering cancer cell death. However, there is no comprehensive account of disulfidoptosis application in cancer therapy. This review comprehensively summarizes the mechanism of disulfidoptosis for cancer treatment, which provides new ideas for cancer treatment.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143904983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-37 Protects Against Ventilator-Induced Lung Injury by Inhibiting NLRP3 Activation","authors":"Xingmeng Xu,&nbsp;Weili Liu,&nbsp;Yan Xu,&nbsp;Yinghong Fan,&nbsp;Fei Han,&nbsp;Jiajia Pan,&nbsp;Guotao Lu,&nbsp;Chenlong Yi,&nbsp;Qingfen Zhang","doi":"10.1002/cbf.70080","DOIUrl":"https://doi.org/10.1002/cbf.70080","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>Mechanical ventilation is an effective strategy for managing acute respiratory distress syndrome (ARDS), but it can also exacerbate lung injury, leading to ventilator-induced lung injury (VILI). To investigate the protective role of interleukin-37 (IL-37) in the pathogenesis of VILI, we used two approaches, human IL-37 transgenic (IL37tg) mice and administration of recombinant human IL-37 (rIL37) in wild-type (WT) mice subjected to mechanical ventilation. Lung histopathology was evaluated, inflammatory cytokine levels (IL-1β, IL-6, TNF-α) were measured, and inflammasome activation was assessed by analyzing NLRP3 and Caspase-1 expression. As a result, IL37tg mice exhibited significantly attenuated lung injury compared to WT controls, characterized by improved histological morphology, reduced lung injury scores, and decreased infiltration of macrophages and neutrophils. Similarly, rIL37 administration markedly reduced lung injury and decreased inflammatory cytokine levels. Immunofluorescence analysis revealed colocalization of the alveolar cell marker surfactant protein D (SP-D) and IL-37. Furthermore, IL-37 suppressed NLRP3 inflammasome activation, as evidenced by reduced NLRP3 and Cleaved-Caspase-1 levels in both the IL37tg mouse model and the rIL37 treatment group. These findings suggest that IL-37 effectively protects against VILI by inhibiting inflammation in lung tissues through inhibition of the NLRP3 inflammasome. Therefore, IL-37 may serve as a potential therapeutic target for the prevention and treatment of VILI in the future.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143908957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Irisin Is a Potential Novel Biomarker and Therapeutic Target Against Kidney Diseases","authors":"Xiu Huang,&nbsp;Xiya Ren,&nbsp;Limei Zhao,&nbsp;Yajie Hao,&nbsp;Zhibo Zhao,&nbsp;Fahui Chen,&nbsp;Jinxiu Zhou,&nbsp;Mengqi Bai,&nbsp;Si Chen,&nbsp;Xiaoshuang Zhou","doi":"10.1002/cbf.70075","DOIUrl":"https://doi.org/10.1002/cbf.70075","url":null,"abstract":"<div>\u0000 \u0000 <p>Kidney diseases, characterized by renal dysfunction, are the leading causes of death worldwide. It is crucial to prevent and treat kidney diseases to reduce their associated morbidity and mortality. Moderate physical exercise has been recognized to be advantageous for kidney health. Irisin is an exercise-induced myokine that was identified in 2012. It plays an important role in energy and bone metabolism, oxidative stress reduction, anti-inflammatory processes, cell death inhibition, and cardiovascular protection. However, the relationship between irisin and kidney diseases have not been fully elucidated. This review explores the role of irisin as a biomarker for kidney disease diagnosis and its associated complications, as well as the mechanisms through which it participates in various cell death pathways, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, irisin secretion levels were discussed to provide a basis for kidney disease prevention and treatment avenues, as well as therapeutic guidance for developing new and promising intervention strategies.</p>\u0000 <p><b>Clinical Trial Registration</b>: None.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143896978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X7 Receptor Facilitates Cardiomyocyte Autophagy After Myocardial Infarction via Nox4/PERK/ATF4 Signaling Pathway","authors":"Shuhong Zhang,&nbsp;Yingying Bi,&nbsp;Kaili Xiang,&nbsp;Yanhong Tang","doi":"10.1002/cbf.70078","DOIUrl":"https://doi.org/10.1002/cbf.70078","url":null,"abstract":"<div>\u0000 \u0000 <p>Myocardial infarction (MI) represents a critical cardiovascular emergency, standing as a leading cause of global mortality. ATP, a typical damage-associated molecular pattern, is stored in cells at high concentrations. Upon cellular injury, hypoxia, or necrosis, substantial quantities of ATP efflux into the extracellular space, activating P2X₇ receptors, thereby initiating multiple signaling cascades. In vivo studies demonstrated coordinated upregulation of P2X₇ and autophagy-related proteins in the infarcted border zone. Transcriptome sequencing revealed Nox4 overexpression in the myocardial tissue post-infarction; furthermore, administration of the P2X₇ receptor antagonist A740003 effectively reduced both autophagy-related protein levels and Nox4 expression. In vitro experiments indicated that hypoxia induced upregulation of Nox4, p-PERK/PERK, ATF4, Beclin-1, and ATG5 in cardiomyocytes, A740003 could inhibit the expression of these proteins, while overexpression of Nox4 counteracted this effect. Collectively, our findings indicated that the P2X₇ receptor expression was elevated in the infarcted border zone following MI and implicated its role in excessive autophagy induced by hypoxia in cardiomyocytes—at least partially through the Nox4/PERK/ATF4 pathway, thereby exacerbating myocardial injury following MI.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 5","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}