Cell Biochemistry and Function最新文献

{"title":"The Mechanisms and Implications of Cardiolipin in the Regulation of Cell Death","authors":"Zhou-zhou Li,&nbsp;Han-xi Xiao,&nbsp;Jian-jie Hu,&nbsp;Wei Xie,&nbsp;Zu-xiu Wang,&nbsp;Yong-ping Pan,&nbsp;Xu-huan Li,&nbsp;Xue-feng Yu","doi":"10.1002/cbf.70066","DOIUrl":"https://doi.org/10.1002/cbf.70066","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiolipin (CL), an exclusive phospholipid, is predominantly found within the confines of the inner mitochondrial membrane, playing an indispensable role in the sustenance of mitochondrial operations and the regulation of cellular energy metabolism. The influence of CL on the pathways of cell death has garnered significant interest in recent scholarly discourse. This review delves into the multifaceted roles of CL across various modes of cell demise, encompassing apoptosis, autophagy, pyroptosis, ferroptosis, necrosis, and necroptosis. The discussion extends to the examination of CL's implications in a clinical context, particularly concerning cardiovascular maladies, neurological degeneration, and oncological conditions. Through an integrative analysis of contemporary research findings, the aim is to elucidate the intricate dynamics of CL's involvement in cell death phenomena. While acknowledging the inherent limitations and the hurdles faced by current research endeavors, the therapeutic potential of CL as a modulator of cell death pathways is nonetheless encouraging. Forthcoming investigations must surmount these obstacles, thereby uncovering the nuanced mechanisms and impacts of CL in the realm of cell death and associated pathologies, potentially paving the way for innovative clinical intervention strategies.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646177","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":"HDAC4-AS1/CTCF Transcriptionally Represses HDAC4 Under Stress, Whereas HDAC4 Inhibits Stress-Induced Syncytiotrophoblast Cellular Pyroptosis by Deacetylating NLRP3 and GSDMD","authors":"Juan Du,&nbsp;Qinghong Ji,&nbsp;Lihua Dong,&nbsp;Lanlan Wang,&nbsp;Gang Xin","doi":"10.1002/cbf.70064","DOIUrl":"https://doi.org/10.1002/cbf.70064","url":null,"abstract":"<div>\u0000 \u0000 <p>Our previous study reported that histone deacetylase 4 (HDAC4) expression is significantly downregulated in placental tissues of pre-eclampsia (PE) pregnancies. Cellular pyroptosis is a key event in the pathogenesis of PE that induces the release of factors into the maternal circulation. The aim of this study is to analyze the role and related molecular mechanisms of HDAC4 in PE trophoblast cell pyroptosis. Hypoxia and lipopolysaccharide (LPS)/ATP-treated immortalized human placental villous trophoblast cells HTR-8/SVneo were utilized to mimic the placental trophoblast cell state in PE. Both hypoxia and LPS/ATP treatments induced significant HTR-8/SVneo cell pyroptosis, whereas HDAC4 overexpression inhibited the induced cell pyroptosis. HDAC4 could bind to NLRP3 and GSDMD proteins, and lead to a decrease in acetylated NLRP3 and GSDMD proteins, thereby inhibiting cell pyroptosis. Hypoxia and LPS/ATP treatment significantly upregulated HDAC4-AS1 levels in HRT-8/SVneo cells. HDAC4-AS1 could bind to <i>HDAC4</i> gene promoter sequences as well as CTCF protein. HDAC4-AS1 overexpression recruited the enrichment of CTCF on <i>HDAC4</i> promoter sequences and further repressed HDAC4 transcription and expression. Targeting the transcriptional regulatory mechanism of HDAC4-AS1/HDAC4 may be able to ameliorate the clinical symptoms of PE maternal by inhibiting cellular pyroptosis in syncytiotrophoblast cells under stress.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646178","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":"Necroptotic Suppression of Lung Cancer Cell Proliferation and Migration: A Comprehensive In Vitro and In Silico Study to Determine New Molecular Targets for Pexidartinib","authors":"Ebru Hacıosmanoğlu-Aldoğan,&nbsp;Dilhan Lama,&nbsp;Hande İpek Yetke,&nbsp;Halil Şenol,&nbsp;Fulya Dal Yöntem","doi":"10.1002/cbf.70068","DOIUrl":"https://doi.org/10.1002/cbf.70068","url":null,"abstract":"<div>\u0000 \u0000 <p>In this study, the cytotoxic effects of pexidartinib (PLX), a tyrosine kinase inhibitor approved for tenosynovial giant cell tumor through inhibition of colony-stimulating factor 1 receptor (CSF1R), against A549 lung adenocarcinoma cells and Beas-2B healthy bronchial cells were investigated by in detailed in-vitro and in-silico studies. Through MTT assays, PLX demonstrated significant inhibition of A549 cell viability with IC₅₀ values of 2.15 and 1.3 µM at 24 and 48 h, respectively, while having minimal effects on Beas-2B cells, with IC₅₀ values of 36.2 and 9.3 µM. The high selectivity index indicates PLX's preferential action against cancerous cells. The mechanism of cell death induced by PLX was further explored using Annexin V/PI staining and flow cytometry, revealing that PLX primarily induces necrosis in A549 cells, with an increase in necrotic cell populations and reduced efficacy at higher concentrations. Western blot analysis showed an upregulation of necroptosis markers (RIP3 and pMLKL) in A549 cells, while apoptotic markers like Caspase-3 remained unchanged. In addition, wound healing assays demonstrated that PLX significantly inhibits A549 cell migration in a dose-dependent manner. Molecular docking studies identified key amino acids involved in PLX binding interactions with target proteins. RIPK1 showed the strongest binding affinity. MD simulations revealed that the PLX-VEGFR2 complex was the most stable. As conclusion, PLX, although approved for tenosynovial giant cell tumors, shows promising potential for lung adenocarcinoma treatment. It selectively inhibits cancer cell viability, induces necroptosis, and reduces cell migration. Its stronger binding to RIPK1 and VEGFR2 more than CSF1R.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143602697","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":"E7HPV16 Oncogene and 17beta-Estradiol Stress, Promotes Oncogenic microRNA Expression Patterns, Cell Proliferation and Cervical Intraepithelial Neoplasia 1.","authors":"Erandi Arvizu-Hernandez, Rodolfo Ocadiz-Delgado, Patricio Gariglio","doi":"10.1002/cbf.70065","DOIUrl":"10.1002/cbf.70065","url":null,"abstract":"<p><p>Cervical cancer (CC) is the second cause of death by a neoplasia in woman in Mexico. Among the factors that contribute to its development are prolonged infection by a high-risk HPV type and the use of estrogens. It is well known that diagnosis at early stages is extremely important since, in most cases, progression towards carcinogenesis could be prevented, hence the importance of finding candidates that serve as early biomarkers. Several studies have shown that the expression level of the tumor suppressor miR-218 is diminished in CC while oncomiR miR-21 is overexpressed. On the other hand, it has been reported that the Potassium calcium-activated channel subfamily M alpha 1 (Kcnma1) oncogene, a known target gene of miR-218, is overexpressed in CC. However, there are few studies on the expression of this oncogene in Cervical Intraepithelial Neoplasia 1 (CIN 1). In this study, the analysis of the K14E7HPV16 carcinogenesis model in young mice (1.5-month-old), showed that a single-dose of 17β-estradiol (E₂) increased both the cell proliferation and the Bcl-2 oncogene expression, as well as promoted the development of CIN 1. Interestingly, the hormonal stress and the E7 expression, favor the physiological response of the organism in transgenic young mice by decreasing the expression levels of the tumor suppressor miR-218 and increasing the expression of the Kcnma1 and Bcl-2 mRNA oncogenes in both, cervical tissue and serum. This work demonstrates the significance of a single E₂ stimulation and the expression of the HPV E7 oncoprotein in the early stage of cervical carcinogenesis. In addition, we provide strong evidence about Kcnma1 oncogene as a target gene of miR-218 and that both could be used as early circulating biomarkers of CC.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":"e70065"},"PeriodicalIF":2.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669213","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":"Characterizing the Role of Endocannabinoid Receptor Cnr1 in Mouse Ovarian Granulosa Cells.","authors":"Jasmine Randhawa, Ejimedo Madogwe, Aire McCall, Jaswinder Singh, Raj Duggavathi","doi":"10.1002/cbf.70070","DOIUrl":"https://doi.org/10.1002/cbf.70070","url":null,"abstract":"<p><p>The endocannabinoid receptors Cnr1 and Cnr2 have been found in reproductive organs such as the oviduct and uterus. These receptors bind to endocannabinoids, the arachinodoylethanolamine (AEA) and arachinodoylglycerol (2-AG), respectively. Both cannbinoid receptors have been investigated for their role in implantation and fertilization. However, not much is explored in terms of their role in ovarian granulosa cells. As these two receptors (especially Cnr1) have affinity towards the major component of Cannabis, tetrahydrocannabinol (THC), its usage raises concerns about the potential effects of THC on ovarian functions. Hence, it is important to characterize the role of endocannabinoid system in the ovarian granulosa cells. The objectives of this study were to use the mouse model to: (1) profile the expression pattern of the Cnr1 and Cnr2 and the endocannabinoid metabolizing enzymes (Faah and Mgll) in granulosa cells and (2) to determine the effect of the Cnr1 antagonist, AM251 on ovarian functions. We found that Cnr1 transcript abundance was higher (p < 0.05) at 4 h hCG than 24 h and 48 h eCG timepoints, whereas Cnr2 transcript decreased (p < 0.05) with follicular development. Conversely, Faah and Mgll transcripts were higher at 14 h hCG (p < 0.05) suggesting their upregulation after ovulation. The ovulation rate was lower in AM251 than vehicle-treated mice (p < 0.05), indicating that Cnr1 signaling may regulate ovulation. Further investigating the effect of AM251, we found that it significantly downregulated Ptgs2 and Pappa (p < 0.05). Overall, these data suggest that Cnr1, an important player in the endocannabinoid system, is important for ovulation.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":"e70070"},"PeriodicalIF":2.8,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677048","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":"Neutrophil Depletion Reduced the Relative Abundance of Unsaturated Long-Chain Fatty Acid Synthesis Microbiota and Intestinal Lipid Absorption","authors":"Xingyu Lu,&nbsp;Yike Xu,&nbsp;Yitong Liu,&nbsp;Fang Li,&nbsp;Qiong Feng,&nbsp;Chun Gao,&nbsp;Dan Liu,&nbsp;Li Zhou,&nbsp;Haizhen Yang,&nbsp;Ji Zhang,&nbsp;Fengmei Cui,&nbsp;Qiu Chen","doi":"10.1002/cbf.70060","DOIUrl":"https://doi.org/10.1002/cbf.70060","url":null,"abstract":"<div>\u0000 \u0000 <p>As immune cells, neutrophils serve as the first line of defense against infections; however, the mechanism by which neutrophils regulate lipid metabolism is unknown. The neutrophil depletion group was treated with 100 μg InVivoMAb anti-mouse Ly6G 6 times, whereas the control group mice were intraperitoneally injected with the same quantity of InVivoMAb rat IgG2a. Body fat content, triglycerides (TGs), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) in the jejunum and ileum, as well as 9 long-chain fatty acids (LCFAs) in the intestinal contents were significantly decreased. Furthermore, genes involved in the absorption of lipids in each segment of the intestine also showed decreased expression. Neutrophil-depletion and control models were administered 25 μCi of ³H-cholesterol by gavage. The distribution of ³H cholesterol in the intestinal segment, heart, liver, serum, and feces was not altered by anti-Ly6G antibodies. Metagenomics was applied to investigate uncultured microorganisms in the intestinal contents to identify bacteria containing lipid metabolism genes. At the species level, 12 bacteria were involved in unsaturated LCFA synthesis, among which 2 increased and 10 decreased. The overall relative abundance of these bacteria decreased from 3.102% to 0.734%. Many genes involved in lipid metabolism were also reduced as a result, such as fatty acid synthase and peroxisome proliferator-activated receptor γ. In conclusion, neutrophil depletion does not affect intestinal lipid absorption in the diet but leads to a decrease in the overall relative abundance of gut bacteria involved in unsaturated LCFA synthesis. Consequently, intestinal lipid synthesis and absorption are reduced.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513469","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":"Recent Advances in Anti-Aging Therapeutic Strategies Targeting DNA Damage Response and Senescence-Associated Secretory Phenotype-Linked Signaling Cascade","authors":"Jawad Nadeem,&nbsp;Razia Sultana,&nbsp;Amna Parveen,&nbsp;Sun Yeou Kim","doi":"10.1002/cbf.70046","DOIUrl":"https://doi.org/10.1002/cbf.70046","url":null,"abstract":"<div>\u0000 \u0000 <p>Aging is considered the contributory accumulation of abruptions occurring through cell signaling cascades, which ultimately cause changes in physical functions, cell fate, and damage across all organ systems. DNA damage response (DDR) also occurs through telomere shortening, tumor formation, mitochondrial dysfunction, and so forth. Cellular aging occurs through cell cycle arrest, which is the result of extended DDR cascade signaling networks via MDC1, 53BP1, H2AX, ATM, ARF, P53, P13-Akt, BRAF, Sirtuins, NAD + , and so forth. These persistent cell cycle arrests initiated by DDR and other associated stress-induced signals promote a permanent state of cell cycle arrest called senescence-associated secretory phenotype (SASP). However, cellular aging gets accelerated with faulty DNA repair systems, and the produced senescent cells further generate various promoting contributors to age-related dysfunctional diseases including SASP. Any changes to these factors contribute to age-related disease development. Therefore, this review explores anti-aging factors targeting DDR and SASP regulation and their detailed signaling networks. In addition, it allows researchers to identify anti-aging targets and anti-aging therapeutic strategies based on identified and nonidentified targets.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143489985","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":"Matrix Stiffness Regulates Interleukin-10 Secretion in Human Microglia (HMC3) via YAP-Mediated Mechanotransduction","authors":"Xue Fang,&nbsp;Haiying Jia,&nbsp;Shaoshan Pan,&nbsp;Qian Liu,&nbsp;Qian Wang,&nbsp;Ye Feng,&nbsp;Weiping Ding,&nbsp;Tianzhi Luo","doi":"10.1002/cbf.70061","DOIUrl":"https://doi.org/10.1002/cbf.70061","url":null,"abstract":"<div>\u0000 \u0000 <p>Microglia, as resident immune cells in the brain, adhere to the extracellular matrix and typically exhibit anti-inflammatory polarization under normal physiological conditions. Despite their pivotal roles, the regulatory effects of extracellular matrix properties on microglial function and the associated molecular mechanisms remain inadequately understood. Here, we elucidate how matrix stiffness modulates interleukin-10 (IL-10) secretion in human microglia (HMC3) via yes-associated protein (YAP)-mediated mechanotransduction. Using soft collagen Ⅰ-coated hydrogels, we observed a substantial reduction in IL-10 secretion, accompanied by a decrease in the expression and nuclear localization of YAP compared to cells adhered to glass substrates. With increasing hydrogel substrate stiffness, the expression and nuclear localization of YAP were enhanced, leading to an elevated secretion of IL-10. Subsequently, to further investigate the relationship between YAP and IL-10, we performed YAP depletion experiments, which revealed that nuclear exclusion of YAP suppressed IL-10 secretion. Interestingly, overexpression of YAP in microglia did not markedly affect IL-10 levels. We seeded YAP-knockdown microglia onto hydrogels of varying stiffness, and no significant differences were observed in IL-10 secretion. Our findings suggested that cytoskeletal polymerization was crucial for the regulation of IL-10 secretion mediated by YAP. Given the crucial role of IL-10 in the tumor microenvironment, we further found shYAP-microglia attenuated the pro-proliferative effect of microglia on gliomas. Besides, when YAP was silenced, actin of human microglia decreased, and their contractility was weakened. In summary, this study identifies YAP as a pivotal molecule in controlling cytokine secretion and sensing matrix stiffness in microglia. These insights offer potential therapeutic avenues for glioma treatment by targeting YAP-mediated pathways in microglial cells.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 3","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143497110","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":"Cell Bio Notes: A New Article Type for Cell Biochemistry and Function","authors":"Raphael Gaudin,&nbsp;Robert J. Heath","doi":"10.1002/cbf.70062","DOIUrl":"https://doi.org/10.1002/cbf.70062","url":null,"abstract":"","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475522","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":"The Influence of Cyanidin-3-Glucoside on the Modulation of Immune Cell Responses by Mesenchymal Stem Cell-Conditioned Medium","authors":"Sumara de Freitas,&nbsp;Edson Naoto Makiyama,&nbsp;Bruna Roberta Oliveira Neves,&nbsp;Iolanda Silva Rafael Pizzolato Cezar,&nbsp;Carlos Eduardo da Silva Gonçalves,&nbsp;Marcelo Macedo Rogero,&nbsp;Ricardo Ambrósio Fock","doi":"10.1002/cbf.70059","DOIUrl":"https://doi.org/10.1002/cbf.70059","url":null,"abstract":"<div>\u0000 \u0000 <p>Mesenchymal stem cells (MSCs) are emerging as promising therapeutic agents due to their immunomodulatory effects, primarily mediated via paracrine signaling. Similarly, anthocyanins, such as cyanidin-3-glucoside (C3G), have demonstrated significant anti-inflammatory properties. In this context, this study investigated the immunomodulatory potential of C3G on MSCs, and subsequent effects on macrophage and lymphocyte responses. Cytotoxicity assays identified 50 µM as the highest nontoxic C3G concentration for MSCs. Flow cytometry confirmed that C3G treatment did not affect MSC viability or cell cycle distribution, even under LPS stimulation. Cytokine production by MSCs was evaluated after treatment with C3G and LPS. While no significant changes were observed in IL-6, IL-10, TGF-β, or PGE₂ levels, IL-1β production was significantly reduced in LPS-stimulated MSCs treated with C3G. Protein expression analysis revealed decreased NFκB phosphorylation in LPS-stimulated MSCs treated with C3G, with no changes detected in STAT-3 or PCNA expression. The immunomodulatory effects of MSC-derived conditioned media on macrophages and lymphocytes were also assessed. In LPS-stimulated macrophages, conditioned media from MSCs reduced the production of IL-1β, IL-6, and IL-12. Interestingly, conditioned media from C3G-treated MSCs specifically decreased TNF-α levels, enhanced IL-10 secretion, and further inhibited NFκB phosphorylation. In LPS-stimulated lymphocytes, conditioned media from C3G-treated MSCs suppressed IL-2 production while increasing IL-10 levels. In summary, these findings demonstrate that conditioned media from C3G-treated MSCs modulates immune cell responses more effectively than C3G alone. C3G influences the paracrine activity of MSCs, resulting in a shift in the secretory profile and subsequent effects on immune cell behavior.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431398","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}