Cell Biology International最新文献_第2页

YTHDF1-Mediated m⁶A Methylation of GLUT1 Promotes Progress and Suppresses Propranolol Sensitivity in Infantile Hemangioma. ythdf1介导的GLUT1 m6A甲基化促进婴儿血管瘤的进展并抑制心得安敏感性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-02 DOI: 10.1002/cbin.70059

Yunfeng Du, Pengyuan Li, Xianghong Du

{"title":"YTHDF1-Mediated m6A Methylation of GLUT1 Promotes Progress and Suppresses Propranolol Sensitivity in Infantile Hemangioma.","authors":"Yunfeng Du, Pengyuan Li, Xianghong Du","doi":"10.1002/cbin.70059","DOIUrl":"https://doi.org/10.1002/cbin.70059","url":null,"abstract":"Early intervention for infantile hemangioma (IH) typically involves the use of the first-line drug propranolol, which can be taken orally or applied topically. However, approximately 10% of patients develop resistance, highlighting the need to elucidate the underlying molecular mechanisms. This study found that the expression of glucose transporter 1 (GLUT1) was significantly increased in IH tissues. Knockdown of GLUT1 significantly inhibited the cell viability, colony formation, and angiogenesis of HemEC cells. Moreover, high GLUT1 levels caused insensitivity to propranolol treatment in IH as HemEC cells showed few significant changes to intracellular GLUT1 protein expression and glycolysis level upon treatment with propranolol, while overexpression of GLUT1 promoted colony formation and increased the IC50 value of HemEC cells with propranolol treatment. The YT521-B homology domain family protein 1 (YTHDF1), an m6A reader in mRNA, was significantly increased in IH tissues compared with normal adjacent tissues. MeRIP-qPCR results showed that YTHDF1 binds to GLUT1 mRNA and promoted its stability and translation efficiency, resulting in GLUT1 upregulation, thereby inhibiting the sensitivity of IH to propranolol. Additionally, YTHDF1 overexpression promoted the ability of colony formation and increased the IC50 value of HemEC cells with propranolol treatment. However, this promotion was reversed by knockdown of GLUT1. Collectively, our results demonstrated that YTHDF1-mediated m6A recognition of GLUT1 is vital in IH development and propranolol insensitivity. The YTHDF1/GLUT1 axis may serve as a potential target for inhibiting IH progression from aggravating and overcoming propranolol resistance in IH.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539144","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}

引用次数: 0

CCP1 Inhibits Pulmonary Fibrosis by Suppressing Fibrotic Progression Through the EIF4B/PI3K/AKT Pathways. CCP1通过EIF4B/PI3K/AKT通路抑制肺纤维化进展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-01 DOI: 10.1002/cbin.70051

Qiang Ren, Yifei Pan, Zhennan Tian, Guiwei Jiao, Xiaomin Liu

{"title":"CCP1 Inhibits Pulmonary Fibrosis by Suppressing Fibrotic Progression Through the EIF4B/PI3K/AKT Pathways.","authors":"Qiang Ren, Yifei Pan, Zhennan Tian, Guiwei Jiao, Xiaomin Liu","doi":"10.1002/cbin.70051","DOIUrl":"https://doi.org/10.1002/cbin.70051","url":null,"abstract":"Pulmonary fibrosis (PF), particularly idiopathic pulmonary fibrosis, is a chronic and fatal disease. However, the precise pathogenic mechanisms underlying this condition remain elusive. We employed LASSO regression and random forest analyses, combined with expression profiling in TGFβ1-induced MRC-5 cells and bleomycin-induced PF mouse models, to identify differentially expressed genes. These analyses revealed that cytoplasmic carboxypeptidase 1 (CCP1) was significantly downregulated in fibrotic conditions. Relevant signaling pathways were further identified through RNA sequencing (RNA-seq). Subsequent functional studies were conducted using qRT-PCR, western blot, hematoxylin and eosin (HE) staining, Masson's trichrome staining, immunohistochemistry (IHC), immunofluorescence, scratch assays, EdU assays, RNA interference, and co-immunoprecipitation (co-IP). Functional studies revealed that CCP1 knockdown promoted cell migration, proliferation, and the transformation of MRC-5 cells into a fibrotic phenotype, as evidenced by increased expression of fibrosis-associated markers (FN1, COL 1α1, and ACTA2) and dysregulated expression of apoptosis-related markers (BCL2 and BAX). Conversely, CCP1 overexpression inhibited these processes. CCP1 was discovered to inhibit the PI3K/AKT signaling pathway by binding to eukaryotic initiation factor 4B (EIF4B). Overexpression of EIF4B activated the fibrotic process and interacted with c-Myc. In vivo studies further demonstrated that CCP1 inhibited PF by suppressing EIF4B to inhibit the PI3K/AKT signaling pathway. In summary, our results demonstrate that CCP1 inhibits the development of PF by suppressing the EIF4B/PI3K/AKT axis. This study offers new perspectives into the pathogenesis of PF and underscores CCP1 as a potential therapeutic target for managing this condition.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539142","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}

引用次数: 0

The Role of IL-6, IL-10 and CRP in Gastrointestinal Cancers. IL-6、IL-10和CRP在胃肠道肿瘤中的作用。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-01 DOI: 10.1002/cbin.70050

Reyhaneh Yarmohammadi, Mina Noroozbeygi, Kimia Didehvar, Aria Rastin, Faezeh Ataei, Mohammad Reza Atashzar, Sahar Shomeil Shushtari

{"title":"The Role of IL-6, IL-10 and CRP in Gastrointestinal Cancers.","authors":"Reyhaneh Yarmohammadi, Mina Noroozbeygi, Kimia Didehvar, Aria Rastin, Faezeh Ataei, Mohammad Reza Atashzar, Sahar Shomeil Shushtari","doi":"10.1002/cbin.70050","DOIUrl":"https://doi.org/10.1002/cbin.70050","url":null,"abstract":"Gastrointestinal (GI) cancers represent a major global health burden, significantly impacts the digestive system. Recent research has focused on the relationship between interleukin-6 (IL-6), interleukin-10 (IL-10), and C-reactive protein (CRP) to deepen understanding of GI cancer-including esophageal, gastric, pancreatic, hepatobiliary, and colorectal cancers-pathogenesis and to enhance diagnostic and therapeutic strategies. Elevated levels of IL-6, IL-10, and CRP have been associated with advanced disease stages and poor prognosis, underscoring their potential utility as biomarkers for disease progression and outcome prediction. Moreover, these markers appear to modulate the sensitivity of GI cancer cells to chemotherapy, suggesting that their assessment in serum and tissue samples could aid therapeutic decision-making and predict treatment responses. In addition to their diagnostic and prognostic value, IL-6, IL-10, and CRP are being investigated as targets for preventive strategies. These findings highlight the potential role of anti-inflammatory interventions in chemoprevention. Overall, studying the interplay among IL-6, IL-10, and CRP has yielded valuable insights into the molecular mechanisms driving GI cancer development and progression. Continued research is essential to fully elucidate these complex interactions and to translate these findings into effective clinical applications for the management of GI malignancies.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539143","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}

引用次数: 0

CALR Type 1-Like Mutations Increase Endoplasmic Reticulum Free Ca²⁺ and Induce ERK1/2 Activation Independent of Thrombopoietin Receptor Activation. CALR 1型样突变增加内质网游离Ca2+并诱导ERK1/2激活，不依赖于血小板生成素受体的激活。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-30 DOI: 10.1002/cbin.70053

Mifra Faiz, Caitlin Dunstan-Harrison, Elizabeth C Ledgerwood

{"title":"CALR Type 1-Like Mutations Increase Endoplasmic Reticulum Free Ca2+ and Induce ERK1/2 Activation Independent of Thrombopoietin Receptor Activation.","authors":"Mifra Faiz, Caitlin Dunstan-Harrison, Elizabeth C Ledgerwood","doi":"10.1002/cbin.70053","DOIUrl":"https://doi.org/10.1002/cbin.70053","url":null,"abstract":"Calreticulin is a multifunctional protein found in the endoplasmic reticulum lumen that is important for calcium homeostasis and glycoprotein folding. Mutations in exon 9 of the CALR gene are the second most common genetic cause of myeloproliferative neoplasms. CALR-mutated megakaryocyte proliferation in myeloproliferative neoplasms involves cytokine-independent constitutive activation of JAK/STAT signaling caused by binding of mutant calreticulin to the thrombopoietin receptor. However, whether the partial or complete removal of wildtype calreticulin from the endoplasmic reticulum has additional effects on megakaryocyte biology is not clear. To explore the impact of calreticulin mutations independent of thrombopoietin receptor signaling we generated type 1-like CALR mutations in K-562 cells, which do not express the thrombopoietin receptor. We confirmed that the loss of endoplasmic reticulum-retention KDEL motif causes the majority of mutant calreticulin to be secreted from cells. The CALR mutated cells have higher endoplasmic reticulum free Ca2+ but basal cytosolic Ca2+ is unchanged. Cells in which the KDEL endoplasmic reticulum retention motif was lost from all CALR alleles had increased ERp57 expression however the unfolded protein response was not induced. The calreticulin mutated cells also showed elevated basal phosphorylation of ERK1/2. Overall, these results suggest that the phenotype of type 1 CALR mutated myeloproliferative neoplasms is not solely due to cytokine independent activation of the thrombopoietin receptor by the mutant calreticulin, and that increased endoplasmic reticulum Ca2+ and/or basal ERK1/2 activation may contribute to the abnormal megakaryocyte proliferation characteristic of CALR mutant myeloproliferative neoplasms.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526536","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}

引用次数: 0

SIRT7-Mediated MVP Desuccinylation Facilitates Tongue Squamous Cell Carcinoma Progression by Activating JAK2/STAT3 Pathway. sirt7介导的MVP去琥珀酰化通过激活JAK2/STAT3通路促进舌鳞状细胞癌进展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-30 DOI: 10.1002/cbin.70048

Zhuo Zhang, Tingting Guo, Xiangyu Zhao

{"title":"SIRT7-Mediated MVP Desuccinylation Facilitates Tongue Squamous Cell Carcinoma Progression by Activating JAK2/STAT3 Pathway.","authors":"Zhuo Zhang, Tingting Guo, Xiangyu Zhao","doi":"10.1002/cbin.70048","DOIUrl":"https://doi.org/10.1002/cbin.70048","url":null,"abstract":"Major vault protein (MVP) plays a contributing role in multifarious cancers, and then its role in Tongue squamous cell carcinoma (TSCC) is uncomprehending. This study aimed to investigate the regulatory effect of MVP on malignant behavior of TSCC cells and its mechanism. We first pointed out the abnormal upregulation of MVP in tumor tissues by immunohistochemistry, western blot, and reverse transcription-quantitative polymerase chain reaction assays. Depletion of MVP hindered TSCC cell viability, migration, and invasion and accelerated apoptosis. Mechanistically, depletion of MVP inactivated Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway. Coumermycin A1 (CA1), a JAK2 agonist, was used to trigger JAK2/STAT3 signaling. Functional experiments demonstrated that CA1 significantly counteracted the inhibitory effects of MVP silencing on cell proliferation, invasion, and migration, as well as the stimulatory effects of MVP silencing on cell apoptosis. Moreover, we discovered that MVP undergoes succinylation and identified Sirtuin 7 (SIRT7) as the desuccinylase for MVP. Addition of SIRT7 promoted the protein stability of MVP in TSCC cells. Further, addition of MVP expedited the viability, migration, and invasion and suppressed apoptosis of TSCC cells, which was partly neutralized following depleted SIRT7. Our findings revealed that MVP desuccinylated by SIRT7 accelerated TSCC progression via regulating JAK2/STAT3 signaling.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526537","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}

引用次数: 0

Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1 表没食子儿茶素-3-没食子酸酯通过调节厚壁菌门抑制胃分泌胰岛素样生长因子-1来减缓良性前列腺增生的发展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-24 DOI: 10.1002/cbin.70032

Tianye Yang, YiQun Shao, Zhong Wang, Chong Liu, Meng Gu

{"title":"Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1","authors":"Tianye Yang, YiQun Shao, Zhong Wang, Chong Liu, Meng Gu","doi":"10.1002/cbin.70032","DOIUrl":"10.1002/cbin.70032","url":null,"abstract":"<div>\u0000 \u0000 Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota—particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio—promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed apoptosis via PI3K/AKT/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/AKT/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes–IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary polyphenols in metabolic urological disorders.</div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"952-964"},"PeriodicalIF":3.3,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474079","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}

引用次数: 0

Tangzhiqing Exacerbates Oxidized Low-Density Lipoprotein-Induced Cell Pyroptosis Through Activation of NLRP3 Inflammasome in Human Umbilical Vein Endothelial Cells. 唐志清通过激活人脐静脉内皮细胞NLRP3炎性体加重氧化性低密度脂蛋白诱导的细胞热亡。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-19 DOI: 10.1002/cbin.70044

Rui Chen, Zhihuan Zhou, Zhihui Song, Wanying Feng, Xinya Ding, Han Zhang, Yi Wang

{"title":"Tangzhiqing Exacerbates Oxidized Low-Density Lipoprotein-Induced Cell Pyroptosis Through Activation of NLRP3 Inflammasome in Human Umbilical Vein Endothelial Cells.","authors":"Rui Chen, Zhihuan Zhou, Zhihui Song, Wanying Feng, Xinya Ding, Han Zhang, Yi Wang","doi":"10.1002/cbin.70044","DOIUrl":"https://doi.org/10.1002/cbin.70044","url":null,"abstract":"Atherosclerosis (AS) is a chronic and progressive inflammatory condition affecting arterial walls. It is widely accepted that the deposition of low-density lipoprotein (LDL) and its adverse impact on endothelial cells (ECs) play a pivotal role in the development of AS. Specifically, oxidized LDL (ox-LDL) has been validated as a trigger for inducing pyroptosis in ECs, thereby contributing significantly to intima inflammation and AS progression. However, the underlying molecular mechanisms require further investigation. In this study, we demonstrated that ox-LDL significantly upregulates the expression of pyrin domain-containing 3 (NLRP3) protein levels in ECs. This upregulation is associated with increased caspase-1 cleavage, interleukin-1β (IL-1β) maturation, and lactate dehydrogenase (LDH) release. Moreover, ox-LDL also upregulates the expression of ASC, caspase-1, GSDMD, IL-1β, and IL-18 proteins. The inhibition of NLRP3-specific inhibitor MCC950 or caspase-1-specific inhibitor VX-765 effectively suppressed the expression of cellular pyroptosis-associated proteins. Our findings highlight the crucial role of Tangzhi Qing (TZQ) in regulating ox-LDL-induced pyroptosis and inflammation through the activation of the NLRP3 inflammasome. This suggests that NLRP3 inflammasome could serve as a promising therapeutic target for mitigating diseases associated with atherosclerosis.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324514","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}

引用次数: 0

Glutathione as a Therapeutic Agent for OxLDL-Induced Endothelial Dysfunction and Atherosclerosis Prevention. 谷胱甘肽作为oxldl诱导的内皮功能障碍和动脉粥样硬化预防的治疗剂。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-13 DOI: 10.1002/cbin.70047

Chathuri Kaushalya Marasinghe, Jae-Young Je

{"title":"Glutathione as a Therapeutic Agent for OxLDL-Induced Endothelial Dysfunction and Atherosclerosis Prevention.","authors":"Chathuri Kaushalya Marasinghe, Jae-Young Je","doi":"10.1002/cbin.70047","DOIUrl":"https://doi.org/10.1002/cbin.70047","url":null,"abstract":"Endothelial dysfunction is a critical contributor to atherosclerosis and cardiovascular diseases, driven by oxidative stress and inflammation induced by oxidized low-density lipoprotein (oxLDL). This study investigates the protective effects of reduced glutathione (GSH) against oxLDL-induced endothelial dysfunction using human umbilical vein endothelial cells (HUVECs) as an in vitro model. Our findings demonstrate that oxLDL exposure significantly reduces cell viability, induces oxidative stress, and promotes endothelial injury by upregulating LOX-1 expression, decreasing nitric oxide (NO) production, and impairing endothelial nitric oxide synthase (eNOS) activity. Pretreatment with GSH effectively restores cell viability, reduces ROS generation, suppresses LOX-1 expression, and preserves NO bioavailability by maintaining eNOS activity. Additionally, GSH enhances the antioxidant defense system by increasing superoxide dismutase, catalase, and glutathione peroxidase levels while reducing lipid peroxidation, as indicated by lower malondialdehyde content. Beyond its antioxidative properties, GSH exhibits antiapoptotic effects by restoring the Bax/Bcl-2 balance, inhibiting cytochrome C release, and suppressing caspase-3 activation, thereby preventing mitochondrial membrane depolarization. Furthermore, GSH mitigates endothelial inflammation by downregulating intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression. These findings highlight GSH's potential as a therapeutic agent for protecting endothelial cells against oxLDL-induced dysfunction by alleviating oxidative stress, apoptosis, and inflammation, ultimately contributing to the prevention of atherosclerosis progression.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282669","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}

引用次数: 0

Menstrual Blood‑Derived Endometrial Stem Cells Protect the Integrity of the Intestinal Barrier by Inhibiting the NF-κB/Snail Signaling Pathway. 经血来源的子宫内膜干细胞通过抑制NF-κB/蜗牛信号通路保护肠道屏障的完整性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-07 DOI: 10.1002/cbin.70040

Tao Ruan, Jiaming Han, Chengxu Xue, Haiyan Liang, Juntang Lin

{"title":"Menstrual Blood‑Derived Endometrial Stem Cells Protect the Integrity of the Intestinal Barrier by Inhibiting the NF-κB/Snail Signaling Pathway.","authors":"Tao Ruan, Jiaming Han, Chengxu Xue, Haiyan Liang, Juntang Lin","doi":"10.1002/cbin.70040","DOIUrl":"https://doi.org/10.1002/cbin.70040","url":null,"abstract":"Inflammatory bowel diseases (IBDs), including Crohn's disease (CD) and ulcerative colitis (UC) are chronic recurrent nonspecific intestinal disease. Current IBD therapeutics cannot fundamentally change the natural course of IBD. Therefore, it is of great significance to find new treatment strategies for IBD. Preclinical and clinical studies have shown that mesenchymal stem cells (MSCs) are a promising therapeutic approach. However, the mechanism by which MSCs alleviate colitis and how MSCs affect intestinal mucosal barrier is still unclear. LPS-exposed human colonic epithelial cancer cell lines Caco2 and HT29. Dextran sulfate sodium (DSS)-induced IBD mouse were treated with MenSCs. We found that LPS downregulates intercellular junction proteins and induces the production of inflammatory cytokines in intestinal epithelial cells. MenSCs reduced paracellular permeability and restored barrier integrity in Caco2 cells. In Vivo, MenSCs mitigated DSS-induced colitis in mice by reducing body weight loss, colonic shortening, and disease activity index scores and by inhibiting the expressions of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α. MenSCs increased the expression of TJ proteins, improved the destruction of tight junction (TJ) structures, and reduced intestinal epithelial permeability. Furthermore, MenSCs could inhibit NF-κB p65 phosphorylation and the expression of Snail and prevent Snail nuclear localization, thereby maintaining tight and adherens junctions. Our findings demonstrate that MenSCs alleviate intestinal inflammation and enhance barrier function by suppressing the NF-κB/Snail signaling axis, offering a promising therapeutic strategy for inflammatory bowel diseases.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246602","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}

引用次数: 0

BUBR1 Facilitated Nerve Regeneration by Modulating STAT3 Phosphorylation, Thereby Alleviating HIE in Neonatal Mice BUBR1通过调节STAT3磷酸化促进神经再生，从而减轻新生小鼠HIE。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-06-05 DOI: 10.1002/cbin.70033

Shuting Chang, Weiqing Huang, Guinan Li, Mi Zhang, Xionghui Wu

{"title":"BUBR1 Facilitated Nerve Regeneration by Modulating STAT3 Phosphorylation, Thereby Alleviating HIE in Neonatal Mice","authors":"Shuting Chang, Weiqing Huang, Guinan Li, Mi Zhang, Xionghui Wu","doi":"10.1002/cbin.70033","DOIUrl":"10.1002/cbin.70033","url":null,"abstract":"<div>\u0000 \u0000 Hypoxic-ischemic encephalopathy (HIE) represents a leading cause of morbidity and mortality among neonates. However, the underlying molecular mechanisms of HIE remain largely elusive. A HIE animal model was established, and neural stem cells (NSCs) underwent oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic HIE in vitro. The HIE-induced brain injury was evaluated using a battery of assessments, including the Morris water maze test, wire hanging test, cylinder test, TTC, TUNEL, IHC, and IF staining. Subsequently, the expressions of budding uninhibited by benzimidazoles related 1 (BUBR1) and signal transducer and activator of transcription 3 (STAT3) were examined using immunoblotting and qRT-PCR. Furthermore, the interaction between BUBR1 and STAT3 was confirmed through co-immunoprecipitation assays. BUBR1 was observed to be downregulated in both the HIE model and in NSCs subjected to OGD/R. Notably, the restoration of BUBR1 expression was found to alleviate the detrimental effects of HIE, primarily by facilitating nerve regeneration. Further investigation revealed that BUBR1 also mitigated OGD/R-induced apoptosis in NSCs. Mechanistically, BUBR1 was shown to regulate the phosphorylation of STAT3, a crucial transcription factor involved in cell survival and regeneration. Moreover, BUBR1 alleviated OGD/R-induced apoptosis of NSCs and promoted nerve regeneration to protect HIE by regulating STAT3 phosphorylation. BUBR1 facilitated nerve regeneration by modulating STAT3 phosphorylation, thereby alleviating HIE.\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 8","pages":"975-988"},"PeriodicalIF":3.3,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224431","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}

引用次数: 0