Journal of Cell Communication and Signaling最新文献

Notch NICD domains form biomolecular condensates 缺口NICD结构域形成生物分子凝聚体

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-26 DOI: 10.1002/ccs3.70039

Tana R. Gazdik, Anamaria Zavala, Henry A. Charlier Jr., Michael A. Detweiler, Jacob J. Crow, Tyler Lawton, David Oke, Saborni Sarker, Allan R. Albig

{"title":"Notch NICD domains form biomolecular condensates","authors":"Tana R. Gazdik, Anamaria Zavala, Henry A. Charlier Jr., Michael A. Detweiler, Jacob J. Crow, Tyler Lawton, David Oke, Saborni Sarker, Allan R. Albig","doi":"10.1002/ccs3.70039","DOIUrl":"https://doi.org/10.1002/ccs3.70039","url":null,"abstract":"Biomolecular condensates are a quickly emerging area of research that strongly impacts how we view the inner workings of the cell itself. Here, we explore the connection between the Notch signaling pathway and nuclear condensate localization. In this study, we hypothesize that activated Notch intracellular domain (NICD) fragments differentially localize into unique nuclear condensates. Using both overexpression and endogenous systems, our results reveal that N1ICD, N2ICD, and N4ICD efficiently localize into subnuclear bodies, whereas N3ICD inefficiently localizes into similar subnuclear puncta. These “notchosomes” appear to be unique because they do not colocalize with markers for other known nuclear puncta. In contrast, we find that N1ICD does colocalize with other known Notch-interacting proteins, including MAML-1, RBPj, AES1, and SKIP1, but not NACK1. Through deletion analysis of the N1ICD C-terminal tail, we identify multiple regions of mouse N1ICD that are necessary for localization into notchosomes, including sequences immediately C-terminal to the ankyrin domain and sequences within the transactivation domain. We also show that N1ICD localization into notchosomes may be important for N1ICD transcriptional activity from some, but not all, Notch-responsive promoters. Collectively, our results show that Notch NICD domains form nuclear localized biomolecular condensates that may be important for transcriptional activity.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144705567","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}

引用次数: 0

Cancer-associated fibroblasts-secreted lactate promotes RNA polymerase III subunit G-mediated epithelial–mesenchymal transition in non-small cell lung cancer by increasing m6A modification of zinc finger protein 384 癌相关成纤维细胞分泌乳酸通过增加锌指蛋白384的m6A修饰，促进非小细胞肺癌中RNA聚合酶III亚基g介导的上皮-间质转化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-25 DOI: 10.1002/ccs3.70037

Ping Li, Xing Yang, Hao Tang, Zhiping Zhou, Bin Liu

{"title":"Cancer-associated fibroblasts-secreted lactate promotes RNA polymerase III subunit G-mediated epithelial–mesenchymal transition in non-small cell lung cancer by increasing m6A modification of zinc finger protein 384","authors":"Ping Li, Xing Yang, Hao Tang, Zhiping Zhou, Bin Liu","doi":"10.1002/ccs3.70037","DOIUrl":"https://doi.org/10.1002/ccs3.70037","url":null,"abstract":"Most advanced non-small cell lung cancer (NSCLC) patients have metastasis, which poses great risks to their survival. As the most abundant components in the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) can induce epithelial–mesenchymal transition (EMT) to promote tumor. This study aimed to explore the potential molecular mechanisms of CAFs-mediated EMT in NSCLC. The gene expression was assessed using RT-qPCR, immunofluorescence, and Western Blot. Cells phenotypes were evaluated through CCK-8, scratch, and transwell assays, respectively. Lactate levels were measured with a commercial kit. The m6A level of zinc finger protein 384 (ZNF384) was measured using methylated RNA immunoprecipitation. The molecular interactions was checked using chromatin immunoprecipitation and dual luciferase reporter assay. ZNF384 was upregulated in NSCLC. ZNF384 knockdown suppressed NSCLC cell proliferation and inhibited EMT-related protein vimentin and Snail, but elevated E-Cadherin. Mechanistically, CAFs-secreted lactate promoted the H3K18 lactylation of methyltransferase-like 3 (METTL3) promoter region and further increased the m6A modification of ZNF384. ZNF384 promoted the transcription of RNA polymerase III subunit G (POLR3G) by binding to POLR3G promoter region. CAFs induced EMT in NSCLC cells by enhancing ZNF384 expression. Additionally, POLRG3 silencing counteracted the promoting effect of ZNF384 overexpression on EMT in NSCLC. CAFs facilitating cell proliferation and EMT by modulating the METTL3/ZNF384/POLR3G axis. It is suggested that CAFS-related TME could be an approach for treating NSCLC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144705456","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}

引用次数: 0

Y-box binding protein 1 stabilizes EP300 mRNA and promotes forkhead box C1 H3K27Ac to aggravate chondrocyte injury in osteoarthritis Y-box结合蛋白1稳定EP300 mRNA，促进叉头盒C1 H3K27Ac加重骨关节炎软骨细胞损伤

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-23 DOI: 10.1002/ccs3.70028

Jingyi Li, Gang Zhou, Te Chen, Qiao Lin, Qiupeng Yang

{"title":"Y-box binding protein 1 stabilizes EP300 mRNA and promotes forkhead box C1 H3K27Ac to aggravate chondrocyte injury in osteoarthritis","authors":"Jingyi Li, Gang Zhou, Te Chen, Qiao Lin, Qiupeng Yang","doi":"10.1002/ccs3.70028","DOIUrl":"https://doi.org/10.1002/ccs3.70028","url":null,"abstract":"Chondrocyte abnormalities play an important role in osteoarthritis (OA), and forkhead box C1 (FOXC1) expression is related to OA progression. Nonetheless, the molecular mechanisms underlying the action of FOXC1 in chondrocytes remain unclear. Rats were subjected to anterior cruciate ligament transection (ACLT) to establish an in vivo OA model, and chondrocytes were subjected to interleukin (IL)-1β to establish an in vitro OA model. Pathological changes in rat cartilage tissues were evaluated using hematoxylin–eosin and safranin O staining. H3K27Ac enrichment in the FOXC1 promoter was analyzed using chromatin immunoprecipitation. Interactions between EP300 and Y-box binding protein 1 (YBX1) were validated using RNA immunoprecipitation and RNA pull-down assay. The expression of YBX1, EP300, and FOXC1 was elevated in ACLT rats and IL-1β-induced chondrocytes. FOXC1 knockdown inhibited apoptosis and inflammatory response in IL-1β-induced chondrocytes. EP300 bound to FOXC1 promoter and promoted H3K27Ac enrichment in the FOXC1 promoter. Additionally, YBX1 bound to EP300 mRNA and enhanced EP300 mRNA stability. YBX1 overexpression promoted cell apoptosis and inflammation of IL-1β-induced chondrocytes, but was reversed by FOXC1 downregulation. YBX1 enhances EP300 mRNA stability and elevates FOXC1 expression by mediating FOXC1 H3K27Ac to promote IL-1β-induced chondrocyte apoptosis and inflammation, thereby exacerbating chondrocyte injury in OA.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70028","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144687950","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}

引用次数: 0

UBD-mediated glycolytic reprogramming promotes M2 macrophage polarization in ovarian cancer immune evasion ubd介导的糖酵解重编程促进卵巢癌免疫逃避中M2巨噬细胞极化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-21 DOI: 10.1002/ccs3.70034

Nana Zhang, Fengming Zhao, Hailong Chen, Juli Wang, Haiyan Li

{"title":"UBD-mediated glycolytic reprogramming promotes M2 macrophage polarization in ovarian cancer immune evasion","authors":"Nana Zhang, Fengming Zhao, Hailong Chen, Juli Wang, Haiyan Li","doi":"10.1002/ccs3.70034","DOIUrl":"https://doi.org/10.1002/ccs3.70034","url":null,"abstract":"Ovarian cancer (OC) is one of the most common malignant tumors in women, with immunotherapy resistance (ITR) being a major challenge. Glycolytic metabolic reprogramming has been shown to play a crucial role in the tumor immune microenvironment and immune evasion, yet the underlying mechanisms remain unclear. This study aims to investigate the role of Ubiquitin D (UBD) in OC immunotherapy, particularly its regulation of macrophage polarization through glycolytic metabolism. Using data from the Cancer Genome Atlas and Clinical Proteomic Tumor Analysis Consortium databases, combined with proteomics techniques, we analyzed the expression of UBD in OC tissues and its correlation with key glycolytic enzymes. Through lentiviral-mediated gene manipulation and in vivo mouse models, we evaluated the effects of UBD on macrophage polarization, glycolytic metabolism, and immunotherapy. The results indicate that UBD promotes M2 macrophage polarization through glycolytic reprogramming, enhancing immune evasion and ITR in OC. Inhibiting UBD or targeting glycolytic pathways may provide new strategies for improving OC immunotherapy.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144672966","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}

引用次数: 0

A comprehensive analysis of the relationship between inflammasomes and autophagy in human tumors: Recent developments 人类肿瘤中炎性小体与自噬关系的综合分析：最新进展

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-16 DOI: 10.1002/ccs3.70035

Sai Liu, Jingzhou Zhang

引用次数: 0

Beyond the tumor: Enhancing pancreatic cancer therapy through glutamine metabolism and innovative drug delivery 超越肿瘤：通过谷氨酰胺代谢和创新药物输送增强胰腺癌治疗

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-09 DOI: 10.1002/ccs3.70033

Min Su, Huan Qin, Jie Shen, Hao An, Yu Cao

{"title":"Beyond the tumor: Enhancing pancreatic cancer therapy through glutamine metabolism and innovative drug delivery","authors":"Min Su, Huan Qin, Jie Shen, Hao An, Yu Cao","doi":"10.1002/ccs3.70033","DOIUrl":"https://doi.org/10.1002/ccs3.70033","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) depends a lot on how it uses glutamine to grow quickly and stay alive. Oncogenic drivers such as KRAS, c-Myc, and HIF-1α increase how much glutamine gets taken up and broken down. Meanwhile, the bacteria in the gut and tumor itself also affect how much glutamine is available throughout the body and near the tumor. This impacts both how the tumor grows and how the immune system can detect and respond to it. Multiple strategies have emerged to disrupt this dependence: glutamine antagonists (DON and its prodrugs DRP-104, JHU-083), small-molecule glutaminase inhibitors (CB-839), antibody–drug conjugates targeting the ASCT2 transporter, and combination regimens pairing glutamine blockade with immune checkpoint inhibitors. Nanoparticle formulations—including pH-sensitive and PEGylated liposomes co-delivering DON and gemcitabine—enable targeted delivery and reduce off-target toxicity. Single-agent treatments do not work so well because the cells can adapt. They boost enzymes such as asparagine synthetase and increase how they burn fatty acids to make up for the lack of glutamine. To overcome these escape routes, future interventions must concurrently target compensatory pathways and integrate biomarker-driven patient selection. Combining glutamine-targeted agents with inhibitors of asparagine synthesis or lipid oxidation, guided by multi-omics profiling, promises a more durable therapeutic benefit and lays the groundwork for personalized treatment of PDAC.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144589549","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}

引用次数: 0

Sirtuin 2 regulates NOD-like receptor protein 3/nuclear factor kappa B axis to promote cartilage repair in osteoarthritis Sirtuin 2调节nod样受体蛋白3/核因子κ B轴促进骨关节炎软骨修复

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-07-03 DOI: 10.1002/ccs3.70031

Xiaotian Chen, Yining Song, Fan Zhang, Fangyan Hu, Zhenfei Ding, Jianzhong Guan

{"title":"Sirtuin 2 regulates NOD-like receptor protein 3/nuclear factor kappa B axis to promote cartilage repair in osteoarthritis","authors":"Xiaotian Chen, Yining Song, Fan Zhang, Fangyan Hu, Zhenfei Ding, Jianzhong Guan","doi":"10.1002/ccs3.70031","DOIUrl":"https://doi.org/10.1002/ccs3.70031","url":null,"abstract":"Osteoarthritis (OA) is a prevalent degenerative joint disease driven by inflammation and cartilage degradation. The NOD-like receptor protein 3 (NLRP3) inflammasome and nuclear factor kappa B (NF-κB) pathway are central to OA-associated inflammation. Sirtuin 2 (SIRT2), an NAD+-dependent deacetylase, regulates inflammation and oxidative stress but its role in OA is not fully understood. This study aims to elucidate how SIRT2 modulates the NLRP3/NF-κB signaling axis to promote cartilage repair in OA. In vivo and in vitro experiments were conducted using OA mouse models and chondrocyte cultures. Single-cell RNA sequencing was performed to identify differentially expressed genes, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. SIRT2's impact on NLRP3 and NF-κB was assessed using Western blotting (WB), real-time PCR, co-immunoprecipitation (Co-IP), and chromatin immunoprecipitation (ChIP-qPCR). SIRT2 was found to deacetylate NF-κB p65, inhibiting NLRP3 activation and reducing inflammatory cytokines. SIRT2 overexpression enhanced chondrocyte proliferation, DNA repair, and mitochondrial function while decreasing reactive oxygen species production. In vivo, SIRT2 significantly improved cartilage repair in OA mice with NLRP3 overexpression attenuating its protective effects. SIRT2 promotes cartilage repair in OA by regulating the NF-κB/NLRP3 axis, reducing inflammation and oxidative stress. This highlights SIRT2 as a potential therapeutic target for OA.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70031","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144550822","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}

引用次数: 0

Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification 核结合SET结构域1通过H3K36me2修饰上调kr<s:1> ppel样因子9/自噬相关14通路，减轻膝关节骨性关节炎软骨铁吊

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-29 DOI: 10.1002/ccs3.70027

Qinglei Yang, Rugang Li, Zhiqiang Hu, Wengang Zhu, Hongying Yu

{"title":"Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification","authors":"Qinglei Yang, Rugang Li, Zhiqiang Hu, Wengang Zhu, Hongying Yu","doi":"10.1002/ccs3.70027","DOIUrl":"https://doi.org/10.1002/ccs3.70027","url":null,"abstract":"Knee osteoarthritis (KOA) is a progressive disease featured by cartilage damage. This study attempts to explore the role of nuclear binding SET domain 1 (NSD1) in KOA cartilage ferroptosis, thereby finding a new target for KOA treatment. Pathological changes, cartilage damage, and inflammatory cytokine levels in the established KOA mouse model were assessed. Primary mouse knee chondrocytes were separated, cultured, and challenged with IL-1β to establish in vitro KOA models. Cell viability was determined, Reactive oxygen species levels and ferroptosis-related factors were measured after interventions with NSD1, krüppel-like factor 9 (KLF9), and acyl-CoA synthetase long-chain family member 4 (ATG14). Furthermore, the enrichment of NSD1 and H3K36me2 on the KLF9 promoter as well as the enrichment of KLF9 on the ATG14 promoter was analyzed. Binding site between KLF9 and ATG14 promoter was assessed. NSD1 was downregulated in KOA mouse cartilage tissues and IL-1β-challenged chondrocytes. KOA severity was alleviated, chondrocyte viability was promoted, and ferroptosis was quenched after NSD1 overexpression. NSD1 strengthened H3K36me2 to upregulate KLF9 expression, and KLF9 transcriptionally activated ATG14 expression. KLF9 or ATG14 knockdown could both partially reverse the protective role of NSD1 overexpression on KOA cartilage ferroptosis. NSD1 enhanced KLF9 expression to improve ATG14 expression via H3K36me2 modification, thus relieving KOA cartilage ferroptosis.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144514678","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}

引用次数: 0

Hypoxic adipose-derived stem cell exosomes as carriers of miR-100-5p to enhance angiogenesis and suppress inflammation in diabetic foot ulcers 低氧脂肪来源的干细胞外泌体作为miR-100-5p的载体，在糖尿病足溃疡中促进血管生成和抑制炎症

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-27 DOI: 10.1002/ccs3.70018

Hong Liu, Fei Hao, Bangtao Chen

{"title":"Hypoxic adipose-derived stem cell exosomes as carriers of miR-100-5p to enhance angiogenesis and suppress inflammation in diabetic foot ulcers","authors":"Hong Liu, Fei Hao, Bangtao Chen","doi":"10.1002/ccs3.70018","DOIUrl":"https://doi.org/10.1002/ccs3.70018","url":null,"abstract":"Diabetic foot ulcer (DFU) is a severe diabetes complication characterized by impaired angiogenesis and chronic inflammation, leading to delayed wound healing. Exosomes (Exo) derived from hypoxic adipose-derived stem cells (H-ADSCs-Exo) show potential as therapeutic carriers. This study investigates the role of H-ADSCs-Exo carrying miR-100-5p in DFU healing. ADSCs were isolated, characterized, and their Exo analyzed via transmission electron microscopy, nanoparticle tracking analysis, and Western blot. Transcriptome sequencing identified miR-100-5p as a key modulator of angiogenesis and inflammation. In vitro, H-ADSCs-Exo enhanced human umbilical vein endothelial cell and fibroblast proliferation, migration, and tube formation. In a rat DFU model, H-ADSCs-Exo administration reduced ulcer size, increased angiogenesis (VEGF/CD31 expression), and decreased inflammatory markers (TNF-α, IL-6). miR-100-5p overexpression further amplified these effects, demonstrating its critical role in Exo-mediated healing. These findings highlight the therapeutic potential of H-ADSCs-Exo in DFU treatment, offering insights into cell signaling mechanisms and paving the way for miRNA-based regenerative therapies.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144503000","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}

引用次数: 0

GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17 GRIN2B通过与KIF17相互作用减轻妊娠中期七氟醚暴露诱导的大鼠神经干细胞的早期分化

IF 3.6 3区生物学

Journal of Cell Communication and Signaling Pub Date : 2025-06-24 DOI: 10.1002/ccs3.70024

Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li

{"title":"GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17","authors":"Mengyuan Li, Yan Hu, Zhonggui Cheng, Qianqian Li","doi":"10.1002/ccs3.70024","DOIUrl":"https://doi.org/10.1002/ccs3.70024","url":null,"abstract":"General anesthetic exposure during pregnancy has neurotoxic effects on the developing brain, causing long-term cognitive dysfunction in the offspring. Sevoflurane exposure during mid-gestation results in premature differentiation of neural stem cells (NSCs), being the crucial factor affecting normal hippocampal functions and contributing to neurocognitive impairment. However, the related molecular mechanism remains unclear. For in vivo assays, pregnant rats were exposed to 3% sevoflurane once on gestational day 14 (G14) or 3 times on G13, 14, and 15 (2 h per day). For in vitro assays, primary rat NSCs were isolated from fetal hippocampus tissues at 24 and 72 h after birth and on postnatal day 28. NSCs were transfected with GRIN2B or KIF17 overexpression plasmids before exposure to 4.1% sevoflurane for one or three consecutive days (2 h per day). Multiple sevoflurane exposures during the mid-trimester triggered NSC premature differentiation and decreased GRIN2B and KIF17 expression in the hippocampus of offspring rats and primary rat NSCs. GRIN2B or KIF17 overexpression attenuated sevoflurane-induced NSC premature differentiation. GRIN2B interacted with KIF17, and KIF17 silencing reversed the inhibition of GRIN2B overexpression on NSC early differentiation. GRIN2B alleviates NSC premature differentiation induced by repeated mid-gestational sevoflurane exposure via interaction with KIF17.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"19 2","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ccs3.70024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472808","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}

引用次数: 0