Cytotechnology最新文献

{"title":"Astragalin inhibits the proliferation of high-risk HPV-positive cervical epithelial cells and attenuates malignant cervical lesions.","authors":"Wei Zeng, Li Chen","doi":"10.1007/s10616-025-00742-6","DOIUrl":"10.1007/s10616-025-00742-6","url":null,"abstract":"<p><p>High-risk human papillomavirus (HPV), especially HPV16 and HPV18, are closely linked to the onset of cervical cancer (CC). Astragalin (AST), a bioactive flavonoid, has been reported to impede CC HeLa cell proliferation. Nevertheless, the mechanism by which AST exerts its tumor-suppressive role in CC remains unclear. HeLa (HPV18-positive) and CaSki (HPV16-positive) cells were exposed to various concentrations of AST. CCK-8 assay, flow cytometry analysis, wound healing, and Transwell assays were employed to examine the AST functions on CC cell aggressiveness. Protein levels were assessed by western blotting. Immunofluorescence staining was used to detect E6, E7, p53, and p-pRb expression. Animal experiments were performed to validate the anti-CC role in vivo. The results showed that AST dose-dependently impaired HeLa and CaSki cell viability and elicited G1 cell cycle arrest. AST restrained CC cell migration and invasiveness. AST inhibited the growth of HeLa-derived xenograft tumors in mice and repressed E6/E7 oncoprotein expression in CC cells and mouse tumor tissues. In conclusion, AST suppresses CC progression by downregulating E6/E7 oncoprotein expression to attenuate CC cell aggressiveness.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00742-6.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"80"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cartilage repair: unleashing PRP's potential in organoid models.","authors":"Mahsa Golshan, Hengameh Dortaj, Zeinab Omidi, Mehdi Golshan, Majid Pourentezari, Mehrdad Rajabi, Ali Rajabi","doi":"10.1007/s10616-025-00739-1","DOIUrl":"10.1007/s10616-025-00739-1","url":null,"abstract":"<p><p>Platelet-rich plasma (PRP) has emerged as a promising biological therapy in regenerative medicine due to its high concentration of growth factors and cytokines, which promote tissue healing and regeneration. In recent years, its application in cartilage tissue engineering has garnered significant attention. This study explores the synergistic interaction between PRP and cartilage organoids, a novel three-dimensional in vitro culture system that closely mimics the structural and functional properties of native cartilage. Cartilage organoids serve as a physiologically relevant model for studying cartilage development, disease progression, and regeneration. By integrating PRP with cartilage organoids, this review aims to enhance chondrogenesis, extracellular matrix synthesis, and cellular proliferation within the organoids. Emerging evidence suggests that PRP supplementation significantly improves chondrocyte viability, growth, and differentiation in cartilage organoids, thereby accelerating their maturation. This combination holds great potential for advancing cartilage repair strategies, providing a robust platform for preclinical studies, and paving the way for innovative therapeutic approaches for cartilage-related injuries and degenerative diseases. These key aspects-chondrogenesis, matrix synthesis, and cellular proliferation-were specifically selected due to their fundamental roles in cartilage tissue engineering and regeneration. Chondrogenesis is crucial for chondrocyte differentiation and maintenance, matrix synthesis ensures the structural integrity and functional properties of regenerated cartilage, and cellular proliferation supports tissue viability and repair. Addressing these factors is essential, as current cartilage regeneration strategies often suffer from limited long-term efficacy and inadequate extracellular matrix production. By elucidating the synergistic effects of PRP and cartilage organoids in these areas, this study seeks to bridge existing knowledge gaps and provide valuable insights for improving regenerative approaches in clinical applications, particularly for osteoarthritis and cartilage defects.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"86"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naringin regulates the cGAS-STING pathway to improve mitochondrial dysfunction and ferroptosis after myocardial ischemia-reperfusion injury.","authors":"Xinwei Zhang, Junjie He, Zhen Xu, Yanna Yang","doi":"10.1007/s10616-025-00762-2","DOIUrl":"10.1007/s10616-025-00762-2","url":null,"abstract":"<p><p>Myocardial ischemia-reperfusion injury (MI/RI) is a crucial complication of reperfusion treatment for myocardial infarction. Naringin (Nar) is a flavonoid with identified cardioprotective functions. This study aimed to explore the protective mechanisms of Nar against MI/RI, specifically focusing on its modulation of the cGAS-STING pathway. An H9c2 cardiomyocyte hypoxia/reoxygenation (H/R) injury model and an MI/R rat model were established. Our findings demonstrated that Nar, at a concentration of 480 μM, exhibited no cytotoxic effects on H9c2 cardiomyocytes and did not inhibit cell proliferation. Nar significantly reduced myocardial cell injury by improving mitochondrial function and decreasing oxidative stress, particularly the stress induced by a ferroptosis activator (Erastin). Additionally, the in vivo MI/R rat model further confirmed that Nar inhibited the activation of the cGAS-STING pathway, thereby attenuating myocardial injury. Collectively, Nar exerts protective effects against MI/RI by regulating mitochondrial dysfunction and ferroptosis, primarily through inhibition of the cGAS-STING pathway.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"103"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyaluronidase induces degenerative effects on intervertebral endplate cells via upregulation of PTGS2.","authors":"Zengxin Jiang, Yutong Gu","doi":"10.1007/s10616-025-00764-0","DOIUrl":"10.1007/s10616-025-00764-0","url":null,"abstract":"<p><p>Hyaluronic acid is widely recognized as a therapeutic target and is currently utilized in medical applications. However, the metabolism of HA during intervertebral disc degeneration has not been fully elucidated. The effects of hyaluronidase on the cartilage endplate remain unclear. The aim of this article is to explore the effects of hyaluronidase on cartilage endplate (CEP) cells and potential molecular mechanisms. Cartilage endplate cells were extracted from the intervertebral endplates of 4-week-old rats. These cells were then treated with hyaluronidase. Cell viability was detected using Cell Counting Kit-8. Cell apoptosis and extracellular matrix degradation were determined using RT-PCR. Additionally, Transcriptome sequencing was performed and prostaglandin-endoperoxide synthase-2 (PTGS2) was identified as the key factor in hyaluronidase-induced degeneration. Furthermore, we inhibited PTGS2 and measured the level of apoptosis mediators to determine its effect on hyaluronidase-induced CEP degeneration. Exposure to hyaluronidase significantly reduced cell viability, induced apoptosis of CEP cells and promoted extracellular matrix degradation in vitro. Hyaluronidase treatment upregulated PTGS2 in CEP cells. Knockdown of PTGS2 alleviated the apoptosis of CEP cells and inihited extracellular matrix degradation caused by hyaluronidase. Hyaluronidase induces endplate cell apoptosis and extracellular matrix degradation in vitro, while PTGS2 functions as a regulatory factor in this process. Inhibiting PTGS2 may serve as an effective treatment for intervertebral disc degeneration.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"104"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Administration with <i>Yangxinshi</i> ameliorates the progression of atrial fibrillation by affecting atrial remodeling and oxidative stress via the activation of the PI3K/AKT signaling.","authors":"Binmei Zhang, Jingxiu Hou, Li Dong, Man Sun, Ying Dong, Yumei Dong","doi":"10.1007/s10616-025-00778-8","DOIUrl":"10.1007/s10616-025-00778-8","url":null,"abstract":"<p><p>Atrial fibrillation (AF) is a common cardiac arrhythmia and constitutes a great global health burden. Traditional Chinese medicine Yangxinshi exerts protective efficacy in cardiovascular diseases. However, its function in AF remains elusive. Here, Yangxinshi attenuated induction and duration of AF in acetylcholine (Ach)-CaCl₂-constructed AF rat model, inducing inhibitory efficacy in susceptibility to AF. Moreover, Yangxinshi decreased AF-evoked atrial enlargement by inhibiting left atrial diameter (LAD) and LA area. Yangxinshi attenuated AF-induced oxidative stress by inhibiting elevation of ROS and 8-OHdG and ameliorated cell apoptosis in atria in AF rats. Moreover, Yangxinshi reduced atrial fibrosis levels, concomitant with decreases in collagen I, collagen III, and α-SMA. The network pharmacological analysis identified 110 common target genes between AF and Yangxinshi, and 6 major active ingredients of Yangxinshi that intersected with AF. GO and KEGG enrichment assay identified 20 pathways related to Yangxinshi targets in AF, among which the PI3K/AKT signaling had the greatest impact. Importantly, inactivation of the PI3K/AKT pathway in AF rats was offset by Yangxinshi. Together, Yangxinshi may attenuate the progression of AF by affecting atrial structural remodeling (atrial enlargement and fibrosis) and oxidative stress injury via the activation of the PI3K/AKT pathway, supporting a promising therapeutic agent for AF.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"121"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12149087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA sequencing identifies <i>MAP1A</i> and <i>PTTG1</i> as predictive genes of aging CD264⁺ human mesenchymal stem cells at an early passage.","authors":"Margaret K Giler, H Alan Tucker, Amanda K Foote, Avery G Francis, Sean D Madsen, Yao-Zhong Liu, Kim C O'Connor","doi":"10.1007/s10616-025-00724-8","DOIUrl":"10.1007/s10616-025-00724-8","url":null,"abstract":"<p><p>Molecular profiles of mesenchymal stem cells (MSCs) are needed to standardize the composition and effectiveness of MSC therapeutics. This study employs RNA sequencing to identify genes to be used in concert with CD264 as a molecular profile of aging MSCs at a clinically relevant culture passage. CD264^- and CD264⁺ populations were isolated by fluorescence-activated cell sorting from passage 4 MSC cultures. CD264⁺ MSCs exhibited an aging phenotype relative to their CD264^- counterpart. Donor-matched CD264^-/+ mRNA samples from 5 donors were subjected to pair-ended, next-generation sequencing. An independent set of 5 donor MSCs was used to validate differential expression of select genes with quantitative reverse transcription PCR. Pairwise differential expression analysis identified 2,322 downregulated genes and 2,695 upregulated genes in CD264⁺ MSCs relative to donor-matched CD264^- MSCs with a Benjamini-Hochberg adjusted <i>p</i>-value (BH <i>p</i> _<i>adj</i> ) < 0.1. Nearly 25% of these genes were unique to CD264^-/+ MSCs and not differentially expressed at a significance level of BH <i>p</i> _<i>adj</i>  < 0.1 in previous RNA sequencing studies of early- vs. late-passage MSCs. Least Absolute Shrinkage and Selection Operator regression identified microtubule-associated protein 1A (<i>MAP1A</i>) and pituitary tumor-transforming gene 1 (<i>PTTG1</i>) as predictive genes of CD264⁺ MSCs. Combined <i>MAP1A</i> and <i>PTTG1</i> expression correctly classified CD264 status of MSC samples with an accuracy of 100%. Differential expression and predictive ability of <i>MAP1A</i> and <i>PTTG1</i> compared favorably with that of existing senescence markers expressed in early passage CD264^-/+ MSCs. This study provides the first linkage of <i>MAP1A</i> to CD264, aging and senescence. Our findings have application as quality metrics to standardize the composition of MSC therapies and as molecular targets to slow/reverse cellular aging.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00724-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"63"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143467289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression and role of CTHRC1 in inflammatory bowel disease in children.","authors":"Heng Tang, Xiang Gao, Zhaofang Wu, Jia Chen, Li Chen, Xiang Du","doi":"10.1007/s10616-025-00705-x","DOIUrl":"10.1007/s10616-025-00705-x","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a chronic, progressive, immune-mediated, gastrointestinal inflammatory disease with increasing occurrences in children. Collagen triple helix repeat containing 1 (CTHRC1), a migration-promoting protein, acts as a tumor-promoting factor in malignant tumors. However, functions and mechanisms of CTHRC1 in children with IBD remain unclear. This study aimed to determine the effects and mechanisms of CTHRC1 on dextran sodium sulfate (DSS)-treated HT-29 cells. HT-29 control cells were exposed to 2% DSS to develop an in vitro IBD model. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to assess CTHRC1 expression in serum of children with IBD and HT-29 cells. Cell viability and apoptosis were assessed using MTT and flow cytometry (FCM). Expressions of cleaved-Caspase3 and Caspase3 were determined by western blotting. The cytokine production (TNF-α, IL-1β and IL-6) in HT-29 cells was measured by ELISA assay. Activation or inactivation of NF-κB signaling pathway was confirmed by western blot assay. Results showed that CTHRC1 expression was upregulated in the IBD serum and HT-29 control cells. The level of CTHRC1 was lower in CTHRC1-siRNA transfected cells than in control siRNA-treated cells. Notably, silence of CTHRC1 markedly enhanced HT-29 cells viability, decreased apoptotic cells, suppressed cleaved-Caspase3 expression, inhibited cleaved-Caspase3/Caspase3 ratio, reduced the production of inflammatory cytokines, and blocked NF-κB signaling pathway induced by DSS. However, these effects were reversed following diprovocim treatment. Thus, that knockdown of CTHRC1 alleviated DSS-induced HT-29 cell injury by inhibiting the NF-κB signaling pathway in vitro, providing a new therapeutic target for IBD in children.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00705-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"44"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The roles of melatonin and potassium channels in relaxation response to ang 1-7 in diabetic rat isolated aorta.","authors":"Nazar M Shareef Mahmood, Almas M R Mahmood, Ismail M Maulood","doi":"10.1007/s10616-025-00720-y","DOIUrl":"10.1007/s10616-025-00720-y","url":null,"abstract":"<p><p>In a circadian cycle, the pineal gland produces and releases melatonin (MEL) into the bloodstream. By activating distinct melatonin receptors, MEL has been shown to variably change vascular endothelial dysfunction (VED) to various vascular beds. This study investigates the interaction of melatonin (MEL) and potassium ion (K⁺) on angiotensin 1-7 (Ang 1-7) vasorelaxant in streptozotocin (STZ)-induced diabetes mellitus (DM) and non-diabetes mellitus (non-DM) male albino rat aortic rings. The isometric tension of isolated aortic rings was assessed by generating a dose-response curve (DRC) for Ang 1-7 using a PowerLab data acquisition system. Accordingly, three experimental sets were carried out. In the first set the aortic rings were exposed MEL and MEL agonist ramelteon (RAM) and MEL antagonist luzindole (LUZ). In the second set, the aortic rings were exposed to various non-selective calcium activated potassium channel (K_Ca) blockers, including tetraethylammonium (TEA), a small and large-conductance calcium-activated K⁺ [(SK_Ca) and (BK_Ca)] channels blocker charybdotoxin (ChTx) and intermediate calcium-activated K⁺ channel (IK_Ca) blocker clotrimazole (CLT). In the third set, the aortic rings were exposed to various selective K⁺ channels blockers, including the selective blocker of K_ATP channel, glibenclamide (Glib), 4-aminopyridine (4-AP), a selective blocker of K_v channels and BaCl₂, delayed inward rectifier K⁺ channels (K_ir) blocker. The results highlight the significant role of MEL in modulating vascular reactivity, particularly in the DM aorta. By enhancing the vasorelaxant effects of Ang 1-7 through mechanisms involving its receptors and antioxidant activities, MEL demonstrates its potential to counteract oxidative stress and VED associated with diabetes. These findings advance the understanding of vascular reactivity in diabetes and suggest MEL as a promising therapeutic agent for improving vascular health in diabetic conditions.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"55"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11799518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incorporating shaken 24-deep-well plate fed-batch culture shortens CHO cell line development time.","authors":"Shunsuke Ohira, Takeshi Omasa","doi":"10.1007/s10616-025-00728-4","DOIUrl":"10.1007/s10616-025-00728-4","url":null,"abstract":"<p><p>In conventional Chinese hamster ovary (CHO) cell line development, static culture is used for early-stage screening, whereas suspension culture is generally used for the manufacturing process. Shaken flask (SF) fed-batch culture allows evaluation with culture mode, which is closer to the final process. However, due to its laborious and low-throughput characteristics, only a limited number of clones can be evaluated. To attain high-throughput fed-batch culture evaluation, a shaken 24-deep-well plate (24 DWP) culture process was developed. 24 DWP culture allows multiple plates to be run in parallel, and is therefore suitable for early-stage screening. One challenge of well plate culture is the nonuniform evaporation rate among wells, which may result in unnecessary bias on clone evaluation. The 'sandwich lid system' introduced here provides a uniform evaporation rate, and showed no significant difference in cell culture performance by well location. 192 antibody-producing CHO clones were evaluated by 24 DWP fed-batch culture, and 30 clones were selected. On comparison of clone sets selected by 24 DWP fed-batch culture and the conventional scheme, average antibody concentration in SF fed-batch culture was 3.6 g/L and 2.9 g/L, respectively. 24 DWP fed-batch culture process showed a high correlation ratio with SF fed-batch culture in antibody productivity and similar cell culture characteristics. These characteristics-high-throughput and sufficient culture volume to support cell culture performance monitoring-indicate that 24 DWP fed-batch culture can be applied in the clone selection stage in place of SF, and will shorten the time required for cell line development.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"64"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839547/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of plasma exosomal microRNAs and bioinformatics analysis of the microRNA-messenger RNA regulatory pathways in mice with status epilepticus.","authors":"Wei Wang, Jian Yin","doi":"10.1007/s10616-025-00708-8","DOIUrl":"10.1007/s10616-025-00708-8","url":null,"abstract":"<p><p>Status epilepticus (SE) is a serious neurological emergency that brings significant risks to health and life. microRNAs (miRNAs) and their targets show involvement in the pathophysiology of SE. We identified plasma exosomal miRNAs and analyzed the miRNA-messenger RNA (mRNA) regulatory pathways in SE mice. Mice were subjected to SE induction by kainic acid injection, and plasma exosome (Exo) extraction. Exo morphology, particle size distribution, and Exo-positive marker proteins were evaluated. Differentially-expressed miRNAs in Exos of SE mice were analyzed and verified by sequencing and RT-qPCR. Functional enrichment analysis on target genes and protein-protein interaction (PPI) network were performed. Hippocampal neuron cells HT-22 were cultured in vitro, and the targeted binding association between Exos-derived miR-205-5p and target genes was invalidated. There were 64 differentially-expressed miRNAs in plasma Exos of SE mice from healthy mice (32 up-regulated, 32 down-regulated). Among the top 10 differentially-expressed miRNAs, 5 were up-regulated, and 5 were down-regulated. The PPI network of collective target genes was developed, including 11 edges and 9 nodes. The genes related to nerve injury were phosphatase and tensin homolog (Pten), glycogen synthase kinase 3 beta (Gsk3b), and leucine-rich repeat kinase 2 (Lrrk2). SE mouse plasma Exos targeted Gsk3b, Lrrk2 and Pten in neuronal cells and reduced cell viability. Plasma exosomal miRNAs of SE mice were differentially expressed, and their target genes participated in the regulation of multiple pathways, mainly related to nervous system development. miR-205-5p could target Gsk3b, Lrrk2 and Pten, and suppress neuronal viability.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00708-8.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 2","pages":"65"},"PeriodicalIF":2.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}