Cytotechnology最新文献

{"title":"Apigenin attenuates hepatocyte senescence in metabolic dysfunction-associated steatotic liver disease by targeting the TGF-β signaling pathway.","authors":"Lijun Cao, Yongna Zhao","doi":"10.1007/s10616-026-01020-9","DOIUrl":"10.1007/s10616-026-01020-9","url":null,"abstract":"<p><p>This study aimed to investigate whether the natural flavonoid apigenin attenuates hepatocyte senescence and ameliorates high-fat diet (HFD)-induced metabolic dysfunction-associated steatotic liver disease (MASLD) by inhibiting the transforming growth factor-β (TGF-β)/Smad signaling pathway. Both <i>in vivo</i> and <i>in vitro</i> experiments were conducted. <i>In vivo</i>, an HFD-induced MASLD model was established in C57BL/6J mice, which were then treated with apigenin. Hepatic steatosis, inflammation, and fibrosis were assessed by histopathological staining, and the expression of hepatocyte senescence markers (p16, p21, and γH2AX) and key proteins of the TGF-β/Smad pathway were detected by western blotting, immunohistochemistry, and immunofluorescence. Serum lipid metabolism and indicators of liver injury were evaluated using biochemical methods. <i>In vitro</i>, senescence was induced in AML12 mouse hepatocytes with palmitic acid (PA), and the cells were treated with apigenin; anti-senescence effects and TGF-β pathway inhibition were confirmed by senescence-associated β-galactosidase (SA-β-gal) staining and western blotting. In the HFD-induced mouse model, apigenin alleviated hepatic steatosis, inflammation, and fibrosis, and reduced serum levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). It also decreased senescence markers (p16, p21, and γH2AX) in liver tissues and inhibited TGF-β expression and Smad2/3 phosphorylation. In the PA-treated AML12 cells, apigenin lowered senescence-associated proteins and SA-β-gal-positive cells while suppressing TGF-β/Smad pathway activation. Overexpression of TGF-β partially reversed the anti-senescence effect of apigenin, whereas pharmacological inhibition of TGF-β receptor I with SB431542 further reduced senescence markers and lipid accumulation. These findings indicate that apigenin may mitigate HFD/PA-induced hepatocyte senescence and MASLD-related pathological changes by inhibiting the TGF-β/Smad signaling pathway, offering new insights into its hepatoprotective effects.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"149"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13328522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390202","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":"Correction: <i>Viscum coloratum</i> (Kom.) Nakai inhibits osteoclastogenesis in RANKL-induced osteoclast differentiation through the PI3K/AKT/mTOR pathway.","authors":"Zhichao Hao, Yuan Liu, Yanfu Wang, Xu Yang, Yan Pan, Qingshan Chen, Lili Zhang, Haixue Kuang, Yuxin Li, Yiran Wang, Bing-You Yang, Yan Liu","doi":"10.1007/s10616-026-00986-w","DOIUrl":"10.1007/s10616-026-00986-w","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-026-00941-9.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"125"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053119","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":"Evaluation of a prototype bioreactor based on slowly rotating drum.","authors":"Alfredo Ambrico, Mario Trupo, Rosaria Alessandra Magarelli, Vincenzo Larocca, Maria Martino, Sergio Modenese, Sirio Vurro","doi":"10.1007/s10616-026-01036-1","DOIUrl":"10.1007/s10616-026-01036-1","url":null,"abstract":"<p><p>In this study, an innovative rotating-drum bioreactor was evaluated and compared with a conventional stirred-tank system for CHO cell fed-batch culture, with particular focus on oxygen transfer, hydrodynamic conditions, and overall bioprocess performance. The novel configuration, based on a slowly rotating perforated drum, enabled efficient oxygenation at low rotational speeds, achieving a higher volumetric mass transfer coefficient (k_La = 0.1087 min⁻¹) despite significantly lower tip speeds. This resulted in stable dissolved oxygen (DO) levels (approximately 40%) throughout a 10-day cultivation. Under these operating conditions, the innovative bioreactor promoted enhanced cell growth, achieving a peak viable cell density (VCD) of 2.55 × 10⁷ cells mL⁻¹ and maintaining high viability (around 91.7% on day 10). Monoclonal antibody production reached 1.3 ± 0.09 g L⁻¹, almost doubling the yield obtained in the stirred-tank reactor. The improved outcomes observed in the innovative bioreactor could be associated with the distinct operating and hydrodynamic conditions established by the system configuration. Nevertheless, further studies are needed to better define the operational limits of the system and optimize process conditions. Future investigations should also assess critical quality attributes, including glycosylation patterns, aggregation, fragmentation, and host cell protein contamination, as well as evaluate the performance of the bioreactor at larger scales.</p><p><strong>Graphical abstract: </strong></p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01036-1.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"162"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13379560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497264","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":"xCELLigence™ RTCA system in cancer biology: innovations in real-time functional profiling.","authors":"Charlene Andraos, Jitcy Saji Joseph, Wells Utembe, Millicent Magogotya, Olumayowa Oriyomi, Oladapo Fagbohun","doi":"10.1007/s10616-026-01000-z","DOIUrl":"10.1007/s10616-026-01000-z","url":null,"abstract":"<p><p>The molecular mechanisms and interactions for the complex cancer pathogenesis are still poorly understood. Traditional and conventional endpoint migration assays such as MTT/XTT/CCK-8, transwell migration, clonogenic, and false positives/negatives assays, do not capture the kinetics of the 3D tumor microenvironment. Therefore, there is the need for high-resolution kinetic data on cancer cell invasion, proliferation, migration, cytotoxicity, adhesion, and differentiation, to understand transient and adaptive responses that are often missed by static measurements for highly effective cancer immunotherapeutics. Here, we review the xCELLigence™ Real-Time Cell Analysis (RTCA) system that represents a major advancement in cancer research by enabling non-invasive, label-free, and continuous monitoring of cellular behaviour through impedance-based technology. Over the years, and particularly since 2020, RTCA has been increasingly applied and relied upon across diverse areas of cancer research, including kinase inhibition, gene silencing, metabolic targeting, immunotherapy, nanomedicine, and three-dimensional tumour models. We first analyse the recent advances in the applications of xCELLigence™ RTCA, with a specific emphasis on how impedance-derived kinetic signatures enhance mechanistic understanding of tumor cell behaviour. We then critically discuss quantitative metrics derived from real-time impedance measurements, compare RTCA with conventional endpoint assays, and highlight its translational relevance for drug development and precision oncology. Finally, we outline current limitations and emerging directions that may further consolidate RTCA as a predictive and integrative platform in preclinical cancer research.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"128"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053241","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":"Magnetic resonance imaging-based Alzheimer's disease detection using an EfficientNet-CMSACCN framework.","authors":"S Sujanthi, A M Ravishankkar, S Ponmaniraj, S Nanthini","doi":"10.1007/s10616-026-01015-6","DOIUrl":"10.1007/s10616-026-01015-6","url":null,"abstract":"<p><p>Alzheimer's Disease (AD) is a degenerative neurological condition characterized by memory loss, cognitive deterioration, and brain tissue shrinkage. Detecting it at an early stage is difficult due to variations in disease progression and the restricted scope of single-modality neuroimaging methods. Magnetic Resonance Imaging (MRI)-based Alzheimer's diagnosis, such as magnetic resonance imaging, offers complementary structural and functional insights, but existing deep learning methods often struggle with data imbalance, high computational complexity, and limited generalization. To fill these research gaps, design an MRI-based EfficientNet feature extraction framework for Alzheimer's stage classification. EfficientNet, equipped with compound scaling, depthwise-separable layers, and squeeze-and-excitation components, enables precise characterization of cortical structures and whole-brain variations while preserving computational efficiency. Extracted features are classified using a Compression-based Multi-Scale Attention Convolutional Network (C-MSACCN), which integrates attention mechanisms and compression strategies to enhance accuracy and reduce model complexity. Furthermore, the Improved Cellular Neighbours Optimiser (ICNO) fine-tunes hyperparameters, striking a balance between exploration and exploitation for optimal convergence and robustness. With 99.9% accuracy, precision, recall, and F1-score on datasets, the model outperforms prior work. Validation confirms consistency, and visualisation methods highlight disease-relevant regions to provide clinical insight.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"146"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13310867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148351147","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":"Gamma-terpinene suppresses the growth of lymphoblastic cancerous cells in vitro<i>,</i> possibly via multiple proposed molecular mechanisms, including apoptosis and gene expression modulation.","authors":"Pooya Baradaran Safa, Maryam Nooshadokht, Maryam Mohit, Maryam Ramezany, Sahar Illaghi-Hoseini, Mahla Lashkari, Hamid Forootanfar, Alireza Keihani, Bagher Amirheidari","doi":"10.1007/s10616-026-01017-4","DOIUrl":"10.1007/s10616-026-01017-4","url":null,"abstract":"<p><p>ALL is recognised as a heterogeneous malignancy affecting lymphocyte precursors. Considering shortcomings of the current treatments, herbal compounds have always been in the focus of attention as novel anticancer candidates, owing to their main advantages like promising levels of bioactivity and toxicity. Accordingly, the anticancer potentials of gamma-terpinene were evaluated on cell-death relevant proteins as well as on Nalm-6 ALL cells alone and in combination with Doxorubicin (Dox). In this study, an optimized form of GT from the RCSB PDB structure databank was docked to Bcl-2 and p21 proteins using MOE software. Nalm-6 cell viability in exposure to GT was measured using dye-exclusion and MTT methods. Initiation of apoptosis was also studied by Annexin-V/PI DNA-staining kit. In addition, cellular mRNA levels of genes coding for hTERT, Bcl-2, Bax, P53, and P21 were quantified and detected by the real-time PCR method. The differences were assessed using SPSS version 26 and statistical data analysis was done by ANOVA (one-way). Dockability of GT in the active cavities of Bcl-2 and P21 was evident, involving at least 11 interacting amino acids. Also, GT exerted dose-dependent cytotoxicity on Nalm-6 cells, exhibiting the IC₅₀ of 27.6 (mM) and selectivity index (SI) of 4.58 in comparison with exposure to PBMC normal cells. Bax, P53 and P21 gene mRNAs were at higher titres in exposure to GT, while the GT-treated cells displayed lower levels of Bcl-2 gene. When applied in combination, GT (10 mM) enhanced the cytotoxicity of Dox (8 nM) against Nalm-6 cells significantly (p > 0.05). Molecular docking, cellular studies, and gene expression analyses suggested that GT possesses promising antileukemic potential on Nalm-6 cells at reasonable selectivity over normal blood cells. However, further investigations, including studies targeting protein level and in vivo validations, are necessary to further proof drugability of this monoterpene product.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"151"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403823","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 role and predictive potential of miR-451-5p in delayed fracture healing.","authors":"Chuangye Qu, Weibing Bao, Wenqi Wang, Xiaozhong Zhu","doi":"10.1007/s10616-026-00994-w","DOIUrl":"https://doi.org/10.1007/s10616-026-00994-w","url":null,"abstract":"<p><p>To explore the predictive value of miR-451-5p in delayed fracture healing (DFH) and its mechanism of action in fracture healing. Patients with normal fracture healing (NFH) and DFH were included in this study. The expression of miR-451-5p in serum was detected by RT-qPCR. The predictive potential of miR-451-5p for DFH was evaluated by ROC analysis, and risk factors influencing DFH were determined using logistic regression analysis. The proliferation, apoptosis and expression levels of osteogenic differentiation markers (ALP, BMP2, OSX) of mouse embryonic osteoblast precursor cells (MC3T3-E1) were detected by CCK-8, flow cytometry, RT-qPCR and western blot. The targeting relationship between miR-451-5p and ATF2 was verified by dual-luciferase reporter assay and RNA pull-down experiments. The level of miR-451-5p in the serum of DFH patients was significantly higher than that in the NFH group. Its sensitivity for predicting DFH was 81.33%, and its specificity was 86.96%. miR-451-5p is an independent risk factor for DFH. Overexpression of miR-451-5p could inhibit the proliferation of osteogenic precursor cells, promote cell apoptosis, and downregulate the expression of osteogenic differentiation markers. miR-451-5p binds to ATF2 and inhibits its expression. Overexpression of ATF2 could reverse the inhibitory effect of miR-451-5p on osteogenic differentiation. During the process of osteogenesis, miR-451-5p negatively regulates cell proliferation and osteogenesis by inhibiting the function of ATF2. Clinically, miR-451-5p has the potential to serve as a biomarker for the early predictive of DFH.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-00994-w.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"139"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293791","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":"Brusatol Induces Ferroptosis in Condyloma Acuminatum Keratinocytes by Suppressing Nrf2 via Inhibition of the PI3K/AKT Pathway.","authors":"WeiQi Wu, Juan Yang, XiuYi Lu, LieHua Deng, LiuYan Wen","doi":"10.1007/s10616-026-01007-6","DOIUrl":"https://doi.org/10.1007/s10616-026-01007-6","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;i&gt;Objective&lt;/i&gt; Condyloma acuminatum (CA), a common sexually transmitted disease caused by human papillomavirus (HPV) infection, is closely associated with the abnormal proliferation and differentiation of host keratinocytes. Brusatol (BRU), a quassinoid compound derived from the medicinal plant Brucea javanica, has gained attention for its ability to regulate multiple biological processes through the phosphoinositide 3-kinase/Protein Kinase B (PI3K/AKT) signaling pathway. It may also reduce Nuclear factor erythroid 2-related factor 2 (Nrf2) expression to induce ferroptosis in cancer cells. However, its regulatory role in ferroptosis of HPV-infected keratinocytes remains unreported. Therefore, this study was designed to examine the role of BRU in inducing ferroptosis in CA keratinocytes via the PI3K/AKT/Nrf2 pathway, with the aim of identifying a promising therapeutic strategy for CA. &lt;i&gt;Methods&lt;/i&gt; To simulate the pathological process of CA, a pEGFP-N1-HPV6 recombinant plasmid vector was transfected into HaCaT human epidermal keratinocyte cells. The cytotoxicity of BRU was determined by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell membrane integrity was assessed via the Lactate Dehydrogenase release assay. Lipid peroxidation accumulation was detected using C11-BODIPY581/591 fluorescent staining. The oxidative stress level was evaluated by measuring the glutathione/oxidized glutathione (GSH/GSSG) ratio. Cellular iron content was measured to assess iron homeostasis. Nrf2 nuclear translocation was examined by immunofluorescence. Cell proportions were analyzed by flow cytometry. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome enrichment analyses were performed to identify signaling pathways involved in BRU-induced ferroptosis. The protein expression levels of Glutathione Peroxidase 4 (GPX4), Solute Carrier Family 7 Member 11 (SLC7A11), Nrf2, phosphorylated-PI3K (p-PI3K)/total-PI3K, and p-AKT/total-AKT were detected by Western blot. The mRNA expression levels of GPX4, SLC7A11, Nrf2, Heme Oxygenase-1, and NAD(P)H Quinone Dehydrogenase 1 (NQO1) were measured by quantitative real-time polymerase chain reaction (RT-qPCR). &lt;i&gt;Results&lt;/i&gt; BRU inhibited the viability of CA keratinocytes (HPV-HaCaT) and induced characteristic features of ferroptosis, including lipid reactive oxygen species (ROS) accumulation (lipid ROS), GSH depletion, increased ferrous iron levels, and downregulation of key ferroptosis regulators (GPX4, SLC7A11). BRU also reduced Nrf2 protein expression and its nuclear translocation. These effects were partially reversed by Ferrostatin-1. KEGG and Reactome pathway enrichment analyses using R software revealed that the PI3K/AKT signaling pathway was the most significantly enriched pathway in KEGG, while the 'Negative regulation of the PI3K/AKT network' pathway was also significantly enriched in Reactome. In vitro, BRU inhibited PI3K and AKT phosphorylation, reduced Nrf2 expression and nuclea","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"144"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13309603/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344038","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":"USP5 inhibits osteogenic differentiation but promotes oxidative stress and M1-like macrophage polarization of human periodontal ligament stem cells via deubiquitinating and stabilizing RIPK1: insights from <i>in vitro</i> and <i>in vivo</i> analyses.","authors":"Jinghong Mao, Ming Qin","doi":"10.1007/s10616-026-01012-9","DOIUrl":"10.1007/s10616-026-01012-9","url":null,"abstract":"<p><p>Chronic periodontitis (CP) is a chronic infectious disease. Ubiquitin-specific protease 5 (USP5), a member of the deubiquitinase family, has garnered significant attention due to its crucial biological functions. In this study, we aimed to explore the function of USP5 in CP development. Human periodontal ligament mesenchymal stromal cells (hPDL-MSCs) were stimulated with LPS. qRT-PCR and western blot assay were performed to determine the expression of USP5, receptor-interacting protein kinase 1 (RIPK1), osteogenic markers, and macrophage polarization markers. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining assays were used to examine ALP activity and ARS quantification. Flow cytometry analysis was used to analyze cell apoptosis. Commercial kits were used to evaluated the levels of oxidative stress indicators. ELISA was performed for the concentrations of inflammatory factors. Co-immunoprecipitation (Co-IP) assay, GST pull-down assay and Ubiquitination assay were applied to analyze the relation between USP5 and RIPK1. USP5 was upregulated in the PDL tissues of CP patients and LPS-triggered hPDL-MSCs. Knockdown of USP5 contributed to the osteogenic differentiation of LPS-treated hPDL-MSCs and repressed the apoptosis, oxidative stress, inflammation, and M1-like macrophage polarization in LPS-treated hPDL-MSCs. Mechanically, USP5 was demonstrated to regulate RIPK1 expression through deubiquitination. Moreover, overexpression of RIPK1 restored the effects of USP5 knockdown on the osteogenic differentiation, apoptosis, oxidative stress injury, and macrophage polarization direction in LPS-treated hPDL-MSCs. USP5 deubiquitinated and stabilized RIPK1 to regulate the osteogenic differentiation, oxidative stress injury and macrophage polarization in CP.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-026-01012-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"152"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13337979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148403788","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":"OGN inhibits apoptosis and ferroptosis via FSHR in human granulosa cells: implications for polycystic ovary syndrome.","authors":"Yu Zhang, Cheng Yin, Jiahui Wang, Jiajia Chen, Cuiping Li, Lijing Liu, Shi Liu","doi":"10.1007/s10616-026-01030-7","DOIUrl":"10.1007/s10616-026-01030-7","url":null,"abstract":"<p><p><i>Background</i> Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by granulosa cell dysfunction, including impaired proliferation, excessive apoptosis, and ferroptosis, which contribute to abnormal follicular development and ovarian dysfunction. This study aims to investigate the effects of Osteoglycin (OGN) on proliferation, apoptosis, and ferroptosis in human ovarian granulosa cells, and to analyze its regulation of follicle stimulating hormone receptor (FSHR), providing insights into granulosa cell dysfunction associated with PCOS. <i>Methods</i> This study investigated the function of OGN in KGN granulosa cells by transfecting them with OGN-plasmid for overexpression or OGN-siRNA for knockdown. Cell viability was assessed using the MTT assay, while apoptosis was analyzed by flow cytometry. Ferroptosis was evaluated by measuring intracellular ROS and MDA levels, and protein expression was examined via Western blotting. Additionally, RT-qPCR and Western blotting were used to assess mRNA and protein levels of FSHR to determine the regulatory effect of OGN on FSHR expression. <i>Results</i> Overexpression of OGN significantly promoted granulosa cell proliferation and inhibited apoptosis, whereas knockdown of OGN suppressed proliferation and induced apoptosis. Mechanistic studies revealed that knockdown of OGN upregulated cleaved-Caspase3 expression, increased intracellular ROS and MDA levels, and reduced GPX4 expression, indicating the activation of both apoptotic and ferroptotic pathways. Furthermore, OGN positively regulated FSHR expression, as FSHR levels were increased with OGN overexpression and decreased following OGN knockdown at both mRNA and protein levels. <i>Conclusion</i> This study demonstrates that OGN plays a critical role in regulating granulosa cell survival and ferroptosis and may contribute to follicular development and PCOS-related ovarian dysfunction by modulating FSHR.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"78 4","pages":"154"},"PeriodicalIF":2.2,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13354735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419591","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}