Folia histochemica et cytobiologica最新文献

{"title":"Molecular mechanism by which dichotomitin inhibits growth and metastasis of gastric cancer MKN-45 cells via the EGFR/ROS signaling pathway.","authors":"Zhao Ning, Quan Quan, Xi-Chun Huang, Jun-Hao Li, Zhe Liu, Cheng-Hao Jin","doi":"10.5603/fhc.113717","DOIUrl":"10.5603/fhc.113717","url":null,"abstract":"<p><strong>Introduction: </strong>Dichotomitin (DC), an isoflavone from Belamcanda chinensis, has anti-inflammatory and antioxidant properties, but its role in gastric cancer (GC) remains unexplored. This study aimed to elucidate the mechanisms by which DC modulates GC cell proliferation, apoptosis, and migration.</p><p><strong>Material and methods: </strong>MKN-45 cells were used for in vitro studies, and xenograft tumor models were established using BALB/c nude mice for in vivo evaluation. Bioinformatics analysis predicted core targets. CCK-8, flow cytometry, wound healing, Transwell, and fluorescence microscopy assays were performed to assess proliferation, cell-cycle distribution, apoptosis, migration, and ROS levels. Expression of proteins in the EGFR/MAPK, EGFR/AKT, and AKT/GSK-3β/β-catenin pathways was determined by Western blotting.</p><p><strong>Results: </strong>In vitro, DC significantly inhibited GC cell proliferation and induced morphological changes. DC induced cell cycle arrest in the G0/G1 phase and promoted mitochondria-dependent apoptosis by modulating EGFR/MAPK signaling, while inhibiting migration through the AKT/GSK-3β/β-catenin pathway. Mechanistically, DC inhibited EGFR activation and elevated ROS levels. The EGFR agonist NSC228155 reversed these effects, confirming dependence on EGFR-ROS signaling. In vivo, DC dose‑dependently inhibited tumor growth, with medium/high doses outperforming 5‑fluorouracil. Histological examination of major organs showed no significant abnormalities, confirming low toxicity at therapeutic doses.</p><p><strong>Conclusions: </strong>DC inhibited proliferation, induced cell cycle arrest and apoptosis, and suppressed migration in GC cells by modulating EGFR-related ROS-dependent signaling pathways.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"166-182"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR-mediated MLH1 disruption suppresses endometrial cancer growth via genomic instability induction and Wnt/β-catenin pathway inhibition.","authors":"Baoling Xing, Xiaoying Zhang, Li Shen, Xinpeng Zhang","doi":"10.5603/fhc.111186","DOIUrl":"10.5603/fhc.111186","url":null,"abstract":"<p><strong>Introduction: </strong>MutL homolog 1 (MLH1) loss is a defining molecular feature of endometrial cancer (EC) and a principal driver of microsatellite instability (MSI). Ishikawa cells harbor intrinsic MLH1 promoter hypermethylation, resulting in reduced but not abolished MLH1 expression and placing these cells in a vulnerable, partially compromised mismatch repair state. This study explores the effects of MLH1 knockdown (MLH1-KD) on MSI, cellular functions, signaling pathways, and tumor growth in Ishikawa EC cells.</p><p><strong>Material and methods: </strong>Using CRISPR/Cas9, we created an MLH1-KD Ishikawa EC cell line, validated through Sanger sequencing, qRT-PCR, western blotting, comet assays, and γ-H2AX analysis. Functional assays assessed proliferation, migration, and cell cycle progression and apoptosis. RNA sequencing identified global transcriptomic changes, and Wnt/β-catenin pathway activity was measured by a dual-luciferase reporter assay. A xenograft model evaluated tumor growth in vivo.</p><p><strong>Results: </strong>MLH1-KD cells showed MSI-H characteristics, increased DNA damage, and downregulation of key EC-related genes. Functionally, MLH1-KD led to significant reductions in cell proliferation and migration, which was accompanied by cell cycle arrest and a marked increase in apoptosis. RNA sequencing revealed profound alterations in the Wnt signaling pathway. Crucially, this was confirmed by a dual-luciferase reporter assay, which showed a significant inhibition of Wnt/β-catenin signaling activity. In vivo, MLH1-KD significantly decreased tumor weight and size in nude mice.</p><p><strong>Conclusions: </strong>In EC cells with pre-existing MLH1 promoter methylation, MLH1-KD leads to MSI-H, enhances genomic instability, disrupts Wnt signaling, impairs cellular functions, and inhibits tumor growth, highlighting Wnt signaling and MSI-H as potential therapeutic targets in EC.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"75-87"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of miR-33b-5p promotes osteoblast differentiation by regulating ABCA1 in cellular and animal models of osteoporosis.","authors":"Erya Miao, Yanli Li, Fan Feng, Yi Cai, Nan Shan","doi":"10.5603/fhc.111371","DOIUrl":"10.5603/fhc.111371","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoporosis is a major health risk for postmenopausal women and is primarily driven by estrogen decline-induced bone loss. As critical post-transcriptional regulators of gene expression, dysregulated microRNAs (miRs) participate in the pathogenesis of osteoporosis by disrupting key signaling pathways that govern bone homeostasis and remodeling. This study investigated the functional role of the miR-33b-5p/ABCA1 axis in cellular and murine models of osteoporosis.</p><p><strong>Material and methods: </strong>Alizarin Red S staining and alkaline phosphatase (ALP) activity assays were performed to detect osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). ABCA1 mRNA and protein levels, as well as osteogenic proteins such as RUNX2, OPN, and OCN, were quantified by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. Dexamethasone (DEX)-stimulated BMSCs were employed as an in vitro osteoporosis model. To overexpress ABCA1 in BMSCs, the cells were transfected with pcDNA3.1 vectors carrying the full-length ABCA1 coding sequence. ABCA1 silencing was accomplished using short hairpin RNA targeting ABCA1 (sh-ABCA1), whereas miR-33b-5p inhibition was achieved using a specific miR-33b-5p inhibitor. The direct interaction between miR-33b-5p and its downstream target ABCA1 was validated using luciferase reporter assays. After an ovariectomized (OVX) mouse model was established, micro-CT was performed to detect bone density by assessing trabecular thickness and trabecular number in femurs.</p><p><strong>Results: </strong>ABCA1 expression increased during osteogenic differentiation of BMSCs, suggesting an essential role in this process. In DEX-treated BMSCs, the ABCA1 level was downregulated. ABCA1 overexpression promoted osteoblast differentiation, as evidenced by increased mineralized nodule formation, upregulation of key osteogenic proteins, and elevated ALP activity. MiR-33b-5p directly interacted with the 3'UTR of ABCA1, with the binding region conserved across multiple species. MiR-33b-5p inhibitors promoted osteogenic differentiation, and this effect was abolished upon ABCA1 depletion via sh-ABCA1. Animal experiments indicated that miR-33b-5p inhibition promoted trabecular bone formation in the femurs of OVX mice, including increased trabecular number and thickness, along with elevated expression of osteoblastic markers. A significant negative correlation between miR-33b-5p and ABCA1 expression levels was observed in bone tissues of experimental mice.</p><p><strong>Conclusions: </strong>Inhibition of miR-33b-5p promotes osteoblastic differentiation by regulating ABCA1 in experimental osteoporosis models.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"99-110"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGFL2-AS1 knockdown enhances erastin-induced ferroptosis-associated changes in oral squamous cell carcinoma.","authors":"Li Li, Ye Yin","doi":"10.5603/fhc.112241","DOIUrl":"10.5603/fhc.112241","url":null,"abstract":"<p><strong>Introduction: </strong>Long non-coding RNA (lncRNA) IGFL2-AS1 has been implicated in oral squamous cell carcinoma (OSCC) progression, whereas its relationship to ferroptosis remains unclear. Erastin is a small-molecule ferroptosis inducer that inhibits system Xc-, reduces cystine uptake and glutathione availability, and thereby promotes lipid peroxide accumulation. We investigated whether IGFL2-AS1 modulates erastin-induced ferroptosis-associated changes through the miR-181a-5p/SLC7A11 axis.</p><p><strong>Material and methods: </strong>Correlations among IGFL2-AS1, miR-181a-5p, and SLC7A11 were analyzed in public HNSC datasets using online bioinformatic tools. RNA immunoprecipitation (RIP)-qPCR and dual-luciferase assays were used to validate the interactions. Erastin-treated OSCC cell lines (Cal-27 and SCC15) were subjected to IGFL2-AS1 knockdown/overexpression or miR-181a-5p modulation for CCK-8 assays, and Cal-27 cells were further used for MDA, GSH, and Fe2+ measurements. Fluorescence staining and immunofluorescence analyses of ROS, SLC7A11, and FTH1 were further performed in Cal-27 cells. In vivo, tumor growth was monitored in xenografts derived from Cal-27 cells with stable IGFL2-AS1 knockdown and treated with erastin or antagomiR-181a-5p.</p><p><strong>Results: </strong>IGFL2-AS1 knockdown or miR-181a-5p overexpression increased the sensitivity of OSCC cells to erastin, as indicated by reduced viability. In Cal-27 cells, this was accompanied by increased MDA and Fe2+ levels and depleted GSH. Mechanistically, IGFL2-AS1 acted as a competing endogenous RNA for miR-181a-5p and regulated the expression of the ferroptosis-related protein SLC7A11. In Cal-27 cells, IGFL2-AS1 knockdown further enhanced erastin-associated ROS fluorescence and reduced SLC7A11 and FTH1 immunoreactivity, whereas miR-181a-5p inhibition partially reversed these changes. In vivo, IGFL2-AS1 silencing enhanced erastin-associated tumor suppression and reduced SLC7A11 expression, while antagomiR-181a-5p partly attenuated these effects.</p><p><strong>Conclusions: </strong>The present data support that IGFL2-AS1 knockdown enhances erastin-induced ferroptosis-associated changes in OSCC, at least in part through the miR-181a-5p/SLC7A11 axis.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"111-124"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Esculetin ameliorates sevoflurane-induced cognitive dysfunction in aged mice by suppressing neuroinflammation via inhibition of NF-κB/NLRP3 signaling.","authors":"Xiaoli Cai, Zhang Tian, Qingyun Zhang, Jing Zhao","doi":"10.5603/fhc.112581","DOIUrl":"10.5603/fhc.112581","url":null,"abstract":"<p><strong>Introduction: </strong>The widely used inhalational anesthetic sevoflurane increases susceptibility to postoperative cognitive dysfunction (POCD), especially among the elderly. Esculetin, a natural coumarin compound derived from Cortex Fraxini, possesses anti-inflammatory and neuroprotective activities. This study aimed to determine whether esculetin mitigates sevoflurane-induced POCD and to clarify its underlying mechanisms.</p><p><strong>Material and methods: </strong>POCD was induced in aged male C57BL/6J mice by 3% sevoflurane inhalation. Esculetin was administered 1 h before each exposure. Learning, memory, and locomotion were evaluated by Morris water maze and open field tests. Hippocampal apoptosis was detected by TUNEL staining and western blotting (WB) of apoptosis-associated proteins. Neuroinflammation was assessed through Iba-1 immunofluorescence, ELISA, WB, and RT-qPCR. NF-κB and NLRP3 inflammasome pathways were analyzed by WB and immunofluorescence. In vitro, HT22 neurons were treated with sevoflurane and/or esculetin, and microglia-mediated neuroinflammation was examined using a BV2-HT22 co-culture system.</p><p><strong>Results: </strong>In aged mice, esculetin alleviated sevoflurane-induced spatial learning and memory impairments. Hippocampal neuronal apoptosis was reduced, as indicated by fewer TUNEL-positive cells and restored expression of Bcl-2, Bax, and cleaved caspase-3. Esculetin also inhibited microglial activation, along with the sevoflurane-induced elevation of proinflammatory cytokines (TNF-α, IL-1β, IL-6) and M1 microglial markers (iNOS, CD68). Mechanistically, esculetin inhibited sevoflurane-triggered phosphorylation of IκBα and p65, as well as NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and caspase-1 upregulation. In vitro, esculetin dose-dependently protected HT22 cells against sevoflurane-induced apoptosis. In the co-culture system, esculetin attenuated microglia-driven neuroinflammation and NF-κB/NLRP3 inflammasome activation in HT22 cells.</p><p><strong>Conclusions: </strong>Esculetin ameliorates sevoflurane-induced cognitive deficits in aged mice by inhibiting hippocampal neuroinflammation and neuronal apoptosis through NF-κB/NLRP3 inflammasome inhibition.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"125-139"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Latent transforming growth factor beta binding protein 1 (LTBP1): roles as a multifunctional extracellular matrix regulator in human disease - from molecular mechanisms to clinical translation prospects.","authors":"Yi Liu, Minming Yi, Huan Wei, Xuewei Gu, Wenyan Liao","doi":"10.5603/fhc.110761","DOIUrl":"10.5603/fhc.110761","url":null,"abstract":"<p><p>Latent transforming growth factor beta binding protein 1 (LTBP1) is a key regulator of the extracellular matrix (ECM). However, its role as a molecular hub that integrates biochemical signals within the mechanical microenvironment across diverse human diseases has not been systematically elucidated. To address this, this review provides an in-depth analysis of the current evidence chain for LTBP1, from basic biology to disease mechanisms. The analysis indicates that through its isoforms, post-translational modifications (PTMs), and dynamic conformation, LTBP1 not only precisely modulates the spatiotemporal activity of TGF-β but also independently orchestrates ECM assembly and mediates direct cell signaling. In disease, LTBP1's function exhibits strong context-dependency: it acts as a \"double-edged sword\" in cancer (driving progression or suppressing growth); it serves as a key pathological mediator in fibrosis, and contributes to structural defects in cardiovascular, neurological, and developmental disorders. These mechanisms lay a solid foundation for its clinical translation: LTBP1 is established as a multidimensional biomarker and constitutes a novel target for a range of intervention strategies, from targeted therapies and cell therapies to functionalized biomaterials. In summary, establishing LTBP1 as a key pathological integrator in systematic studies, provides a new framework and direction for understanding common mechanisms of complex diseases and developing precision medicine strategies.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"1-25"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fundamental research on the treatment of periodontitis with Kangfuxin (KFX) extended-release gel.","authors":"Jianzhao Ding, Ye Zhang, Qiyan Li, Bin Gong, Rui Yang, Yanli Tang","doi":"10.5603/fhc.110856","DOIUrl":"10.5603/fhc.110856","url":null,"abstract":"<p><strong>Introduction: </strong>Periodontitis, a chronic inflammatory disease that severely compromises oral health and is linked to systemic disorders, has attracted increasing research attention. Kangfuxin (KFX), an ethanol extract derived from Periplaneta americana (L.) with documented anti-inflammatory and tissue-regenerative properties, remains unexplored for localized periodontal therapy. This study investigated whether KFX extended-release gel (KFX-ERG) could inhibit the progression of periodontal disease and provide potential support for the treatment of periodontitis.</p><p><strong>Material and methods: </strong>We selected the optimal concentration from different component ratios of KFX-ERG for subsequent experiments. In vivo, a periodontitis model was established in rats, and pathological changes in periodontal tissue were examined using histological and micro-computed tomography (micro-CT) analyses.</p><p><strong>Results: </strong>Micro-computed tomography revealed that KFX-ERG reduced alveolar bone resorption in experimental periodontitis in rats. Histopathological analysis further revealed markedly reduced inflammatory cell infiltration and concurrently elevated osteoblast density in periodontal tissues of the KFX-ERG group.</p><p><strong>Conclusions: </strong>This study establishes a theoretical foundation for the therapeutic application of KFX-ERG in mitigating periodontitis progression and demonstrates its significant potential to promote periodontal tissue regeneration, thereby offering promising translational prospects for clinical regenerative periodontal therapy.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"150-163"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing GJB2 attenuates IL-1β-induced chondrocyte injury by activating Nrf2/HO-1 signaling and preserving mitochondrial function.","authors":"Hongyi Pan, Lianguo Wu","doi":"10.5603/fhc.111194","DOIUrl":"10.5603/fhc.111194","url":null,"abstract":"<p><strong>Introduction: </strong>Mitochondrial oxidative stress is a key driver of inflammation-induced chondrocyte dysfunction and cartilage degeneration. However, the molecular regulators linking inflammatory signaling to mitochondrial impairment in chondrocytes remain incompletely understood.</p><p><strong>Material and methods: </strong>Public transcriptomic datasets were analyzed using differential expression analysis, weighted gene co-expression network analysis (WGCNA), and screening for oxidative stress-related genes to identify osteoarthritis (OA)-associated hub genes. An IL-1β-induced CHON-001 chondrocyte injury model was established, and the GJB2 gene, which encodes connexin 26, was silenced using siRNA. Cell viability, oxidative stress, apoptosis, Nrf2/HO-1 signaling, and mitochondrial membrane potential were evaluated.</p><p><strong>Results: </strong>Integrated bioinformatics analysis of multiple GEO datasets identified GJB2 as a key oxidative stress-related hub gene. IL-1β stimulation significantly increased GJB2 expression and induced oxidative stress, apoptosis, and mitochondrial dysfunction. GJB2 knockdown reduced reactive oxygen species (ROS) accumulation, attenuated inflammatory responses, inhibited apoptosis, restored Nrf2 nuclear translocation and HO-1 expression, and preserved mitochondrial membrane potential.</p><p><strong>Conclusions: </strong>GJB2 promotes inflammation-associated oxidative injury and mitochondrial dysfunction in chondrocytes. Silencing GJB2 activates the Nrf2/HO-1 antioxidant pathway and confers cytoprotective effects, identifying GJB2 as a critical regulator and highlighting connexin-mediated redox signaling as a potential therapeutic target for cartilage degeneration.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"196-209"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of STAT1 alleviates oxidative damage in retinal pigment epithelial cells and exhibits neuroprotective effects in autoimmune optic neuritis by upregulating IFI30 lysosomal thiol reductase.","authors":"Siqi Ma, Jiajia Yuan","doi":"10.5603/fhc.104300","DOIUrl":"10.5603/fhc.104300","url":null,"abstract":"<p><strong>Introduction: </strong>Oxidative damage-induced retinal pigment epithelial (RPE) cell apoptosis and optic nerve inflammation and demyelination are closely related to the pathogenesis of optic neuritis (ON). STAT1 has been found to be activated in the retina and optic nerve of ON rats. This study aimed to determine whether STAT1 depletion exerts neuroprotective effects against ON in both cellular and animal models.</p><p><strong>Material and methods: </strong>ARPE-19 cells were stimulated by H₂O₂ to induce oxidative stress, followed by STAT1 and IFI30 silencing. CCK-8 and flow cytometry assays assessed ARPE-19 cell viability and apoptosis. RT-qPCR, Western blotting, DCFH-DA staining, and commercial kits detected the levels of STAT1, IFI30, apoptosis markers, and antioxidant/oxidative markers. CHIP and luciferase reporter assays validated the binding between STAT1 and IFI30 promoter. Female C57BL/6 mice were immunised with myelin oligodendrocyte glycoprotein (MOG) peptide (MOG35-55) to induce experimental autoimmune encephalomyelitis, an animal model of ON. Optic nerve inflammation, demyelination, axonal loss, and retinal ganglion cell (RGC) apoptosis in encephalomyelitis (EAE) mice after STAT1 knockdown were evaluated via haematoxylin and eosin, luxol fast blue, immunofluorescence, and Brn3a-TUNEL double staining.</p><p><strong>Results: </strong>STAT1 silencing reversed the H₂O₂-induced increase of cell apoptosis and oxidative stress and the decrease in cell viability in ARPE-19 cells. STAT1 bound with the IFI30 promoter region and negatively regulated its expression. IFI30 knockdown antagonised the protection of STAT1 silencing against H₂O₂-induced oxidative stress and apoptosis in ARPE-19 cells. STAT1 depletion alleviated optic nerve inflammation, demyelination, axonal loss, and RGC apoptosis in EAE mice.</p><p><strong>Conclusions: </strong>STAT1 silencing exhibits neuroprotective effects against ON by upregulating IFI30.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"11-27"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of O-GlcNAcylation in pulp tissue and dental pulp stem cells of healthy dental organs.","authors":"María Cristina Franco-Arellanes, Perla Xóchitl Toledo-Valdes, Cynthia Díaz-Hernández, Risk Díaz-Castillejos, Eunice Daysi García-Reyes, Saira Karina Ramírez-Thomé, Beatriz Xóchitl Ávila-Curiel, María Cristina Castañeda-Patlán, Edgar Zenteno, Carlos Josué Solórzano-Mata","doi":"10.5603/fhc.103756","DOIUrl":"10.5603/fhc.103756","url":null,"abstract":"<p><strong>Introduction: </strong>O-GlcNAcylation is a post-translational modification in which a single N-Acetyl-D-Glucosamine (GlcNAc) molecule is added to Ser or Thr residues of proteins. The O-N-acetylglucosaminyl transferase (OGT) enzyme is responsible for adding GlcNAc to the target proteins and N-acetyl-β-D-glucosaminidase (OGA) that removes the GlcNAc residue. O-GlcNAcylation has been described in the pathophysiology of several diseases; however, little has been studied in dental tissue. The aim of the present work is to characterise the product of O-GlcNAcylation and its enzymes at the tissue level in the dental pulp, as well as its expression in dental pulp stem cells (DPSCs) both in situ and in vitro. This enables the recognition of the behaviour of O-GlcNAcylation in pulp tissue without pathology.</p><p><strong>Material and methods: </strong>Pulp tissue was obtained from 10 healthy donors, and the expression of O-GlcNAc, OGT, and OGA was analysed using immunofluorescence with specific antibodies in different regions of the dental pulp. DPSCs were isolated, cultured, and identified with anti-STRO1 (antibody specific for human CD34+ cells, useful for DPSC identification). The expression of O-GlcNAc in DPSCs was confirmed in vitro through Western blot.</p><p><strong>Results: </strong>Different regions of the dental pulp and DPSCs express O-GlcNAc and the enzymes OGT and OGA. O-GlcNAc and OGT expression was more prominent in the odontoblastic layer, cell-rich zone, and in the central core. OGA was distributed throughout the pulp tissue with lower immunoreactivity compared to OGT.</p><p><strong>Conclusions: </strong>Our results suggest that O-GlcNAcylation may play a relevant role in human dental pulp homeostasis and in physiology of DPSCs.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"1-10"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}