Histology and histopathology, Vol.41, Nº2, (2026)
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- ItemOpen AccessA redefinition of prognosis: Invasive carcinoma with metastasis originating from microglandular adenosis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Xiaochun Fei; Dan Chen; Biología Celular e HistologíaAim. To investigate the clinicopathological features, immunophenotype, diagnosis, and prognosis of invasive carcinoma originating from microglandular adenosis. Methods. Two cases of invasive carcinoma originating from microadenosis were analyzed in the Department of Pathology of the Ruijin Hospital affiliated with the Medical College of Shanghai Jiaotong University. Histopathological morphology, immuno-histochemical staining, and prognosis were observed. Results. (1) Histopathological morphology: microscopically, the tumor showed small clusters and nests of infiltrative growth; a few areas showed tubules, and some eosinophilic secretions were observed in the lumen. (2) Immunohistochemistry and molecular genetics: Case 1 was partly positive for S-100, positive for SOX-10, and negative for ER, PR, and HER2 (2+). The result of HER2 gene amplification was negative. Breast and liver tissue lesions in Case 2 were positive for S-100 and SOX-10 but negative for ER and HER2. PR was positive in the liver lesions but showed moderate to strong expression in approximately 80% of the staining. Myoepithelial markers (p63 and calponin) showed loss of myoepithelium around the nests of invasive cancers. TP53 (R213Ter) showed somatic gene variations, and no exon amplification or deletion was detected in BRCA1/2. Conclusion. Invasive carcinoma originating from microadenosis has the same immunophenotype as microadenosis, and its prognosis is difficult to determine.
- ItemOpen AccessADAMTS4 is expressed in different cells and tissues in leprosy skin lesions: A potential biomarker and therapeutic target for leprosy and its reactional phenomena(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Rafael Dantas Soares; Igor Bueno Garrido; Natália Silveira Virgili; Luciana Raquel Vincenzi Fachin; Patricia Sammarco Rosa; Ana Paula Fávaro Trombone; Andrea de Faria Fernandes Belone; Cleverson Teixeira Soares; Biología Celular e HistologíaIntroduction. A disintegrin and metallo-proteinase with thrombospondin motifs-4 (ADAMTS4), a metalloproteinase involved in extracellular matrix (ECM) degradation, is implicated in several pathological conditions. This study evaluated ADAMTS4 in leprosy skin lesions. Methods. In total, 519 skin samples were selected, including 20 healthy controls (HC) and 499 samples with leprosy skin lesions. Leprosy lesions were divided into tuberculoid range “T” (n=95), lepromatous range “L” (n=115), type 1 reaction (n=120), type 2 reaction (n=128), and lesions in regression (n=41). Following standardization with an anti-ADAMTS4 marker, all samples were subjected to immunohistochemistry (IHC). Marker expression in cells or tissues with moderate or intense staining intensity (2+ or 3+) was considered positive, and the absence of or weak expression (0 or 1+) was considered negative. Results. ADAMTS4 was expressed in several cells involved in the inflammatory processes of leprosy, particularly macrophages and fibroblasts, and in different skin tissues affected by leprosy lesions. Marker expression was remarkable in different tissues affected by leprosy lesions compared with the control group. Conclusion. ADAMTS4 expression in different leprosy lesions and their reaction phenomena suggest its contribution to disease progression and reactive inflammatory amplification, indicating ADAMTS4 as a potential biomarker and therapeutic target in leprosy.
- ItemOpen AccessCORM-3 mitigates hypoxia/reoxygenation-induced injury in neonatal rat cardiomyocytes by regulating mitochondrial-mediated apoptosis and complex IV activity(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Qingsheng Niu; Xiaojuan Yang; Junwei Zheng; Xiaohong Wang; Fang Du; Biología Celular e HistologíaBackground. Myocardial ischemia-reperfusion injury (MIRI) is a major contributor to myocardial infarction and leads to significant myocardial dysfunction. Mitochondria, crucial for cellular energy production, are particularly susceptible to damage during ischemia/reperfusion (I/R) events. Carbon monoxide-releasing molecule-3 (CORM-3), a water-soluble compound that releases carbon monoxide (CO), has demonstrated multiple protective effects against I/R injury. Mitochondria are recognized as selective targets for CO’s protective actions in cells. Purpose. This study aimed to explore whether CORM-3 mitigates cardiomyocyte injury during hypoxia/reoxygenation (H/R) by regulating the mitochondrial-mediated apoptosis pathway and mitochondrial respiration. Methods. Neonatal rat cardiomyocytes were cultured and randomly assigned into four groups: control group, H/R group (hypoxia for three hours followed by reoxygenation for six hours), CORM-3 group, and inactivated CORM-3 (iCORM-3) group. CORM-3 and iCORM-3 (12.5 μmol/L) were administered at the onset of hypoxia. Mitochondrial ultrastructure was assessed using transmission electron microscopy. The protein levels of caspase-3, caspase-9, mitochondrial cytochrome c, and cytosolic cytochrome c were analyzed via western blot. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) were measured by flow cytometry. ATP levels were quantified using an ATP Assay Kit, and mitochondrial respiratory chain complex IV activity was determined using a cytochrome oxidase activity colorimetric assay kit. Results. CORM-3 effectively reduced myocardial mitochondrial structural damage induced by H/R and downregulated the expression of caspase-3, caspase-9, and cytosolic cytochrome c. Moreover, CORM-3 inhibited cytochrome c release from mitochondria and enhanced mitochondrial membrane potential. Additionally, CORM-3 diminished ROS production and increased the activity of mitochondrial respiratory complex IV in cardiomyocytes. CORM-3 also alleviated the decline in ATP levels following H/R. The protective effects were lost when using inactivated CORM-3 (iCORM-3), suggesting that CO is the active mediator. Conclusion. The results indicate that CORM-3 effectively alleviates myocardial injury during H/R by inhibiting mitochondria-mediated apoptosis and enhancing mitochondrial respiratory function
- ItemOpen AccessAmygdalin improves ovarian function by inhibiting oxidative stress and inflammation in premature ovarian failure mice(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jintao Han; Jianyuan Li; Jin Yao; Wenwei Jiang; Biología Celular e HistologíaBackground. Menstrual stoppage, follicular dysplasia, and hypergonadotropic hypoestrogenism in women under forty are among the symptoms of premature ovarian failure (POF). This study aimed to explore the role and mechanism of amygdalin on ovarian function in a POF mouse model. Methods. A POF mouse model was established via injection of D-galactose (D-gal), followed by amygdalin treatment. Histological staining of ovarian tissues was applied to determine follicular development and granulosa cell apoptosis. Levels of malondialdehyde (MDA), glutathione peroxidase (GSH-px), and superoxide dismutase (SOD) were measured in ovarian tissues. Enzyme-linked immunosorbent assay was used to detect levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), progesterone (P), estradiol (E2), anti-Müllerian hormone (AMH), and reactive oxygen species (ROS) in serum, and tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels in ovaries. Results. D-gal increased levels of FSH, LH, ROS, MDA, TNF-α, IL-1β, IL-6, Bax, atretic follicles, and granulosa cell apoptosis, and decreased P, E2, AMH, SOD, GSH-px, Bcl-2, and primordial, primary, secondary, and total follicles (p<0.01). Amygdalin with different concentrations reversed the effects of D-gal on mice (p<0.05). Conclusion. Amygdalin improved ovarian function in POF mice through inhibiting oxidative stress, inflammation, and granulosa cell apoptosis. These results suggested that amygdalin may be a potential antioxidant for POF treatment.
- ItemOpen AccessThe effects of polysaccharides from Schizophyllum commune (Fr.) on amyloid-β and GFAP-induced neuronal injury in hippocampal regions of hyperlipidemia-affected rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Wanida Chuaikhongthong; Uraporn Vongvatcharanon; Manaras Komolkriengkrai; Udomlak Matsathit; Wipapan Khimmaktong; Natyamee Thipthong; Biología Celular e HistologíaAims. The hippocampal region is an essential area for memory. Alzheimer's disease (AD) continues to impact this brain region. It is caused by the accumulation of amyloid-β (Aβ) along with neurofibrillary tangles, together with glial fibrillary acidic protein (GFAP) expression, which causes loss of synapses, resulting in memory problems. Consuming a high-fat diet (HFD) causes the abnormal production of certain neuro-transmitters through the gut-brain axis system, resulting in hippocampal neuron damage. Therefore, this study examined the effects of polysaccharides from Schizophyllum commune (Fr.) or split-gill mushroom (SG) in rats induced with an HFD. Methods. The Y-maze test assessed spontaneous alternation percentages and short-term memory in all rat groups, while H&E and Cresyl violet staining revealed alterations in the characteristics of neurons across treatment groups. Immunofluorescence was employed to identify the expressions of neurodegenerative and inflammatory proteins. Results. The short-term memory was evaluated using the Y-maze test, which found that the spontaneous alternation percentage was lower in the HFD group and higher in the HFD+SG group compared with the control group. Alterations in neuron characteristics were revealed by Cresyl violet and H&E staining. The HFD group was found to have necrotic neurons; however, the HFD+SG group had less damage than the HFD group. Immunofluorescence observations indicated the expression of Aβ and GFAP proteins; the HFD group showed an increase in Aβ and GFAP accumulation, whereas in the HFD+SG group, these were significantly reduced. Conclusions. The study demonstrated improvements in hippocampal neurons, suggesting that polysaccharides from SG may be able to lessen the harm caused to the brain by consuming an HFD.
- ItemOpen AccessElectroacupuncture preconditioning attenuates acute lung injury in mice through transient receptor potential vanilloid 4-mediated anti-inflammation via inhibiting the p38 MAPK signaling pathway(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jiangtian Yan; Nina Yin; Wan Liu; Zhigang Wang; Lin Zeng; Biología Celular e HistologíaThe objective of this study was to investigate the protective effect of electroacupuncture (EA) preconditioning on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. The changes in inflammatory factors and total protein content in bronchoalveolar lavage fluid (BALF) were quantified using enzyme-linked immunosorbent assay (ELISA) and bicinchoninic acid assay (BCA). Hematoxylin and eosin (H&E) staining was employed to assess the extent of lung injury, while Ly-6G immunohistochemistry was used to examine the infiltration of inflammatory cells. Western blot analysis was employed to detect the expression of TRPV4 and proteins associated with the mitogen-activated protein kinase (MAPK) signaling pathway. In comparison with the sham-operated group, the model group demonstrated an elevated production of inflammatory factors in the BALF, augmented total protein content, elevated lung injury score, increased number of Ly-6G-positive cells, upregulation of TRPV4 expression in the lung, and enhanced p38 phosphorylation. The aforementioned pathological changes were significantly improved by EA preconditioning. Furthermore, the protective effect of EA preconditioning on ALI mice was verified by the use of GSK1016790A, an agonist of TRPV4, which demonstrated that this effect is exerted through the TRPV4-mediated p38 MAPK signaling pathway.
- ItemOpen AccessMuscle atrophy following anterior cruciate ligament reconstruction: A narrative review(Universidad de Murcia, Departamento de Histología e Histopatología, 2026) Kaneguchi, Akinori; Ozawa, Junya; Biología Celular e HistologíaMuscle weakness is a common issue following anterior cruciate ligament (ACL) reconstruction and is closely linked to muscle atrophy. Preventing or reducing this atrophy is a key goal of rehabilitation. This review summarizes current knowledge on muscle atrophy after ACL reconstruction, including its spatial distribution, time course, underlying mechanisms, and potential interventions. Atrophy affects multiple lower limb muscles and may be influenced by the type of graft used. Tendon harvesting appears to negatively impact the muscle belly of the donor muscle, while atrophy may also occur in the contralateral limb independently of graft harvesting. Muscle atrophy is often already present before surgery and tends to worsen postoperatively. Although partial recovery may occur, long-term deficits are frequently observed. At the muscle fiber level, evidence is inconsistent regarding which fiber types are more vulnerable to atrophy. A transient shift toward faster fiber types has been reported after surgery. On the cellular and molecular level, satellite cell depletion via apoptosis may hinder muscle regrowth and thereby contribute to persistent muscle atrophy. Concurrently, increased expression of myostatin, atrogin-1, and muscle RING-finger-1, along with postoperative inflammation, may promote protein degradation, further exacerbating muscle atrophy. Rehabilitation strategies that involve early immobilization or non-weight bearing may exacerbate atrophy. Interventions such as eccentric training, neuromuscular electrical stimulation, blood flow restriction training, pharmacological agents, and nutritional support demonstrate potential, but no definitive treatment has been established. Future studies using appropriate animal models to clarify the molecular mechanisms of muscle atrophy will be crucial for developing effective therapies.
- ItemOpen AccessLocal amifostine administration mitigates chemotherapy-induced esophageal mucosal damage: A novel approach for targeted treatment in a rabbit model(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Junqin Zhang; Bin Wang; Yaxing Li; Biología Celular e HistologíaObjective. Effective preventive measures for radiotherapy and chemotherapy-induced esophagitis are currently lacking. This study aims to investigate the local impact of chemotherapeutic agents on normal esophageal tissue and assess the cytoprotective effects of amifostine against chemotherapy-induced esophageal injury. Methods. Twenty-four New Zealand white rabbits were randomly assigned to the control group, which only received saline; the cisplatin (DDP) group, which received 0.25 mg/ml of the chemotherapeutic drug (DDP); and the combined treatment group, which received pre-treatment with 0.8 mg/ml amifostine followed by 0.25 mg/ml DDP. Each group consisted of eight rabbits. A custom-made balloon device for targeted esophageal drug delivery was inserted into the esophagus, followed by the infusion of DDP and/or amifostine into the created space. After six days, rabbits were euthanized, and esophageal specimens were examined for mucosal damage. Results. Macroscopically, compared with the control group, the DDP group exhibited significant thickening, edema, mucosal ulceration, and congestion in the infused esophageal region. Conversely, the combined treatment group showed mild thickening and a smooth or mildly congested mucosal surface. Microscopically, the DDP group displayed extensive mucosal detachment, edema, dilated submucosal blood vessels, and substantial infiltration of inflammatory cells. The combined treatment group exhibited partial mucosal detachment and moderate inflammatory cell infiltration in the submucosal and muscular layers, with few inflammatory cells in the muscle layer. Conclusion. This study provided evidence that damage caused by the local infusion of DDP might be reduced by pre-treatment of the cytoprotective agent amifostine.
- ItemOpen AccessEmpagliflozin protected kidney function in CKD rat through suppressing hypoxic and fibrotic signalings mediated inflammation and EMT(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jui-Ning Yeh; Tsuen-Wei Hsu; John Y. Chiang; Ben-Chung Cheng; Pei-Hsun Sung; Shun-Cheng; Chi-Ruei Huang; Pei-Lin Shao; Hon-Kan Yip; Chih-Chao Yang; Biología Celular e HistologíaBackground. This study tested the hypothesis that PI3K/Akt/GSK3β and TGF-β/Smad2/3 signaling play essential roles in mediating the epithelial-mesenchymal transition (EMT) and fibrosis, resulting in the deterioration of renal function and parenchyma in chronic kidney disease (CKD) rats, which is reversed by early empagliflozin treatment. Methods and results. NRK-52E cells were divided into the A1 (NRK-52E), A2 (NRK-52E + 200 μM p-Cresol), A3 (NRK-52E + 200 μM p-Cresol + 50 μM empagliflozin), B1 (NRK-52E), B2 (NRK-52E + 5 ng/mL TGF-β1) and B3 (NRK-52E + 5 ng/mL TGF-β1 + 50 μM empagliflozin) groups. Compared with those in the A1 group, the expression levels of proteins related to the EMT (TGF-β1/p-Smad2/p-Smad3/α-SMA), extracellular matrix (MMP2/9) and EMT (IGF-1) activators were significantly higher in the A2 group, but these changes were significantly reversed in the A3 group, whereas the protein expression levels of antifibrotic markers (TIMP1/TIMP2) exhibited the opposite pattern to the EMT-related proteins among the groups (all p<0.001). The expression of these proteins, along with the other EMT markers (snail, fibronectin, and vimentin) related to cellular function/protein expression, also exhibited an identical pattern to the A1 to A3 groups among Groups B1 to B3 (all p<0.001). Adult male SD rats were categorized into Groups 1 (sham-operated control), 2 (CKD) and 3 (CKD + empagliflozin). On Day 56 after CKD induction, the renal artery resistive index (RARI) was significantly higher in Group 2 than in Groups 1 and 3 and significantly higher in Group 3 than in Group 1 (all p<0.0001). The expression of EMT (Snail/α-SMA/ fibronectin/vimentin/TGF-β1/p-Smad2/3), apoptotic (cleaved caspase-3/cleaved-PARP), inflammatory (HIF-1α/IL-1β/TNF-α/MPO/MMP-2/MMP-9), and cell stress signaling (p-PI3K/p-Akt/GSK-3β) proteins and the cellular kidney injury score, expression of fibrosis and EMT markers (Snail/vimentin)/glomerular-hyper-cellularity/fibrocellular crescent formation displayed an identical pattern, whereas the cellular expression of podocyte components (podocin/synaptopodin/ZO-1) displayed the opposite pattern to the RARIs among the groups (all p<0.0001). Conclusions. Empagliflozin protected kidney function and architecture mainly by suppressing fibrosis, cellular oxidative stress signaling, the EMT and inflammation.
- ItemOpen AccessLoss of PDE10A is associated with metastasis of colon adenocarcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Nicholas Nuechterlein; Vinny Ha; Allison Shelbourn; Ashis Chowdhury; Yeshavanth K Banasavadi-Siddegowda; Jerzy Lasota; Markku Miettinen; Patrick J. Cimino; Sumaita Arowa; Biología Celular e HistologíaPhosphodiesterase 10A (PDE10A), located on cytoband 6q27, acts as a haploinsufficient tumor suppressor in glioblastoma, where its loss drives aggressive tumor behavior and is associated with a proneural-to-mesenchymal (PN-MES) shift. Lever-aging bioinformatic analyses of The Cancer Genome Atlas (TCGA) pan-cancer dataset, we identified gastrointestinal carcinomas, specifically stomach adenocarcinoma and colon adenocarcinoma, as cancers where 6q27/PDE10A loss is prognostic. In both stomach adenocarcinoma and colon adenocarcinoma, PDE10A loss was associated with reduced overall survival (OS) and progression-free survival (PFS). Additionally, PDE10A loss correlated with increased lymphatic invasion and higher AJCC pathologic nodal stage in colon adenocarcinoma. In an independent institutional cohort, immunohistochemical analysis showed lower PDE10A expression in metastatic colon adenocarcinomas compared to primary tumors. Furthermore, PDE10A loss and decreased protein expression corresponded with an epithelial-to-mesenchymal transition (EMT) phenotype in both cohorts, consistent with the known PN-MES shift observed in glioblastoma. In summary, PDE10A loss in colon adenocarcinoma is associated with decreased OS and PFS, more frequent lymphatic invasion, higher pathologic nodal stage, metastatic disease, and an EMT phenotype.
- ItemOpen AccessPU.1 aggravates hepatic sinusoidal obstruction syndrome by upregulating PTBP1 and activating the Wnt/β-catenin pathway(2026) Yang, Li; Ju, Honglin; Chen, Zhiyuan; Cheng, Siqi; Liu, Ya; Wang, Xiangyang; Biología Celular e HistologíaObjective. Hepatic sinusoidal obstruction syndrome (HSOS) is a disease characterized by damage to hepatic sinusoidal endothelial cells (HSECs). This research investigates the role and regulatory pathway of PU box-binding protein (PU.1) in the progression of HSOS. Methods. We established an in vivo HSOS model through peritoneal administration of monocrotaline (MCT). Primary murine HSECs were isolated and treated with various concentrations of MCT to establish an in vitro HSOS model. PU.1 knockdown was achieved using lentiviral shRNA constructs, and its impact on oxidative stress, PTBP1 expression, β-catenin mRNA stability, and Wnt/β-catenin signaling was evaluated through kits, RT-qPCR, and western blot. Dual-luciferase and chromatin immunoprecipitation assays were conducted to assess the interaction between PU.1 and the PTBP1 promoter. The molecular association between PTBP1 and β-catenin mRNA was confirmed through RNA pull-down and RIP assays. Results. PU.1 was upregulated in MCT-induced HSOS, contributing to elevated oxidative stress and activation of the Wnt/β-catenin pathway. PU.1 directly enhanced PTBP1 transcription, which stabilized β-catenin mRNA and sustained Wnt/β-catenin signaling. PU.1 knockdown alleviated oxidative stress, reduced liver damage, and disrupted the PTBP1-β-catenin interaction, leading to Wnt/β-catenin activity inhibition. Overexpression of PTBP1 reversed the protective effects of PU.1 knockdown, reinstating oxidative stress and reactivating Wnt/β-catenin signaling. Conclusion. PU.1 facilitated HSOS pathogenesis by promoting the transcriptional activity of PTBP1 and activating the Wnt/β-catenin pathway. Targeting PU.1 can serve as a promising therapeutic strategy for reducing oxidative stress and liver damage in HSOS.
- ItemOpen AccessRecent progress in macrophage- mediated tendon injury and healing(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Yining Zhang; Yanzhao Dong; Xiaodi Zou; Ahmad Alhaskawi; Fangyu Yi; Sohaib Hasan Abdullah Ezzi; Vishnu Goutham Kota; Mohamed Hasan Abdulla Hasan Abdulla; Haiying Zhou; Alenikova Olga; Sahar Ahmed Abdalbary; Jinhui Liang; Hui Lu; Weijie Zhou; Biología Celular e HistologíaRecently, the role of macrophages in tendon repair has received increased attention. These cells are versatile, playing multiple roles, such as defending the host, engulfing debris, producing growth factors, and releasing substances that can both promote and alleviate inflammation. Within the scope of tendon repair and tendinopathy resolution, macrophages are essential contributors. However, the current understanding of macrophage involvement in tendon healing remains limited. Hence, understanding macrophages' impact on tendon healing is of considerable importance for devising innovative treatment approaches. It is crucial to examine the precise role that macrophages play in tendon recovery, as it provides new understanding that can propel both research and the development of therapeutic methods aimed at enhancing tendon recovery moving forward
- ItemOpen AccessTau aggregation(Universidad de Murcia, Departamento de Histología e Histopatología, 2026) Domene-Serrano, Indalo; Santa-María, Ismael; Hernandez, Felix; Avila, Jesús; Biología Celular e HistologíaMicrotubule-associated protein tau is predominantly expressed in neurons in the form of multiple isoforms generated by alternative splicing. These isoforms differ in the presence of either three or four microtubule-binding repeats. These binding regions not only regulate tau’s interaction with microtubules but are also critically involved in its pathological self-aggregation. Such aggregates are a defining feature of a group of neurodegenerative disorders collectively referred to as tauopathies. In this work, we examine the mechanisms underlying tau self-aggregation, the molecular and cellular factors that drive this process, and the structural features of tau aggregates. Aggregates composed of isoforms with three versus four microtubule-binding repeats display distinct morphologies, which serve as pathological hallmarks for different tauopathies. Finally, we discuss potential therapeutic strategies aimed at preventing or promoting the clearance of tau aggregates.
- ItemOpen AccessITGAX promotes Th17-cell differentiation and drives pathogenesis in pediatric ulcerative colitis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Dong Zhan; Wanying Xie; Biología Celular e HistologíaBackground. Pediatric ulcerative colitis (UC) is an inflammatory bowel disease characterized by dysregulated immune responses and intestinal inflammation, often more severe than adult-onset UC. Th17 cells play a crucial role in UC pathogenesis but the mechanisms regulating their differentiation and recruitment in pediatric UC remain incompletely understood. Methods. Transcriptomic analysis of pediatric UC patients and weighted gene co-expression network analysis (WGCNA) were performed to identify key dysregulated genes. The functional role of the candidate gene ITGAX was investigated using in vitro Th17 differentiation assays with siRNA knockdown and an in vivo dextran sodium sulfate (DSS)-induced UC mouse model with intrarectal siRNA administration. Results. WGCNA identified ITGAX, SOCS3, CXCL1, CASP1, and CXCL11 as core upregulated genes in pediatric UC, with ITGAX being a novel candidate regulator of Th17 cells. ITGAX knockdown in naive CD4+ T cells impaired Th17 differentiation and IL-17A production in vitro. In the DSS-induced UC mouse model, intrarectal ITGAX siRNA ameliorated colonic inflammation and ulceration, suppressed IL-17A levels, and selectively reduced the expansion of IFNγ-IL-17+ Th17 cells in the colon. Conclusion. ITGAX is a key promoter of Th17-cell differentiation and expansion, contributing to the pathogenesis of pediatric UC. Targeting ITGAX may represent a potential therapeutic strategy for pediatric UC by modulating aberrant Th17 responses.
- ItemOpen AccessNeuN expression in health and disease: A histological perspective on neuronal heterogeneity(Universidad de Murcia, Departamento de Histología e Histopatología, 2026) Moon, Joongbum; Hyeon Ahn, Ji; Won, Moo-Ho; Biología Celular e HistologíaNeuronal nuclei (NeuN), also known as Rbfox3, is a widely used neuronal marker for identifying postmitotic neurons in both basic neuroscience and diagnostic neuropathology. Since its discovery, NeuN immunoreactivity has enabled accurate neuron counting, injury assessment, and anatomical mapping. However, accumulating evidence demonstrates that NeuN is not universally expressed across all mature neurons. Specific neuron types, such as olfactory mitral cells, cerebellar Purkinje cells, and retinal photoreceptors, consistently lack NeuN immunostaining despite functional maturity. Moreover, NeuN expression is dynamically regulated under pathological conditions. In ischemia-reperfusion (I/R) injury, neurodegenerative diseases (e.g., Alzheimer’s and Parkinson’s), and traumatic brain injury or epilepsy, selected for their representative diversity in pathophysiological stress (ischemic, degenerative, and mechanical), NeuN downregulation may reflect functional compromise, stress responses, or reversible transcriptional changes rather than irreversible cell loss. These findings highlight the limitations of interpreting NeuN negativity as neuronal death. This review synthesizes recent findings on NeuN expression patterns, molecular mechanisms regulating its presence or absence, and the implications for research and diagnosis. We propose that NeuN should not be regarded as a binary marker but rather as a dynamic indicator of neuronal state. Multi-marker strategies and molecular tools such as spatial transcriptomics and RNA sequencing are suggested to improve the resolution of neuronal analysis. As histological and transcriptomic approaches converge, NeuN’s role will likely expand from a structural identifier to a contextual readout of neuronal integrity and function.