European Journal of Histochemistry最新文献

{"title":"Discovering ferroptosis in biliary epithelium during liver fibrosis.","authors":"Romina Mancinelli, Arianna Casini, Stefano Leone, Ludovica Ceci, Rosa Vaccaro, Antonella Di Sotto, Giorgio Vivacqua, Rosemarie Heyn, Ludovica Garro, Marco Tagliafierro, Filippo Maria Bassi, Emanuele Bocci, Andrea Bassi, Luigi Pannarale, Antonio Franchitto, Paolo Onori, Eugenio Gaudio","doi":"10.4081/ejh.2026.4615","DOIUrl":"https://doi.org/10.4081/ejh.2026.4615","url":null,"abstract":"<p><p>Ferroptosis is an iron-dependent regulated cell death characterized by iron accumulation and lipid peroxidation. The liver represents the primary site of iron-overload injury due to its role in iron metabolism, but the potential role of ferroptosis in the biliary epithelium is yet unknown. The study investigated the recruitment of ferroptosis under control conditions and after bile duct ligation (BDL), highlighting the effects of ferroptosis inducers and inhibitors in a cell line of cholangiocytes. In addition, we identified iron deposits through Perls Prussian blue as well as the presence of proteins such as ferritin, transferrin receptor 1 (CD71), glutathione peroxidase-4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4). The results showed an increase in the expression of ferritin, CD71 and ACSL4 in the BDL model, whereas GPX4 was reduced in the cholestatic model in comparison to the control. In addition, sorafenib failed to trigger ferroptosis in cholangiocytes, whereas erastin was a potent inducer. Conversely, ferrostatin-1 (Fer-1) did not inhibit ferroptosis, while β-mercaptoethanol (βME) could protect cholangiocytes from ferroptosis-induced cell death. All these findings are important for understanding the involvement of ferroptosis in cholangiocyte pathophysiology and may support additional studies regarding the possible application of ferroptosis modulators in the treatment of liver fibrosis.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149289743","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":"RRP12 knockdown inhibited inflammation and p53/NF-κB pathway and alleviated heterotopic ossification in mice.","authors":"Yuchen Hu, Zihao Zeng, Wen Jin, Chenggang Wang, Xiaofeng Liu, Yusheng Sun, Qing Gao","doi":"10.4081/ejh.2026.4730","DOIUrl":"10.4081/ejh.2026.4730","url":null,"abstract":"<p><p>Heterotopic ossification (HO) is a pathological process, featured by the aberrant mature bone tissue in soft tissues outside the normal skeletal system, commonly occurring following trauma or major joint surgery. Ribosomal RNA Processing 12 Homolog (RRP12) has been confirmed to display multiple roles in ribosome synthesis, DNA damage, cell cycle and cell differentiation processes. However, the regulatory influences of RRP12 in HO progression keep vague and require further investigation. In this project, it was illustrated that RRP12 expression was markedly up-regulated in HO mice. Inhibition of RRP12 retarded the progression of HO in mice. Furthermore, RRP12 knockdown alleviated inflammation. Besides, it was revealed that suppression of RRP12 inactivated the p53/NF-κB pathway. Lastly, in bone marrow mesenchymal stem cells (BMSCs), it was verified that knockdown of RRP12 suppressed osteogenic differentiation of BMSCs. In conclusion, RRP12 knockdown inhibited inflammation and p53/NF-κB pathway and alleviated HO in mice. This study not only expands the current understanding of the molecular underpinnings of HO but also identifies RRP12 as a potential actionable target for therapeutic intervention. Nonetheless, further investigations are warranted to delineate the upstream regulators of RRP12 and to evaluate its translational feasibility in clinical settings.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128448","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":"Short- and long-term effects of dronedarone on Cav3.1- and Cav3.2-T-type calcium channel current.","authors":"Xuan Jiang, Jianan Xu, Honghou He, Zelong Cao, Da Liu, Zhiyan Chen, Ligang Ding, Mingqi Zheng","doi":"10.4081/ejh.2026.4534","DOIUrl":"10.4081/ejh.2026.4534","url":null,"abstract":"<p><p>T-type calcium channels (TTCCs), including the Cav3.1 and Cav3.2 subtypes, play a critical role in regulating cardiac electrical activity. Their abnormal expression is closely associated with arrhythmias and cardiac dysfunction caused by myocardial infarction (MI). Dronedarone, a multi-target antiarrhythmic drug, is widely used to treat atrial fibrillation and atrial flutter but has shown adverse effects under pathological conditions such as MI. This study aims to investigate the direct effects and underlying mechanisms of dronedarone on TTCCs. Using neonatal rat cardiomyocytes, HEK293T cells transfected with Cav3.1 and Cav3.2, and MI rat model, we systematically analyzed the effects of dronedarone on TTCC activity. Dronedarone significantly inhibited Cav3.2 channel activity with an IC50 of 9.20 µM, while its effect on Cav3.1 was weaker (IC50 = 46.41 µM). Chronic treatment with dronedarone also slowed the activation and inactivation kinetics of TTCCs. In vivo experiments demonstrated that dronedarone exacerbated myocardial damage and fibrosis in the MI model. These findings suggest that dronedarone inhibits TTCC activity, particularly the Cav3.2 subtype, and alters its kinetic properties. This study reported the electrophysiological effects of dronedarone on T-type calcium channels, providing new insights into its electrophysiological properties and potential role in adverse cardiac events.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13688010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225073","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":"Dopamine beta-hydroxylase mediates atherosclerosis progression by regulating copper metabolism <i>via</i> PHOX2A.","authors":"Qingquan Xue, Guilin Feng, Jiqiong Hu, Fangkuan Li, Shusen Tang","doi":"10.4081/ejh.2026.4586","DOIUrl":"https://doi.org/10.4081/ejh.2026.4586","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a major cardiovascular disease whose underlying molecular mechanisms remain incompletely understood. This study investigates the role of dopamine beta-hydroxylase (DBH) in AS pathogenesis and its regulation of copper metabolism via the transcription factor PHOX2A. Through transcriptomic profiling of aortic tissues from ApoE⁻/⁻ mice fed a high-fat diet, we identified 2891 differentially expressed genes (DEGs) between AS and control mice, with DBH being significantly upregulated. DBH expression was also elevated in the serum of AS patients and in ox-LDL-treated human vascular smooth muscle cells (HVSMCs). Mechanistically, we demonstrate that PHOX2A directly activates the DBH promoter, and that DBH knockdown attenuates ox‑LDL‑induced apoptosis and lipid accumulation in HVSMCs while PHOX2A overexpression exacerbates these effects. Importantly, DBH knockdown in ApoE⁻/⁻ mice not only reduced atherosclerotic plaque burden and improved serum lipid profiles but also restored serum copper concentrations and altered the expression of cuproptosis‑related proteins (FDX1, LIAS, DLAT). These findings identify DBH as a key mediator of AS progression linked to PHOX2A‑dependent regulation of copper metabolism and cuproptosis, suggesting that targeting the DBH/PHOX2A axis may represent a novel therapeutic strategy for AS.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149289754","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":"Sinensetin ameliorates osteoarthritis progression by modulating the NF-κB/NLRP3 signaling pathway and suppressing chondrocyte pyroptosis.","authors":"Zhendong Liu, Ruizhou Liu, Hongwei Yue, Peilai Liu, Rui Wang","doi":"10.4081/ejh.2026.4587","DOIUrl":"https://doi.org/10.4081/ejh.2026.4587","url":null,"abstract":"<p><p>Sinensetin (SIN) is a natural flavonoid with potential anti‑inflammatory effects. This study investigated whether SIN ameliorates osteoarthritis (OA) and explored its underlying mechanisms. In vitro, SIN (0.05-1 μg/mL) protected human OA chondrocytes from IL‑1β‑induced viability loss. Transcriptome sequencing and molecular docking identified SERPINA3 as a candidate target of SIN. SIN reduced the expression of NLRP3, GSDMD, and ASC, inhibited pyroptotic morphology, decreased TUNEL‑positive cells and LDH release, and lowered IL‑1β and IL‑18 secretion in IL‑1β‑treated chondrocytes. Knockdown of SERPINA3 reversed these effects, suggesting that SIN acts through SERPINA3 to inhibit the NLRP3 inflammasome. In a rat DMM‑induced OA model, SIN (20 mg/kg/day for 6 weeks) alleviated pain, reduced OARSI scores, improved cartilage matrix staining (Safranin O, Masson's trichrome), attenuated synovial hyperplasia and posterior capsule adhesions, and decreased plasma IL‑1β and IL‑18 levels. Western blot of rat cartilage confirmed that SIN suppressed GSDMD and NLRP3 expression. These results indicate that SIN ameliorates OA progression by inhibiting SERPINA3‑mediated NF‑κB/NLRP3‑driven chondrocyte pyroptosis. SIN may be a potential therapeutic candidate for OA.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128469","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":"Emerging role of nuclear phospholipase C-β1 in lung cancer.","authors":"Ilaria Versari, Sara Salucci, Anna Bartoletti Stella, Stefania Benini, Marco Gambarotti, Camilla Sbrighi, Paola Ulivi, Andrea Ambrosini Spaltro, Mirko Traversari, Franco Stella, Beatrice Aramini, Irene Faenza","doi":"10.4081/ejh.2026.4774","DOIUrl":"10.4081/ejh.2026.4774","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is a highly aggressive malignancy accounting for approximately 85% of all lung cancer cases. To better understand its pathology and prognosis, this study focused on the molecular profiling of tissues and clinical outcomes derived directly from lung cancer patients. Recently, the involvement of phospholipase enzymes in cancer has been highlighted, as they are involved in crucial cellular signaling pathways. The mRNA and protein expression levels of phospholipase C (PLC) isoforms were analyzed in biopsies from NSCLC patients. Utilizing Kaplan-Meier plotter database, the prognostic role of PLCs could be assessed. Researchers identified significant changes in mRNA and protein expression levels of various PLC isoforms in patient biopsies. Notably, PLCβ1 was found to be overexpressed in every tumor sample. In addition, the use of KM-Plotter hypothesized an association between elevated PLCβ1 levels and poorer survival outcomes, emphasizing the variations due to patient-specific factors, such as tumor stage and smoking history. Immunohistochemistry performed on patient-derived samples revealed a clear contrast in protein localization. In tumor tissues, PLCβ1 was predominantly found in the nucleus, whereas in adjacent healthy tissues, it remained almost exclusively in the cytoplasm. Nuclear localization is known to be linked to cell cycle modulation; therefore, it may represent a critical event in cancer development. The study highlighted critical alterations in PLC isoforms observed within the patient population. These findings demonstrate that PLCβ1 is significantly upregulated in malignant tissues and correlates with adverse clinical outcomes. Consequently, PLCβ1 may serve as a candidate biomarker, warranting further investigation into its potential role in the management and treatment of NSCLC patients.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149289749","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":"AFF3 regulates ferroptosis and malignant progression in bladder cancer cells <i>via</i> the NRF2/GPX4 signaling axis.","authors":"Song Chen, Xiangyun Li, Peiqin Zhan, Tianjiao Luo, Jiansong Wang","doi":"10.4081/ejh.2026.4756","DOIUrl":"https://doi.org/10.4081/ejh.2026.4756","url":null,"abstract":"<p><p>Bladder cancer (BCa) is a common malignancy of the urinary system, and its malignant progression is closely associated with ferroptosis. As a transcriptional regulator in the AFF family, AFF3 participates in the regulation of gene expression in multiple diseases; however, its role in BCa and its relationship with ferroptosis remain unclear. This study aimed to investigate the role of AFF3 in BCa progression and the molecular mechanism through which it regulates ferroptosis. AFF3 expression was examined through bioinformatics analysis and experiments in clinical tissues and cells. AFF3 was overexpressed in UM-UC-3 cells, and cell proliferation and migration were assessed using CCK-8, colony formation, and Transwell assays. Ferroptosis was evaluated using BODIPY 581/591 C11, MDA, and ferroptosis-related protein assays, and rescue experiments were performed with the ferroptosis inhibitor Fer-1. A subcutaneous xenograft model was established in nude mice, and the NRF2 activator TBHQ was used to verify the in vivo role and mechanism of AFF3 in regulating ferroptosis. Our results revealed that AFF3 was expressed at low levels in BCa. Functionally, AFF3 overexpression inhibited BCa cell proliferation, colony formation, and migration; promoted the accumulation of lipid ROS and MDA; downregulated GPX4 and SLC7A11 expression; and increased sensitivity to ferroptosis. Notably, Fer-1 partially reversed these effects. Mechanistically, AFF3 upregulated KEAP1 and inhibited NRF2 nuclear translocation, thereby reducing GPX4 expression; conversely, TBHQ partially reversed these molecular and functional changes. In vivo animal experiments further confirmed that AFF3 overexpression inhibited xenograft growth and promoted ferroptosis-related changes, whereas TBHQ attenuated the regulatory effects of AFF3. Overall, these findings demonstrate that AFF3 exerts tumor-suppressive effects in BCa by promoting KEAP1 expression and inhibiting NRF2 nuclear translocation and GPX4-mediated antioxidant defense, thereby enhancing the sensitivity of tumor cells to ferroptosis and suppressing the malignant progression of BCa.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149247295","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":"Histopathological evaluation of RPL5 expression in triple-negative breast cancer: an integrated immunohistochemical and transcriptomic study.","authors":"Bing Zhao, Peiyuan Yu, Li Li, Zhenhui Zhao, Xiner Zhang","doi":"10.4081/ejh.2026.4599","DOIUrl":"10.4081/ejh.2026.4599","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by high invasiveness, limited therapeutic options, and unfavorable clinical outcomes. Ribosomal protein L5 (RPL5), a component of the large ribosomal subunit, has been implicated in ribosome biogenesis, translational regulation, and p53-associated cellular processes. This study investigated the immunohistochemical expression pattern of RPL5 in TNBC tissues and explored its potential biological significance through integrated transcriptomic analyses. Tumor tissues from 37 patients with TNBC and 7 adjacent non-tumorous breast tissues were collected from the Affiliated Tumor Hospital of Xinjiang Medical University between December 2017 and December 2023. RPL5 protein expression was evaluated by immunohistochemistry, and its association with clinicopathological characteristics was analyzed. Public transcriptomic datasets from TCGA-BRCA and GEO were further used to validate RPL5 expression patterns in TNBC. Co-expression analysis and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to investigate potential biological functions and signaling pathways associated with RPL5. Immunohistochemical analysis demonstrated significantly lower RPL5 protein expression in TNBC tissues compared with adjacent normal breast tissues (p=0.001). In contrast, transcriptomic analyses revealed significantly higher RPL5 expression in TNBC compared with non-TNBC breast cancer subtypes (p<0.001). No significant associations were observed between RPL5 expression and clinicopathological parameters, including age, tumor size, menopausal status, TNM stage, histological grade, or lymph node metastasis (all p>0.05). Survival analysis showed no significant difference in overall survival between patients with high and low RPL5 expression. Functional enrichment analyses indicated that RPL5-related genes were predominantly involved in ribosome biogenesis, translational regulation, and p53-related signaling pathways. These findings suggest that abnormal RPL5 expression may be associated with TNBC biology through ribosome-related programs, although causal roles require functional validation. RPL5 may represent a potential histopathological and molecular indicator associated with TNBC biology, although its precise functional role requires further experimental validation.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13535662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148563483","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":"LncRNA RP11-708J19.2 promotes colorectal cancer progression by binding to SIRT7 <i>via</i> regulating H3K18ac.","authors":"Jiali Ma, Xianglong Tian, Yiwen Qiu, Chen Zhao, Jinghui Wang, Rongrong Jia","doi":"10.4081/ejh.2026.4560","DOIUrl":"10.4081/ejh.2026.4560","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a prevalent malignancy with a complex genetic basis. Recent genome-wide association studies (GWAS) have identified a susceptibility locus at 3p21.31, however, the functional SNP(s) underlying the association between the 3p21.31 region and CRC remain to be elucidated. In this study, we identified rs2101247 as the potential functional SNP and further demonstrated that rs2101247 is significantly associated with the expression of the nearby long non-coding RNA (lncRNA) RP11-708J19.2 (ENSG00000271161.1). Functional experiments showed that RP11-708J19.2 is upregulated in CRC tumor tissues, and its knockdown reduces cell viability while promoting apoptosis in SW1116 and HCT116 cell lines. Mechanistically, RP11-708J19.2 interacts directly with the deacetylase SIRT7, modulating histone H3K18 acetylation (H3K18ac). Specifically, RP11-708J19.2 knockdown leads to a significant upregulation of H3K18ac levels, implicating a SIRT7-mediated epigenetic pathway in CRC progression. Our findings elucidate a novel functional SNP-lncRNA axis that contributes to CRC pathogenesis, providing potential biomarkers for early detection and therapeutic targets for intervention.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13530957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148563468","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":"Immunocytochemical staining for lymphatic and blood vessels with frozen sections: using LYVE-1 for lymphatic vessel and von Willebrand factor for blood vessel marker.","authors":"Tatsuo Tomita, Kunie Mah","doi":"10.4081/ejh.2026.4564","DOIUrl":"10.4081/ejh.2026.4564","url":null,"abstract":"<p><p>Almost all human tissues are supplied with lymphatic vessels, yet histological structure and function of lymphatic vessels is still elusive. Most immunocytochemical studies have been performed with the routinely formalin-fixed and paraffin-embedded tissue. This study aimed to investigate lymphatic and blood vessels immunocytochemically with frozen sections to explore the masked lymphatic and blood vessels in the routinely processed normal tissues. Several normal monkey tissues were frozen in liquid propane, and frozen sections were immunostained for lymphatic and blood vessels using LYVE-1 for lymphatic vessels and von Willebrand factor for blood vessels. In the liver, sinusoids were immunostained panlobularlly for LYVE-1 compared to LYVE-1 immunostaining limited in the pericentral lobe with the routinely processed liver. In the Jejunal villi, lacteals were surrounded by scattered mall venous capillaries. In the large intestines, a few longitudinal lymphatic vessels were detected in lamina propria. Pancreatic islets were surrounded by baskets of rich venous capillaries. Glomerular capillaries were diffusely positive for von Willebrand factor, suggesting leaking capillaries for von Willebrand factor. Prostate had scattered lymphatic and numerous blood vessels in the stroma with nerve bundles in the fibrous capsule. Many lymphatic and blood vessels were immunostained only in frozen sections, which were not immunostained in the routinely processed tissues. Routine processing masks antigen sites of lymphatic and blood vessels. Therefore, immunocytochemical staining with frozen sections is superior to routinely embedded tissues and this immunostaining would further add histopathological information on tumor spread and liver and kidney biopsies.</p>","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"70 3","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13530947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148801020","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}