Journal of Histochemistry & Cytochemistry最新文献_第3页

Contribution of Cardiac CD34⁺ Stromal Cells to Post-Myocardial Infarction Repair in Middle-Aged Rats. 心肌CD34 +基质细胞在中年大鼠心肌梗死后修复中的作用

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-05-01 Epub Date: 2026-04-12 DOI: 10.1369/00221554261434317

Daniel T Schneider, Eduard I Dedkov

{"title":"Contribution of Cardiac CD34⁺ Stromal Cells to Post-Myocardial Infarction Repair in Middle-Aged Rats.","authors":"Daniel T Schneider, Eduard I Dedkov","doi":"10.1369/00221554261434317","DOIUrl":"10.1369/00221554261434317","url":null,"abstract":"This study investigated the spatiotemporal dynamics of cardiac CD34⁺ stromal cells (SCs) during the reparative/proliferative phase of post-myocardial infarction (MI) healing. A transmural, non-reperfused MI was induced in middle-aged male Sprague-Dawley rats via left anterior coronary artery ligation, and proliferating cells were labeled with 5-bromo-2'-deoxyuridine. Hearts were collected at days 3, 7, and 14 after MI and analyzed using histology and immunohistochemistry. We found that the myocardial interstitium and coronary vessel adventitia harbored a population of cardiac CD34⁺ SCs. Following MI, activated CD34⁺ SCs expanded from the peri-infarct region across the healing wound through proliferation and migration, often alongside activated fibroblasts/myofibroblasts. While α-SMA⁺ myofibroblasts accumulated at pro-fibrotic granulation tissue sites, CD34⁺ SCs preferentially repopulated residual endomysial scaffolds spared by phagocytic macrophages. Over time, expanding fibrotic tissue progressively overtook these regions, leading to disappearance of CD34⁺ SCs. Importantly, clusters of CD34⁺ SCs accumulated at the scar border around the stumps of surviving cardiac myocytes, seemingly facilitating integration of endomysial connective tissue from non-infarcted myocardium into the developing fibrotic scar matrix. Collectively, these findings suggest that, unlike α-SMA⁺ myofibroblasts, cardiac CD34⁺ SCs seemed to support regenerative rather than fibrotic repair during post-MI wound healing by contributing to the preservation of myocardial stromal architecture.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"285-310"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147674061","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}

引用次数: 0

Loss of Macrophage Migration Inhibitory Factor (MIF) Alters the Timing of Ventral Prostate Maturation in Mice. 巨噬细胞迁移抑制因子（MIF）的缺失改变了小鼠腹侧前列腺成熟的时间。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-05-01 Epub Date: 2026-03-25 DOI: 10.1369/00221554261431897

Júlia Eduarda Mesquita Matos, Marina das Graças Carneiro E Silva, Laura Eduarda Dinato Sudário, Luiz Felipe Fernandes Peixoto, Renata Graciele Zanon, Daniele Lisboa Ribeiro

{"title":"Loss of Macrophage Migration Inhibitory Factor (MIF) Alters the Timing of Ventral Prostate Maturation in Mice.","authors":"Júlia Eduarda Mesquita Matos, Marina das Graças Carneiro E Silva, Laura Eduarda Dinato Sudário, Luiz Felipe Fernandes Peixoto, Renata Graciele Zanon, Daniele Lisboa Ribeiro","doi":"10.1369/00221554261431897","DOIUrl":"10.1369/00221554261431897","url":null,"abstract":"This study investigated the contribution of macrophage migration inhibitory factor (MIF) for the development of ventral prostate in pubertal and adult mice. Mice aged 30 or 60 days from C57BL/6 WT (wild-type) and MIF-/-(knockout) strains were studied. Histological analysis, immunohistochemistry (smooth muscle alpha-actin, vimentin, PCNA, WNT5a), serum testosterone, and western blotting for ERK1/2 were performed. Thirty-day-old MIF-/- mice exhibited higher testosterone serum levels, and the ventral prostate presented enlarged luminal area as well as decreased collagen and smooth muscle cell content. Regarding cell proliferation, there was an important reduction in MIF-/- mice of both ages. In addition, MIF-/- 30 mice presented elevated ERK activation and WNT5a scores in the prostate. This study showed that developmental change expected only at adulthood of prostate is already very evident at 30 days of age in MIF-/- mice, anticipating the pubertal development. Thus, MIF has a stimulative role in proliferation and also modulates androgenic stimuli in the prostate, which can contribute to gland development from puberty to adulthood.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"359-372"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512571","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}

引用次数: 0

Corrigendum to "Triple Staining Including FOXA2 Identifies Stem Cell Lineages Undergoing Hepatic and Biliary Differentiation in Cirrhotic Human Liver". “包括FOXA2在内的三重染色识别肝硬化人类肝脏和胆道分化的干细胞谱系”的勘误表。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-05-01 Epub Date: 2026-03-10 DOI: 10.1369/00221554261432912

引用次数: 0

FGF2 Boost for Driving Forebrain Organoid Maturation Under Static Conditions. 静态条件下FGF2促进前脑类器官成熟

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-05-01 Epub Date: 2026-04-24 DOI: 10.1369/00221554261433071

Eleonora Grecu, Cristina Maxia, Cristina Dolciotti, Paolo Bongioanni, Renata Del Carratore, Michela Isola, Ignazia Mocci, Maria Antonietta Casu, Federico Picciau, Daniela Murtas, Andrea Diana

{"title":"FGF2 Boost for Driving Forebrain Organoid Maturation Under Static Conditions.","authors":"Eleonora Grecu, Cristina Maxia, Cristina Dolciotti, Paolo Bongioanni, Renata Del Carratore, Michela Isola, Ignazia Mocci, Maria Antonietta Casu, Federico Picciau, Daniela Murtas, Andrea Diana","doi":"10.1369/00221554261433071","DOIUrl":"10.1369/00221554261433071","url":null,"abstract":"Forebrain organoids (FOs) closely replicate key features of human brain, but often develop necrotic cores due to oxygen diffusion limits, resulting in disassembly. While dynamic culture devices can mitigate this, they add variability and diverge from adult cerebral static environment. Inspired by allometric scaling principles of brain growth, we developed a uniform, static culture protocol applying a 1-day transient high-dose Fibroblast Growth Factor 2 (100 ng/ml) treatment before neural induction. This acted as a proliferative stimulus, promoting long-term viability and structural integrity. Using human embryonic stem cells, early-FOs with diameters of 500-1000 µm achieved an 83.33% survival rate at 20 days in vitro (DIV). Area and volume increased significantly during 60 DIV culture period, but between 30 and 60 DIV they plateaued, indicating a transition from neural development to maturation. Weight increased until 30 DIV, but it significantly dropped between 30 and 60 DIV, possibly reflecting the formation of lumen-like structures. At 60 DIV, immunofluorescence revealed organized PAX6+ ventricle-like structures, where SOX2 marked neural progenitors, TUJ1 and MAP2 indicated mature neurons, GFAP identified astrocytes, and SYN1 highlighted emerging synaptic networks. This scalable protocol supports robust FOs generation, providing optimization and practical improvement within established frameworks to advance precision medicine.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"267-284"},"PeriodicalIF":1.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773719","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}

引用次数: 0

Distinct Single-Cell Expression Pattern of the Soluble Epoxide Hydrolase and Cytochrome p450 Epoxygenases in Human and Mouse Small Intestinal Epithelia. 可溶性环氧化物水解酶和细胞色素p450环氧化酶在人和小鼠小肠上皮中不同的单细胞表达模式。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2025-12-25 DOI: 10.1369/00221554251403631

Leyu Sun, Amy Tang, Jie Liao, Guang-Yu Yang

{"title":"Distinct Single-Cell Expression Pattern of the Soluble Epoxide Hydrolase and Cytochrome p450 Epoxygenases in Human and Mouse Small Intestinal Epithelia.","authors":"Leyu Sun, Amy Tang, Jie Liao, Guang-Yu Yang","doi":"10.1369/00221554251403631","DOIUrl":"10.1369/00221554251403631","url":null,"abstract":"Lipid signaling molecules are essential for maintaining intestinal mucosal barrier homeostasis. Over 80% of polyunsaturated fatty acids (PUFAs) are metabolized through the cytochrome P450 epoxygenase (CYP)-soluble epoxide hydrolase (sEH) axis, generating bioactive epoxy and diol fatty acids. However, the expression patterns and functional roles of these enzymes in the intestinal epithelium remain poorly defined. To address this, we used RNAscope in situ hybridization and publicly available single-cell RNA sequencing (scRNAseq) datasets to map the cell-type-specific expression of PUFA-metabolizing enzymes in the small intestine. In humans, we identified three major epithelial expression patterns: (1) stem-cell-dominant (CYP2E1), (2) enterocyte-dominant (CYP1A1), and (3) widespread expression across epithelial subsets for key CYP epoxygenases (CYP2C8, 2C9, 2C18, 2C19, 2J2, 2S1), sEH, and additional CYPs (3A4, 4A11, 4F2, 4F3, 4F8, 4F12). In mice, five distinct expression patterns were found: (1) stem cell and transit-amplifying cells (CYP2E1), (2) transit-amplifying dominant (CYP4F18), (3) transit-amplifying and enterocytes (CYP2C44), (4) enterocyte-dominant (CYP1A1), and (5) broadly expressed across all epithelial clusters (sEH, CYP2B10, 2S1, 2C55, 4F13, 4F16). Furthermore, in a radiation-induced small-bowel injury-regeneration model, we observed dynamic changes in CYP expression patterns. These findings provide the first high-resolution single-cell atlas of CYP-sEH axis enzymes in the intestinal epithelium, offering key insights into their potential roles in epithelial differentiation, injury response, and mucosal barrier integrity. This foundational work enables future studies to define the biological functions and therapeutic relevance of PUFA-derived lipid mediators in intestinal health and disease.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"163-179"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12743005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833985","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}

引用次数: 0

Transforming Growth Factor-β Drives Epithelial Mesenchymal Transition and Reduces Synthesis of Unelaborated O-GalNAc Glycans in Breast Cancer Cells. 转化生长因子-β在乳腺癌细胞中驱动上皮间质转化并减少未加工的O-GalNAc聚糖的合成

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2026-02-28 DOI: 10.1369/00221554261416994

Joanna Cull, Ryan C Pink, Priya Samuel, Susan A Brooks

{"title":"Transforming Growth Factor-β Drives Epithelial Mesenchymal Transition and Reduces Synthesis of Unelaborated O-GalNAc Glycans in Breast Cancer Cells.","authors":"Joanna Cull, Ryan C Pink, Priya Samuel, Susan A Brooks","doi":"10.1369/00221554261416994","DOIUrl":"10.1369/00221554261416994","url":null,"abstract":"SummaryAltered O-glycosylation of cancer cells is frequently associated with metastasis and poor prognosis. During metastasis, cells must also lose their epithelial characteristics and become mesenchymal and motile, termed epithelial-mesenchymal transition (EMT). While it is established that transforming growth factor beta-1 (TGF-β1) can induce EMT, the effect of cytokine-induced EMT on O-glycosylation of breast cancer cells has not previously been explored. MCF-7 and T47-D breast cancer cells were treated with TGF-β1 over a time course of up to 7 days. Morphological changes were assessed using confocal microscopy and quantified; levels of EMT marker expression were assessed using immunofluorescence with confocal microscopy and western blot. The effect of TGF-β1 on synthesis of unelaborated Tn antigen was explored using Helix pomatia agglutinin (HPA) labelling. TGF-β1 treatment induced morphological changes, resulting in an elongated, mesenchymal-like phenotype, and a reduction of epithelial marker E-cadherin but did not detectably induce mesenchymal markers N-cadherin or vimentin. It also resulted in a significant reduction in unelaborated Tn antigen, detected by HPA labelling. These observations are consistent with TGF-β1 inducing an 'early' or partial EMT state over this timeframe, and a concomitant change in O-glycosylation, consistent with the synthesis of more elaborated O-glycan structures; such glycoplasticity may function in metastasis. (J Histochem Cytochem XX:XXX-XXX, XXXX).","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"193-214"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12950527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147321758","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}

引用次数: 0

Akkermansia muciniphila Selectively Reshapes Small Intestinal Cell Populations. 嗜粘杆菌选择性地重塑小肠细胞群。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2026-02-16 DOI: 10.1369/00221554261417734

Rachel Edens-Valentine, Kristen A Engevik, Melinda A Engevik, Amy C Engevik

{"title":"Akkermansia muciniphila Selectively Reshapes Small Intestinal Cell Populations.","authors":"Rachel Edens-Valentine, Kristen A Engevik, Melinda A Engevik, Amy C Engevik","doi":"10.1369/00221554261417734","DOIUrl":"10.1369/00221554261417734","url":null,"abstract":"The gastrointestinal tract harbors a dynamic microbial ecosystem that interfaces with the intestinal epithelium. Among this community, Akkermansia muciniphila, a mucin-degrading microbe, has garnered attention for its impact on gut health. While well studied in the colon, its influence on the small intestine remains underexplored. To examine direct effects of A. muciniphila, we used gnotobiotic mice. Germ-free mice were inoculated with Brain Heart Infusion (BHI) media or 10⁹ viable A. muciniphila in BHI. After 21 days, small intestinal tissue was collected. Fluorescence in situ hybridization confirmed A. muciniphila colonization. Immunofluorescence staining revealed increased epithelial cell proliferation, unchanged goblet cell numbers, but altered mucus composition with reduced fucose residues. Tuft cell numbers and group 2 innate lymphoid cells (ILC2s) were also elevated in A. muciniphila-colonized mice. Analysis of conditioned media and the A. muciniphila genome identified succinate production, a metabolite known to expand tuft cells. Thus, A. muciniphila alone is sufficient to increase tuft cells in the small intestine, potentially via succinate signaling. These findings reveal a novel role for A. muciniphila in regulating gastrointestinal homeostasis.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"215-233"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12913043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146202035","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}

引用次数: 0

Targeting CCNB1 Repressed Cartilage Degradation Induced by Inflammation Through NF-κB Pathway in Osteoarthritis. 靶向CCNB1通过NF-κB途径抑制炎症诱导的骨关节炎软骨降解。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2026-02-23 DOI: 10.1369/00221554251410643

Hua Li, Yuxue Qiao, Mengshuang Ding, Yirong Liu

{"title":"Targeting CCNB1 Repressed Cartilage Degradation Induced by Inflammation Through NF-κB Pathway in Osteoarthritis.","authors":"Hua Li, Yuxue Qiao, Mengshuang Ding, Yirong Liu","doi":"10.1369/00221554251410643","DOIUrl":"10.1369/00221554251410643","url":null,"abstract":"Inflammation contributes to osteoarthritis, and cyclin B1 (CCNB1) dysregulation is implicated. Understanding its role and regulation is crucial for developing targeted therapies against this degenerative disease. Mice chondrocytes were acquired from C57BL/6 wild-type mice and treated with interleukin (IL)-1β for inflammation induction, followed by assays for cell viability, apoptosis, inflammatory mediators, cartilage markers, and nuclear factor kappa B (NF-κB) pathway. CCNB1 was knocked down or upregulated in chondrocytes, respectively. The modified Hulth method was used to establish osteoarthritis model. The knee joint was visualized using micro-computed tomography, and histopathologic evaluation was carried out by immunohistochemistry staining, Safranin O/fast green, and hematoxylin and eosin staining for cartilage degradation markers. CCNB1 knockdown inhibited IL-1β-caused decrease in cell viability and increase in apoptosis of chondrocytes. Inflammatory mediators in IL-1β-treated chondrocytes were decreased after CCNB1 knockdown. CCNB1 knockdown reduced the expression of MMP-13 and ADAMTS-5, while elevated collagen II and aggrecan accumulation, alongside with NF-κB inactivation, in chondrocytes administered with IL-1β. Targeting inhibition of CCNB1 reduced the production of inflammation regulators, decreased cartilage degradation, and blocked NF-κB pathway activation. Targeting CCNB1 may serve as a potential therapeutic strategy for osteoarthritis by reducing inflammation, protecting cartilage, and modulating the NF-κB pathway.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"235-248"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12932133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147275699","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}

引用次数: 0

Lamina Propria Collagen Architecture in Interstitial Cystitis/Bladder Pain Syndrome. 间质性膀胱炎/膀胱疼痛综合征的固有层胶原结构。

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2026-01-17 DOI: 10.1369/00221554251410640

Hannah Ruetten, Raymond Xu, Harrison Martin, Dylan T Wolff, Wencheng Li, Kaylee Ferrara, L McKenna Huse, Robert J Evans, Gopal Badlani, Stephen J Walker

{"title":"Lamina Propria Collagen Architecture in Interstitial Cystitis/Bladder Pain Syndrome.","authors":"Hannah Ruetten, Raymond Xu, Harrison Martin, Dylan T Wolff, Wencheng Li, Kaylee Ferrara, L McKenna Huse, Robert J Evans, Gopal Badlani, Stephen J Walker","doi":"10.1369/00221554251410640","DOIUrl":"10.1369/00221554251410640","url":null,"abstract":"Interstitial cystitis/bladder pain syndrome (IC/BPS) is a heterogeneous condition of uncertain etiology. We assessed bladder collagen characteristics in phenotypically characterized IC/BPS patient subgroups that may influence pathophysiology. Forty-four females (30 IC/BPS; 14 non-IC/BPS) were included. Patients were divided into groups based on Hunner lesions (HL; N=14 or non-HL; N=16) and anesthetic bladder capacity (BC) (BC≤500 cc; low BC; N=17 or BC>500 cc; non-low BC; N=13). Bladder biopsy tissue slides were stained with hematoxylin and eosin or picrosirius red and semi-quantitatively analyzed by a pathologist. CT-FIRE software was used to quantitatively assess lamina propria collagen. All patients with IC/BPS had lower collagen fiber density independent of subgroup (p<0.0001-0.0038) compared to controls. HL had more peri-muscular collagen accumulation (p=0.0061), more acute inflammation (p=0.0364), more severe chronic inflammation (p=0.0088), and narrower collagen fibers than non-HL and controls. Non-low-BC patients had lower collagen density (p=0.0075) and straighter collagen fibers (p=0.0127) than low BC. Low-BC patients had narrower collagen fibers than control (p=0.0096). IC/BPS, regardless of subgroup, is associated with a bladder lamina propria with diminished collagen density. HL, non-low-BC, and low-BC subgroups have unique collagen characteristics. These findings suggest a collagen fiber destruction and redistribution process, which differs by subgroup, and may contribute to pathophysiology of IC/BPS.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"129-142"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12812059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989531","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}

引用次数: 0

Differential Expression of Histamine H₃ Receptor In Healthy, Preneoplastic, and Tumoral Pancreatic Tissue: A Pilot Study. 组胺H3受体在健康、肿瘤前和肿瘤胰腺组织中的差异表达：一项初步研究

IF 1.5 4区生物学

Journal of Histochemistry & Cytochemistry Pub Date : 2026-03-01 Epub Date: 2026-01-01 DOI: 10.1369/00221554251410292

Daniela Speisky, Melisa B Nicoud, Alejandro Iotti, Karina Formoso, Paolo Lauretta, María Teresa García de Dávila, Vanina A Medina

{"title":"Differential Expression of Histamine H3 Receptor In Healthy, Preneoplastic, and Tumoral Pancreatic Tissue: A Pilot Study.","authors":"Daniela Speisky, Melisa B Nicoud, Alejandro Iotti, Karina Formoso, Paolo Lauretta, María Teresa García de Dávila, Vanina A Medina","doi":"10.1369/00221554251410292","DOIUrl":"10.1369/00221554251410292","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related death worldwide, with a mortality rate almost equal to its incidence, highlighting the urgent need for novel biomarkers and therapeutic targets. This pilot study aims to investigate the potential value of histamine H3 receptor (H3R) as a prognostic biomarker for this lethal disease. We analyzed the H3R expression in PDAC using the RNA sequencing data set from The Cancer Genome Atlas (Pan-Cancer Atlas). In addition, H3R protein levels were evaluated by immunohistochemistry in 27 PDAC samples and compared with adjacent preneoplastic pancreatic tissue of the same patient, and with 10 non-related healthy pancreatic tissues. This preliminary study shows that the H3R is barely expressed in healthy tissue. Interestingly, H3R was detected in 96% of PDAC samples, and its expression in tumoral tissue was significantly higher when compared with its expression in preneoplastic tissue, and it was associated with a better prognosis in terms of overall survival. Present findings suggest that H3R may serve as a potential prognostic biomarker in PDAC. Future research aimed at elucidating the role of H3R in PDAC biology and its prognostic value in larger patient cohorts is warranted.","PeriodicalId":16079,"journal":{"name":"Journal of Histochemistry & Cytochemistry","volume":" ","pages":"181-191"},"PeriodicalIF":1.5,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12759016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889322","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}

引用次数: 0