Histology and histopathology最新文献

{"title":"Expression and prognostic value of PIM-1 kinase in gliomas.","authors":"Zelin Li, Hu Wang, Guangxiu Wang, Anling Zhang, Chen Wang, Lidong Mo, Zhifan Jia, Xiaoguang Tong","doi":"10.14670/HH-18-845","DOIUrl":"10.14670/HH-18-845","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore the correlation of PIM-1 with the clinicopathological features and prognosis of patients.</p><p><strong>Methods: </strong>The MTERF3 mRNA and protein expression levels in tissues were detected by western blot and immunohistochemistry. The expression and survival of PIM-1 in patients with glioma were analysed using the Gene Expression Profiling Interactive Analysis database, the Gene Expression Database of Normal and Tumor Tissues 2, and the Chinese Glioma Genome Atlas database. The relationship between PIM-1 expression and immune cells and chemokines was analysed using the Tumor Immune Estimation Resource Version 2.0 tool and the Tumor and Immune System Interactions Database. A Kaplan-Meier plot was used to estimate the correlation between PIM-1 expression and the survival of patients with glioma.</p><p><strong>Results: </strong>The expression of PIM-1 was upregulated in glioma and was positively correlated with tumour grade. The expression of PIM-1 was significantly inhibited on the second day after transfection (<i>p</i><0.05), and the inhibition was most obvious on the sixth day (<i>p</i><0.01). The results of the co-expression pattern of PIM-1 showed that the expression of 5,012 genes was positively correlated with PIM-1, while the expression of 3,651 genes was negatively correlated with PIM-1. Macrophages (<i>p</i><0.001), myeloid dendritic cells (<i>p</i><0.001), NK cells (<i>p</i><0.001), CD4 T cells (<i>p</i><0.001), cancer-associated fibroblasts (<i>p</i><0.001), and neutrophils (<i>p</i><0.001) were positively correlated with the expression of PIM-1 in low-grade glioma.</p><p><strong>Conclusion: </strong>PIM-1 is overexpressed in glioma and is related to the prognosis of glioblastoma multiforme, and PIM-1 may be a prognostic biomarker and therapeutic target for glioma.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1117-1129"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681759","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":"DNMT1 silencing induces KIR2DL1/2/3 expression via methylation to alleviate graft-<i>versus</i>-host disease after allogeneic hematopoietic stem cell transplantation.","authors":"Ping Zhang, Shuling Yu, Miao Zhou, Xiao Yan, Huiling Zhu, Lixia Sheng, Yi Zhang, Shujun Yang, Guifang Ouyang","doi":"10.14670/HH-18-818","DOIUrl":"10.14670/HH-18-818","url":null,"abstract":"<p><p>Natural killer (NK) cells are the promoters in graft-<i>versus</i>-host disease (GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT), while demethylation can regulate NK cell function. We explored the mechanism of demethylation regulating NK cell function to affect GVHD after allo-HSCT. BALB/c mice were transfused with C57BL/6 mouse-derived NK and bone marrow cells to establish GVHD models, followed by isolation and <i>in-vitro</i> expansion of NK cells. NK cell purity, cytokine levels, proliferation, and cytokine-producing NK cell levels were measured via flow cytometry. KIR2DL1/2/3 methylation was tested by Methylation-specific polymerase chain reaction (MSP), with determination of mouse survival and GVHD scores. KIR2DL1/2/3 and DNMT1 expression was detected through qRT-PCR and/or western blot. Methylation levels were upregulated and KIR2DL1/2/3 expression was downregulated in GVHD mouse model-derived NK cells following IL-2 stimulation. DNMT1 silencing promoted KIR2DL1/2/3 expression, proliferation, and the secretion of Granzyme, Perforin, and Interferon-γ (IFN-γ) in C57BL/6 mouse-derived NK cells. DNMT1 silencing also enhanced mouse survival, reduced GVHD scores, promoted KIR2DL1/2/3 expression on the NK cell surface, and increased the secretion of Granzyme, Perforin, IFN-γ, and the number of cytokine-producing NK cells in the spleen, liver, and lung tissues of the models. Collectively, DNMT1 silencing induced KIR2DL1/2/3 expression in NK cells through reducing methylation to alleviate GVHD after allo-HSCT.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1061-1071"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464135","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":"Betulinic acid isolated from <i>Betula platyphylla</i> induces apoptosis and reduces the mTOR/PI3K/AKT signaling pathway in endometrial cancer cells.","authors":"Gözde Korkusuz, Ceren Oy, Mücahit Secme, Duygu Gok Yurtseven, Sema Serter Kocoglu","doi":"10.14670/HH-18-960","DOIUrl":"https://doi.org/10.14670/HH-18-960","url":null,"abstract":"<p><p>Endometrial cancer is one of the most common gynecological cancers worldwide, and an average of 42,000 women die each year. Chemotherapy, radiotherapy, and surgery are among the treatments available for endometrial cancer. Currently, drugs used for chemotherapy have had limited success in increasing the cure rate. Betulinic acid, a lupane-type triterpene widely found in the plant kingdom, has attracted attention for cancer treatment in recent years due to its ability to inhibit tumor growth and induce cell apoptosis. The aim of this study is to investigate the mTOR pathway-mediated anticancer effects of betulinic acid in human endometrial cancer cells. The effect of betulinic acid on Ishikawa cell viability was determined by the CCK-8 method. Its effect on the expression of genes involved in apoptosis and the mTOR pathway was assessed by real-time PCR. The effect on protein expression in the mTOR pathway was evaluated with immunohistochemistry and western blot, and the effects on apoptosis via Annexin V. Betulinic acid reduced Ishikawa endometrial cancer cell proliferation. Betulinic acid administration caused a significant decrease in Bcl2 (<i>P</i>=0.008) expression and increased caspase-8 (<i>P</i>=0.001) expression in Ishikawa cells. The results of Annexin V supported the idea that betulinic acid administration triggered apoptosis in Ishikawa cells. The mean rate of apoptotic cells in the betulinic acid group was 22±3.23%, while it was 2.31±0.2% in the control group (<i>P</i>=0.02). Betulinic acid caused a significant decrease in the expression of AKT1 (<i>P</i>=0.0001) and a significant increase in the expression of RAPTOR (<i>P</i>=0.00002). Betulinic acid administration also significantly decreased protein expression in the mTOR pathway. The percentage of p-PI3K, p-AKT, and p-mTOR-positive cells in Ishikawa cells was 89.39±5.19%, 74.84%±5.07, and 82.02%±6.14, respectively, in the control group. In the betulinic acid group, these values were 49.12±19.12% (<i>P</i>=0.002), 44.46±7.39% (<i>P</i><0.001), and 53.70±8.94% (<i>P</i><0.001), respectively. This study showed that betulinic acid decreased Ishikawa cell proliferation, triggered apoptosis, and decreased mTOR signaling; thus, betulinic acid may be a potential anticancer agent for the treatment of endometrial cancer.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18960"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642447","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":"Identification of new tissue markers for the monitoring and standardization of penile cancer according to the degree of differentiation.","authors":"Carlos Casanova-Martín, Diego Liviu Boaru, Oscar Fraile-Martinez, Cielo Garcia-Montero, Diego De Leon-Oliva, Patricia De Castro-Martinez, Maria José Gimeno-Longas, Julia Bujan, Natalio García-Honduvilla, Luis G Guijarro, Raquel Gragera, Laura Lopez-Gonzalez, Miguel A Saez, Connie Ferrara-Coppola, Víctor Baena-Romero, Raul Diaz-Pedrero, Melchor Alvarez-Mon, María Val Toledo-Lobo, Miguel A Ortega","doi":"10.14670/HH-18-846","DOIUrl":"10.14670/HH-18-846","url":null,"abstract":"<p><p>Penile cancer is an uncommon disease compared with other urological tumors and is more common in low- and middle-income countries. Risk factors include age, ethnicity, smoking, hygiene, and human papillomavirus infection. Although carcinoma of the penis can be cured in up to 80% of cases if detected early, late diagnosis drastically reduces survival rates, especially in metastatic cases. More than 95% of cases are squamous cell carcinomas, and the degree of cell differentiation is a key histopathological factor, distinguishing between poorly (P), moderately (M), and well-differentiated (W) carcinomas, with verrucous carcinoma (V) having the best prognosis due to its low metastatic capacity. This study analyses the differential expression of several biomarkers related to cell proliferation and cell cycle, inflammation, epigenetics, and autophagy (cell cycle (IRS-4, Ki-67, RB1, CDK4, cyclin D1, ERBB2, β-catenin, and MAGE-A), inflammation (COX2, NLRP3, and AIF-1), epigenetics (HAT-1) and autophagy (ULK-1 and ATG9A) in penile carcinoma according to the degree of differentiation. Immunohistochemical techniques were performed on 34 penile squamous cell carcinoma (PSCC) samples classified into subtype V (N=6), and groups P (N=9), M (N=9), and W (N=10). The findings suggest a differential expression of molecules according to the degree of cell differentiation, with a higher differential expression of molecules according to the degree of cell differentiation, suggesting that the proteins studied could have predictive value. The study highlights the complexity of PSCC and the need for future studies to explore translational applications and search for new biomarkers to improve clinical management and understanding of this disease.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1013-1039"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142728157","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":"Therapeutic potential of CD73⁺ mesenchymal stem cells for myocardial infarction and beyond.","authors":"Huifang Hou, Miaoyun Zheng, Kai Pan, Guodong Wang, Zongjin Li, Qiong Li","doi":"10.14670/HH-18-859","DOIUrl":"10.14670/HH-18-859","url":null,"abstract":"<p><p>Extracellular adenine nucleotides serve as crucial signaling molecules and influence a broad spectrum of physiological and pathological processes. CD73, the rate-limiting enzyme in the metabolism of extracellular adenine nucleotides, is ubiquitously expressed on various cell types, particularly stem cells. CD73⁺ mesenchymal stem cells (MSCs) have emerged as promising candidates for therapeutic applications due to their immunomodulatory and pro-regenerative properties. Numerous studies have highlighted the crucial role of CD73 in mediating tissue protection in myocardial infarction (MI). In this review, a brief overview of the cell type-specific expression, regulatory effects of CD73 on MSCs, and proangiogenic and immunomodulatory mechanisms is provided, with a focus on current findings concerning the protective functions of CD73 in the context of MI within the framework of stem cell therapy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"993-1003"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881898","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":"Biomechanical and histological analyses of a multilayer stent in a swine model of suprarenal aortic aneurysm.","authors":"Allana Maryel Tobita, Anna Paula Weinhardt Baptista Strazzi, Maria Fernanda Cassino Portugal, Nelson Wolosker, Ricardo Aun, Frederico de Lima Jacy Monteiro, Erasmo Simão da Silva, Igor Rafael Sincos","doi":"10.14670/HH-18-842","DOIUrl":"10.14670/HH-18-842","url":null,"abstract":"<p><strong>Objectives: </strong>To analyze and compare, in an animal model, the treatment of thoracoabdominal aneurysms with multilayer stents and its hemodynamic effects through the biomechanical and histological analysis of the aortic wall in contact with the stent.</p><p><strong>Methods: </strong>Large White pigs were randomized into two groups: Stent (n=6) and Control (n=5, non-stent). All animals were subjected to the creation of a suprarenal aneurysm with a bovine pericardial patch. In the Stent group, a multilayer stent was implanted immediately after aneurysm formation. After four weeks, all animals were subjected to angiographic assessment and intravascular ultrasound, and the stent was explanted before euthanasia for histological and biomechanical analyses.</p><p><strong>Results: </strong>At histological analysis, the groups did not differ significantly in maximum thickness of the intima (<i>p</i>=0.526), media (<i>p</i>=0.129), or adventitia (<i>p</i>=0.662). Thrombus formation was observed in 100% of the animals on the intima and media layers of the stented aorta vs. none in the Control group (<i>p</i>=0.048). At biomechanical analysis, no statistical differences were observed in aortic wall elasticity (<i>p</i>=0.158), strength (<i>p</i>=0.360), or thickness (<i>p</i>=0.323).</p><p><strong>Conclusion: </strong>We identified thrombosis of the aneurysmal sac through the presence of thrombi on the intima of the aorta in 100% of the animals in the Stent group; as for the biomechanical analysis, this study showed no statistical differences in vessel wall thickness, strength, and elasticity between groups.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1005-1012"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647350","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":"Fortunellin attenuates sepsis-induced acute kidney injury by inhibiting inflammation and ferroptosis via the TLR4/NF-κB pathway.","authors":"Liu Tianzhi, Yanmin Zhang, Xiujuan Liu, Zhigang Zuo","doi":"10.14670/HH-18-841","DOIUrl":"10.14670/HH-18-841","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the potential protective effect of fortunellin in sepsis-induced acute kidney injury (AKI) and its underlying mechanisms.</p><p><strong>Methods: </strong>Lipopolysaccharide (LPS)-treated human kidney proximal tubular epithelial (HK-2) cells were used as a cell model and sepsis-induced AKI was induced by cecal ligation and puncture (CLP) surgery in mice. Cell Counting Kit-8 (CCK8) assays and flow cytometry analysis were performed to examine the viability of HK-2 cells. Enzyme-linked immunosorbent assay (ELISA) was performed to investigate the content of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) <i>in vivo</i> and <i>in vitro</i>. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and free iron (Fe²⁺) were measured as indicators of ferroptosis. The phosphorylation levels of Interleukin-1 Receptor-Associated Kinase 4 (p-IRAK4), p65 (p-65), and inhibitor of kappa B alpha (p-IκBα) were detected by western blot as an indication of nuclear factor kappa-B (NF-κB) pathway activation.</p><p><strong>Results: </strong>Our cell and animal experiments revealed that fortunellin exhibits significant anti-inflammatory and cytoprotective properties. Fortunellin counteracted LPS-induced cellular damage in HK-2 cells, enhancing cell survival and suppressing the secretion of pro-inflammatory cytokines. Additionally, fortunellin demonstrated potent antioxidant effects, reducing MDA and Fe²⁺ levels while increasing SOD activity and GSH content. The protective effect of fortunellin was further corroborated in the mouse model of sepsis-induced AKI. Notably, fortunellin suppressed activation of the TLR4/NF-κB pathway in the AKI model, as evidenced by decreased levels of p-p65 and p-IκBα proteins.</p><p><strong>Conclusion: </strong>Fortunellin ameliorates inflammation and oxidative stress in sepsis-induced AKI, possibly through the modulation of the TLR4/NF-κB pathway. These findings suggest fortunellin's potential as a therapeutic agent for sepsis-associated AKI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1083-1093"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619271","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":"Exploring pathological targets and advancing pharmacotherapy in autism spectrum disorder: Contributions of glial cells and heavy metals.","authors":"Dhrita Chatterjee, Kousik Maparu, Shamsher Singh","doi":"10.14670/HH-18-870","DOIUrl":"10.14670/HH-18-870","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) is a globally recognized neurodevelopmental condition characterized by repetitive and restrictive behavior, persistent deficits in social interaction and communication, mental disturbances, etc., affecting approximately 1 in 100 children worldwide. A combination of genetic and environmental factors is involved in the etiopathogenesis of the disease, but specific biomarkers have not yet been identified. Due to the lack of clinical evidence, fluctuations in symptoms, and difficulties in <i>in-vitro</i> and <i>in-vivo</i> modeling, developing medications for ASD is quite difficult. Although several drugs are used to treat autism, only risperidone and aripiprazole have received FDA approval in the United States. Epidemiological studies have suggested that maternal exposure to valproic acid (VPA), acetaminophen, propionic acid, and metals, such as cadmium (Cd), lead (Pb), arsenic (As), and mercury (Hg), may contribute to the development of various neurodevelopmental disorders. Pathological targets directly implicated in the disease include excitatory-inhibitory (E/A) imbalance, hyperserotonemia, GSK-3 inhibition, and Akt pathway activation. However, while a combination of pharmacotherapy, behavioral, and nutritional/dietary interventions has been found to be the most effective conventional therapy to date, many patients have chosen to implement particular dietary supplements for reducing ASD symptoms. In this review, we briefly describe various pathological targets and their roles in the pathophysiology of ASD and treatment strategies, including some future research directions.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"979-991"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143004635","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":"USP33 promotes pulmonary microvascular endothelial cell pyroptosis by stabilizing TRAF2 through deubiquitination.","authors":"Jianping Liang, Junbo Chen, Pengfei Xu","doi":"10.14670/HH-18-835","DOIUrl":"10.14670/HH-18-835","url":null,"abstract":"<p><strong>Objective: </strong>Inhibiting the pyroptosis of human pulmonary microvascular endothelial cells (HPMECs) is a promising therapeutic modality for acute lung injury (ALI). Given the undefined effect of ubiquitin-specific protease 33 (USP33) and tumor necrosis factor receptor-associated factor 2 (TRAF2) on pyroptosis in lung injury, this study investigates their roles in the pyroptosis of HPMECs during ALI.</p><p><strong>Methods: </strong>The hypoxia/reoxygenation (H/R)-induced model was constructed in HPMECs. Cell viability, cytotoxicity, and cell death were determined by the cell counting kit-8 (CCK-8), Lactate dehydrogenase (LDH), and Hoechst-PI staining, respectively. Western blot and qRT-PCR were used to detect protein and gene expression levels of pyroptosis-related markers, respectively. The TRAF2 ubiquitination level was measured via immunoprecipitation.</p><p><strong>Results: </strong>USP33 and TRAF2 expressions were elevated in H/R-induced HPMECs. Knockdown of USP33 increased cell viability and inhibited cellular pyroptosis, accompanied by decreases in IL-1β, IL-18, and Caspase-1. USP33 stabilized TRAF2 by deubiquitination. TRAF2 overexpression reversed the effect of USP33 silencing on suppressing HPMEC pyroptosis.</p><p><strong>Conclusion: </strong>USP33 stabilizes TRAF2 by deubiquitination to promote HPMEC pyroptosis during ALI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1073-1081"},"PeriodicalIF":2.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590648","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":"ADAMTS4 is expressed in different cells and tissues in leprosy skin lesions: A potential biomarker and therapeutic target for leprosy and its reactional phenomena.","authors":"Cleverson Soares, Igor Garrido, Rafael Soares, Natália Virgili, Luciana Fachin, Patricia Rosa, Ana Paula Trombone, Andrea Belone","doi":"10.14670/HH-18-959","DOIUrl":"https://doi.org/10.14670/HH-18-959","url":null,"abstract":"<p><strong>Introduction: </strong>A disintegrin and metalloproteinase 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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18959"},"PeriodicalIF":2.5,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636936","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}