Histology and histopathology最新文献

{"title":"Lysophosphatidylcholine negatively reverses the effects of human umbilical cord-derived mesenchymal stem cells on high glucose-induced cell dysfunction.","authors":"Xian Liu, Yong Chai, Han Liu, Yao Zhao, ChunYi Liu, Rui Luo, Qiang Gan","doi":"10.14670/HH-18-927","DOIUrl":"https://doi.org/10.14670/HH-18-927","url":null,"abstract":"<p><strong>Background: </strong>Increasing attention has been attracted to the application of human umbilical cord-derived mesenchymal stem cells (HUCMSCs) in the cell therapy of various diabetic complications, including diabetic retinopathy (DR). Lysophosphatidylcholine (LPC) has been reported to induce cell apoptosis and an inflammatory response. The present study aimed to investigate the mechanism of HUCMSCs in high glucose (HG)-treated retinal microvascular endothelial cells (RMECs) and the effect of LPC on this mechanism.</p><p><strong>Methods: </strong>To mimic DR <i>in vitro</i>, RMECs were treated with HG. Flow cytometry analysis was used to identify HUCMSCs and the expression of their surface markers. The apoptosis of RMECs was also accessed using flow cytometry analysis. A CCK-8 assay was performed to measure the viability of RMECs. ELISA was used to detect the concentration of inflammatory cytokines (TNF-α, IL-6, and IL-1β) in RMECs. The protein expression of tight junction proteins in RMECs was examined using western blot analysis.</p><p><strong>Results: </strong>HUCMSCs were identified to present positive markers (CD105, CD73, and CD90) and loss of negative markers (CD45, CD34, and HLA-DR). In RMECs, HG significantly induced a decrease in cell viability and an increase in cell apoptosis and tight junction proteins. Moreover, HG treatment promoted the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) and facilitated oxidative stress. However, these dysregulated cellular behaviors were alleviated by the treatment of the culture medium of HUCMSCs. Furthermore, LPC treatment reversed the effect of HUCMSCs on HG-induced RMEC injury and impaired the blood-retinal barrier. Moreover, the effect of HUCMSCs on the inflammatory response and oxidative stress of RMEC was also neutralized by LPC treatment.</p><p><strong>Conclusion: </strong>LPC reverses the effects of HUCMSCs on HG-induced RMEC dysfunction, impaired blood-retinal barrier, inflammation, and oxidative stress.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18927"},"PeriodicalIF":2.5,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998570","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":"The evolution of mast cells across all vertebrate classes: The mystery continues.","authors":"Stefano Bacci","doi":"10.14670/HH-18-926","DOIUrl":"https://doi.org/10.14670/HH-18-926","url":null,"abstract":"<p><p>The paper examines what the mast cell, a cell that arose in urochordates and reached humans with the same morphological profile, is used for. Activated mast cells contribute to the regulation of the local immune response and major inflammation and healing processes with the help of a broad range of mediators. Located primarily at the interface between the host and the external environment, mast cells are widely distributed. The local microenvironment directly affects mast cell development, phenotype, and function, which in turn affects the cells' capacity to identify and react to different stimuli by releasing a variety of physiologically active mediators. By interacting with a range of other cells involved in physiological and immunological responses, mast cells can react to changes in their surroundings and serve as first responders in dangerous situations. Consequently, the mast cell's crucial function in innate and adaptive immunity, including immunological tolerance, has come to light more frequently. On the other hand, mast cell malfunction has identified these cells as the primary culprits in a number of autoimmune illnesses, cancer, and chronic allergic/inflammatory conditions.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18926"},"PeriodicalIF":2.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989877","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":"Antagonism of GPR4 with NE 52-QQ57 alleviates gestational diabetes mellitus-induced placental insults mediated by inhibiting NF-κB.","authors":"Fang Li, Zongxu Qiao, Jinhui Feng, Yaning Wang, Xiaohui Zhao","doi":"10.14670/HH-18-925","DOIUrl":"https://doi.org/10.14670/HH-18-925","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) refers to a diabetic condition observed in pregnant women, significantly affecting both the health of the mother and the growth of the offspring. G protein-coupled receptor 4 (GPR4) is a receptor widely distributed across various tissues, but its role in GDM remains unclear. Our research aims to investigate the role of GPR4 in GDM and explore the potential therapeutic effects of its antagonist, NE 52-QQ57, in treating this condition. First, we found that GPR4 was expressed in placental tissues. Mice were divided into three groups: wild-type, db/+ pair-fed, and db/+ pair-fed + NE 52-QQ57. GPR4 expression was significantly higher in the db/+ pair-fed mice compared with wild-type mice. Markedly increased blood glucose and serum insulin levels were observed in GDM mice on gestational days (GD), accompanied by disrupted lipid profiles, all of which were significantly alleviated by NE 52-QQ57. Moreover, undesirable fetal outcomes, including increased fetal mortality, decreased fetal weight, reduced crown-rump length, and decreased placental weight, were observed in GDM mice, however, all were notably improved by NE 52-QQ57. Increased oxidative stress (OS) and the release of inflammatory cytokines were observed in GDM mice, but these were significantly reversed by NE 52-QQ57. Additionally, activated nuclear factor κ-B (NF-κB) signaling in placental tissues of GDM mice was significantly suppressed by NE 52-QQ57. Collectively, antagonism of GPR4 protected against GDM-induced placental damage in mice, confirming the critical role of GPR4 in the development of GDM.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18925"},"PeriodicalIF":2.5,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998257","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":"Liquid biopsy of circulating tumor cells: From isolation, enrichment, and genome sequencing to clinical applications.","authors":"Keqin Tan, Hong Zhu, Xuelei Ma","doi":"10.14670/HH-18-924","DOIUrl":"https://doi.org/10.14670/HH-18-924","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs), shed from primary tumors into the bloodstream, play a crucial role in metastasis and hold great potential in cancer diagnosis, prognosis, and treatment monitoring. Conventional CTC detection using epithelial biomarkers like epithelial cell adhesion molecule (EpCAM) for immunocapture overlooks mesenchymal-like CTCs with high metastatic potential, spurring the development of non-immunocapture technologies that use biophysical traits for enrichment. Innovations in microfluidic platforms and multi-parametric sorting improve isolation efficiency and address related challenges. Breakthroughs in single-cell genomic and transcriptomic sequencing enable in-depth molecular characterization of CTCs. Clinically, CTC enumeration and molecular profiling are emerging as real-time tools for assessing therapeutic response and predicting outcomes, especially in metastatic breast, prostate, and colorectal cancers. This review focuses on CTC isolation, enrichment techniques, their applications in different tumors, downstream analysis progress, and potential in precision medicine.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18924"},"PeriodicalIF":2.5,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063531","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":"KIF22 promotes the proliferation and immune escape of endometrial cancer cells by activating the STAT3/PDL1 pathway.","authors":"Chaoqun Wang, Chaohe Zhang","doi":"10.14670/HH-18-923","DOIUrl":"https://doi.org/10.14670/HH-18-923","url":null,"abstract":"<p><strong>Objective: </strong>Endometrial cancer (EC) is a common gynecologic malignancy with high morbidity and mortality. Kinesin Family member 22 (KIF22) is regarded as a critical oncogene, but its functions in EC progression remained elusive. Hence, this research elucidated the role of KIF22 in EC development and studied the possible mechanism.</p><p><strong>Methods: </strong>KIF22 expression in EC and the relationship with the overall survival of EC cases were determined by GEPIA and online K-M plotter. After transfection with sh-KIF22, cell viability and invasion were evaluated utilizing CCK-8 and Transwell assays. The content of IFN-γ, IL-2, and TNF-α was assessed utilizing an ELISA assay. The protein levels of p-STAT3, STAT3, and PD-L1 were examined using western blot. A xenograft tumor was constructed to assess tumor growth.</p><p><strong>Results: </strong>KIF22 was elevated in EC, with high KIF22 levels presenting poor overall survival. Additionally, silenced KIF22 restrained EC cell viability, invasion ability, and STAT3/PD-L1 pathway, enhanced the viability of CD8+ T cells, and elevated the levels of IFN-γ, IL-2, and TNF-α. Moreover, the rescue assay revealed that STAT3 overexpression counteracted the inhibitory effect of silenced KIF22 on EC cell proliferation, invasion and immune escape. Furthermore, silenced KIF22 repressed EC tumor growth and p-STAT3 and PD-L1 levels, and elevated the IFN-γ level <i>in vivo</i>.</p><p><strong>Conclusion: </strong>The findings demonstrated that KIF22 was elevated in EC and correlated with a poor prognosis. Silenced KIF22 repressed cell proliferation, invasion, and immune escape via suppressing the STAT3/PD-L1 pathway in EC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18923"},"PeriodicalIF":2.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018687","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":"Luteoloside ameliorates sepsis-induced acute lung injury via AMPK-ULK1 pathway-mediated autophagy.","authors":"Bo Xu, Min Huang, Hang Qi, Cheng Liu, Hongzhou Xu, Liang Cai","doi":"10.14670/HH-18-922","DOIUrl":"https://doi.org/10.14670/HH-18-922","url":null,"abstract":"<p><strong>Background: </strong>Septic patients are at high risk of acute lung injury (ALI). Luteoloside is a flavonoid isolated from natural herbs and has many beneficial effects. This study aimed to investigate the protective role of luteoloside in sepsis-induced ALI.</p><p><strong>Methods: </strong>Sepsis was induced by cecal ligation and puncture (CLP) in C57BL/6 mice. Inflammation was induced by lipopolysaccharide (LPS) in MLE-12 cells. The survival rate over 12 days, histological changes in lung and heart, pulmonary edema, vascular leakage, hypoxemia, and inflammation were examined. Apoptosis was detected by TUNEL staining <i>in vivo</i> and flow cytometry <i>in vitro</i>. The levels of autophagy-related proteins, the AMPK/ULK1 pathway, and the NLRP3 inflammasome were evaluated by western blotting. Cell viability was estimated by MTT assays. LC3 expression was evaluated by immunofluorescence staining.</p><p><strong>Results: </strong>Luteoloside attenuated lung and cardiac injury, pulmonary edema, vascular leakage, hypoxemia, and inflammation and improved the survival of septic mice. Luteoloside (20 mg/kg) had no toxic effect on the heart, liver, spleen, and kidney in normal mice. Luteoloside enhanced autophagy to inhibit apoptosis <i>in vivo</i> and <i>in vitro</i>, and autophagy induction was responsible for the protective effect of luteoloside. Luteoloside activated AMPK/ULK1 signaling to enhance autophagy. Luteoloside also inhibited the activation of the NLRP3 inflammasome in LPS-challenged MLE-12 cells.</p><p><strong>Conclusion: </strong>Overall, luteoloside activates AMPK/ULK1 signaling to stimulate autophagy, thereby inhibiting apoptosis and alleviating sepsis-induced ALI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18922"},"PeriodicalIF":2.5,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981494","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":"PLEKHG2 and the PLEKHG family: Linking Rho family GTPases to neural development and disorders.","authors":"Katsuya Sato, Masashi Nishikawa, Koh-ichi Nagata, Hiroshi Ueda","doi":"10.14670/HH-18-921","DOIUrl":"https://doi.org/10.14670/HH-18-921","url":null,"abstract":"<p><p>Rho family small GTPases (Rho GTPases) are key regulators of cellular morphology, primarily through their control of the actin cytoskeleton. They play crucial roles in various cellular processes, including cell division, adhesion, and migration. The activity of Rho GTPases is tightly regulated by specific guanine nucleotide exchange factors (GEFs), which facilitate the exchange of GDP for GTP, thereby activating the GTPases. In the human genome, RhoGEFs are categorized into two major families: the DOCK family, comprising 11 members characterized by dedicator of cytokinesis (DOCK) homology regions, and the Dbl family, consisting of 64 members that contain a diffuse B-cell lymphoma (Dbl) homology domain. This review focuses on the pleckstrin homology and RhoGEF domain containing G (PLEKHG) family within the Dbl family of RhoGEFs, which remains largely uncharacterized. We summarize their structure and function, with a particular emphasis on PLEKHG2, discussing its regulatory mechanisms, interactions with various molecules, and its involvement in neural functions.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18921"},"PeriodicalIF":2.5,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005744","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":"Histological and molecular characterization of endolymphatic sac tumor reveals key differences from its primary differential diagnosis, choroid plexus papilloma.","authors":"Lea L Friker, Rebecca Klein, Ralf Clauberg, Tobias Goschzik, Julian P Layer, Ursula Gies, Michael Hölzel, Ulrich Herrlinger, Andreas Waha, Torsten Pietsch, Gerrit H Gielen","doi":"10.14670/HH-18-920","DOIUrl":"https://doi.org/10.14670/HH-18-920","url":null,"abstract":"<p><p>Endolymphatic sac tumors (ELSTs) are rare, slow-growing neoplasms of the inner ear. Microscopically, they exhibit papillary-cystic and glandular histomorphology, closely resembling their primary differential diagnosis, choroid plexus papilloma (CPP). Through in-depth histological, immunohistochemical, and molecular analysis, we identified distinct characteristics of ELST that facilitate its identification and aid in differentiating it from CPP. Immunohistochemical staining that best discriminated between ELST and CPP included EMA, S-100 protein, EpCAM, cytokeratin, transthyretin, CD34, PTEN, PAX8, and YAP. In contrast to CPP, pan-cancer DNA panel next-generation sequencing frequently revealed pathogenic <i>VHL</i> gene alterations in ELST. In conclusion, comprehensive immunohistochemistry enhances the identification of this rare tumor type and helps prevent misdiagnosis. Furthermore, the detection of <i>VHL</i> gene alterations additionally supports the diagnosis of ELST.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18920"},"PeriodicalIF":2.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995090","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":"Immunohistochemical evidence for hyaline-like cartilage formation after autologous matrix-induced chondrogenesis for osteochondral lesions of the talus: Case reports of 2 patients.","authors":"Fabian Krause, Helen Anwander, Birgit Schäfer","doi":"10.14670/HH-18-919","DOIUrl":"https://doi.org/10.14670/HH-18-919","url":null,"abstract":"<p><strong>Objectives: </strong>As a surgical option for osteochondral lesions of the talus, autologous matrix-induced chondrogenesis (AMIC^®) combines bone marrow stimulation, filling of subchondral defects, and application of a collagen bilayer matrix. The purpose of the study was to analyze the cartilage at the treated defect site in two patients.</p><p><strong>Methods: </strong>Two patients underwent revision surgery (14 and 36 months after the index AMIC^® procedure) for failure due to ligamentous instability. During revision, the repair cartilage was evaluated regarding its integration, presence of fissures, thinning, or firmness. Samples for histologic evaluation were taken from the centre of the treated site. The samples were examined using standard histological and immunohistochemistry techniques.</p><p><strong>Results: </strong>During the revision arthroscopy, the regenerated cartilage was the same color but softer than the surrounding cartilage, superficially frayed, without fissures and even with the level of the original cartilage, but not completely stable on the subchondral bone. Histology revealed the presence of Safranin-O-positive fibrocartilage-like tissue. Additionally, cartilaginous-like tissue was found in the 36-month biopsy. IHC revealed a fraction of collagen type II positive cells in the fibrocartilage-like tissue as well as a collagen type II positive extracellular matrix. The cartilaginous tissue of the 36-month biopsy revealed a homogeneous collagen type II stain.</p><p><strong>Conclusions: </strong>The presence of collagen type II within the tissue indicates its transformation into hyaline-like cartilage at 14 months after AMIC^® continuing up to 36 months. While second-look arthroscopies and histological analyses are rare, the data presented here demonstrate cartilage regeneration, with a progressive formation of a hyaline-like cartilaginous tissue in the talus after AMIC^®.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18919"},"PeriodicalIF":2.5,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005849","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":"Liver morphology and histological alterations related to reproductive phases of female silver croaker <i>Plagioscion squamosissimus</i> (Acanthuriformes, Sciaenidae).","authors":"Yane Caroline Horas Do Nascimento, Amanda Pereira Dos Santos Silva, Bruna Caroline Kotz Kliemann, Igor Paiva Ramos, Lidiane Franceschini, Rosilene Luciana Delariva, Letícia de Oliveira Manoel, Cristieli Fernanda Belancieri Souza, Alexandre Ninhaus Silveira, Rosicleire Veríssimo-Silveira","doi":"10.14670/HH-18-918","DOIUrl":"10.14670/HH-18-918","url":null,"abstract":"<p><p>This study describes the morphology of the liver tissue, histological alterations, and their relationships with the reproductive phases of the female silver croaker <i>Plagioscion squamosissimus</i>. We tested the hypothesis that histological alterations in liver tissue can occur at the expense of the reproductive phase of the female and that climatic factors, such as rainfall, interfere with the reproductive phases and, consequently, promote histological alterations. Histological analysis of the liver showed liver tissue with hepatocytes, bile ducts, blood vessels, sinusoids, intrahepatic pancreas, and phagocytic cells. The histological alterations observed were vacuolization and cytoplasmic degeneration, aggregates of melanomacrophages, hyperemia, and vascular congestion, with cytoplasmic vacuolization, cytoplasmic degeneration, and vascular congestion being the most frequent. We observed that the frequency of cytoplasmic vacuolization increased throughout gonadal development with a decrease in the spawning-capable phase, and that cytoplasmic degeneration and vascular congestion were more frequent in the suitable spawning phase. In addition, relationships between histological alterations, hepatosomatic index, gonadosomatic index, reproductive phases, and rainfall were also observed, showing that alterations were more frequent in periods with higher rainfall and reproductive phases when females were ready to reproduce. In short, histological alterations may be subject to the reproductive phases of females, which are influenced by rainfall, as observed in many studies. Thus, this study presents the morphology of the liver tissue of <i>P. squamosissimus</i>, and the results shed light on the importance of considering the reproductive phases in studies evaluating histological alterations in the liver.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18918"},"PeriodicalIF":2.5,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968269","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}