Folia histochemica et cytobiologica最新文献

{"title":"Upregulation of SIRT1 ameliorates apoptosis of rat nucleus pulposus cells under oxidative stress through FoxO1/β-catenin pathway.","authors":"Hongtao Hu, Sheng Wang, Haijun Teng, Sishun Zhao, Weisheng Hong","doi":"10.5603/fhc.104395","DOIUrl":"10.5603/fhc.104395","url":null,"abstract":"<p><strong>Introduction: </strong>Age-related degenerative changes in intervertebral discs (IVDs) can lead to lower back pain, and even paralysis. This topic is therefore garnering growing attention in an increasingly ageing society. The oxidative stress-induced degenerative process is a major contributor to apoptosis in nucleus pulposus cells. However, the regulatory mechanism of NAD-dependent protein deacetylase Sirtuin-1 (SIRT1) on apoptosis in oxidative stress-induced rat nucleus pulposus cells remains unclear.</p><p><strong>Material and methods: </strong>Rat nucleus pulposus cells (NPCs) were induced to undergo degenerative changes through H₂O₂ exposure, simulating the ageing oxidative stress process. Subsequently, the SIRT1 activator SRT2104 was employed to explore the impact of SIRT1 on the expression of markers of ageing oxidative stress process in NPCs. The FoxO1 inhibitor AS1842856 was used to investigate the role of the downstream signalling pathway FoxO1/β-catenin in ageing NPCs under the influence of SRT2104. TUNEL staining and other assays such as CCK were used to observe the effects of H₂O₂ on cell apoptosis and viability, respectively. The influence of the aforementioned treatments on the ageing phenotype was observed through β-galactosidase staining, immunofluorescence staining, flow cytometry analysis, and protein electrophoresis.</p><p><strong>Results: </strong>Under H₂O₂-induced oxidative stress, both the mRNA and protein levels of SIRT1 decreased in rat NPCs. Conversely, specific activation of SIRT1 inhibited apoptosis and reduced the expression of senescence-associated secretory phenotype (SASP) and ageing-related proteins. Meanwhile, inhibiting FoxO1 expression with AS1842856 significantly upregulated β-catenin protein levels, suppressing the apoptosis process in ageing NPCs under oxidative stress.</p><p><strong>Conclusions: </strong>These results suggest that activation of the SIRT1/FoxO1/β-catenin axis can diminish ageing-related phenotypes and cell apoptosis in NPCs, inhibiting the oxidative stress-induced ageing process triggered by H₂O₂. These findings may offer a new perspective for the treatment of intervertebral disc degeneration (IDD) in the future.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"53-64"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149835","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":"MiR-494-3p knockdown promotes osteogenic differentiation of bone marrow mesenchymal stem cells in ovariectomised rats by targeting Sirt1/TLR4/NF-κB pathway.","authors":"Jianping Lei, Song Guo, Jiabing Kuang, Bo Shen, Zixi Li","doi":"10.5603/fhc.104450","DOIUrl":"10.5603/fhc.104450","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoporosis is a bone disease characterised by low bone mass, deterioration of bone tissue, and disruption of bone microarchitecture. MicroRNAs have been found to play an important role in osteoporosis. MicroRNA (miR)-494 is inhibited during bone angiogenesis, and its overexpression reduces osteogenic differentiation gene expression. Sirtuin 1 (Sirt1) is a histone deacetylase with multiple cellular activities including increasing bone mass and delaying the onset of osteoporosis. MiR-494-3p has been predicted in computer-assisted bioinformatics analysis to target the 3'UTR of Sirt1 mRNA. The aim of the present study was to assess the effect of miR-494-3p on ovariectomy (OVX)-induced osteoporosis in rats and the relevant mechanisms.</p><p><strong>Material and methods: </strong>Osteoporosis in female rats was induced by OVX, and bone microarchitectural changes were evaluated by means of microCT. MiR-494-3p and Sirt1 expression in femurs were evaluated by RT-qPCR or Western blotting. Bone marrow mesenchymal stem cells (BMSCs) were isolated from rat femurs and identified by flow cytometry. Then, BMSCs were transfected with miR-494-3p inhibitor/mimic, si-Sirt1 and negative controls as well as pcDNA3.1-TLR4 and empty pcDNA3.1 vector. Osteogenic cell differentiation was assessed via Alizarin Red, alkaline phosphatase (ALP) and Oil Red O staining.</p><p><strong>Results: </strong>MiR-494-3p level was upregulated, and Sirt1 mRNA and protein levels were downregulated, in femurs of OVX rats. Functionally, miR-494-3p inhibited osteogenic differentiation of cultured rat BMSCs. Mechanistically, miR-494-3p regulated the Sirt1 3'UTR to activate TLR4/NF-κB signalling, and Sirt1 inhibition and TLR4 overexpression reversed the enhancing effect of miR-494-3p knockdown on osteogenic differentiation.</p><p><strong>Conclusions: </strong>MiR-494-3p represses osteogenic differentiation of BMSCs in OVX rats through Sirt1/TLR4/NF-κB signalling.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"65-78"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149953","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":"VE1 immunohistochemistry as a screening tool for BRAFV600E mutation in lung adenocarcinoma: evidence from a Montenegro National Cohort.","authors":"Branko Campar, Mirjana Miladinovic, Janja Raonic, Ivana Curovic, Milana Panjkovic","doi":"10.5603/fhc.108990","DOIUrl":"10.5603/fhc.108990","url":null,"abstract":"<p><strong>Introduction: </strong>Lung cancer remains the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) representing the majority of cases. Molecular profiling of NSCLC has identified multiple genomic alterations, including BRAFV600E mutation, which occurs in 1-5% of patients, predominantly in adenocarcinomas. Detection of this mutation is clinically relevant due to the availability of targeted therapies. Immunohistochemistry using the VE1 antibody offers a rapid and practical screening method, although interpretation criteria and methodological variability remain challenging.</p><p><strong>Material and methods: </strong>This study represents the first systematic evaluation of BRAFV600E immunohistochemical (IHC) and molecular status in the Montenegrin population. A total of 135 patients undergoing surgical resection for primary lung adenocarcinoma were analyzed retrospectively. Clinicopathological data were collected, and tissue microarrays (TMA) were constructed. Immunohistochemical staining was performed with the VE1 monoclonal antibody, and results were scored based on cytoplasmic staining intensity and homogeneity. Positive cases, along with matched negative controls, were further analyzed using fully automated Biocartis Idylla real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>VE1 IHC positivity was observed in 7 patients (5.2%), with strong, homogeneous staining (3+) in 2 cases. BRAFV600E mutations were confirmed by PCR exclusively in these 3+ cases, giving a prevalence of 1.5% overall and 28.6% relative to IHC-positive cases. Statistical analysis demonstrated perfect concordance between strong, homogeneous VE1 staining and PCR results. Weak or focal staining presented interpretative challenges, highlighting the need for standardized criteria and molecular confirmation.</p><p><strong>Conclusions: </strong>Immunohistochemistry using VE1 antibody is a reliable and accessible initial screening tool for BRAFV600E mutation in lung adenocarcinoma. Strong, homogeneous cytoplasmic staining predicts mutation status with high accuracy, while weak or heterogeneous staining requires confirmatory molecular testing. The present findings provide essential local epidemiological data and support universal IHC testing to guide personalized therapy in NSCLC.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"177-184"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145586522","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":"Tectochrysin alleviates high-glucose-induced retinal pigment epithelial cell injury through Nrf2/HO-1 activation.","authors":"Yuan Sui, Chengsen Zhang, Bingbing Jiang, Wei Li, Shuang Wang","doi":"10.5603/fhc.107923","DOIUrl":"10.5603/fhc.107923","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic retinopathy involves retinal pigment epithelium (RPE) dysfunction. Tectochrysin is a natural flavonoid and antioxidant. However, its effects on retinal pigment epithelial cells remain unveiled. In this study, the investigation undertook the question of whether tectochrysin could protect human adult RPE cells ARPE-19 from high-glucose (HG) damage. Also the potential regulatory mechanism was explored.</p><p><strong>Material and methods: </strong>Cell counting assay 8 (CCK8) was used to measure cell viability in ARPE-19 cells with tectochrysin treatment for 72 h to confirm the potential cytotoxicity. Furthermore, cells were treated by HG (40 mM glucose) for 48 h with or without tectochrysin treatment (5 or 10 μg/mL). Then cell viability, apoptosis and Reactive Oxygen Species (ROS) levels were evaluated using CCK8, flow cytometry and DCFH-DA fluorescence methods. Migration capacity was evaluated using wound healing and Transwel assays. In addition, malondialdehyde (MDA) content, glutathione (GSH), and Fe2+ levels were also examined with kits. Protein expression of ferroptosis markers (ACSL4, GPX4), EMT-related proteins (E-cadherin, vimentin, Snail), and Nrf2/HO-1 were determined using western blotting.</p><p><strong>Results: </strong>In ARPE-19 cells tectochrysin (5 or 10 μg/mL) significantly reversed HG-induced cytotoxicity, reducing apoptosis, ROS, MDA and Fe2+ levels, and increasing GSH. Tectochrysin reversed HG-induced ferroptosis-related protein ACSL4 and restored HG-inhibited GPX4 expression. In addition, tectochrysin inhibited HG-induced cell migration and vimentin and Snail levels and restored expression of HG-inhibited mesenchymal marker E-cadherin. Moreover, tectochrysin activated the Nrf2/HO-1 pathway.</p><p><strong>Conclusions: </strong>The findings demonstrate that tectochrysin protects ARPE-19 cells from HG-induced injury by inhibiting apoptosis, ferroptosis and EMT while activating Nrf2/HO-1 signaling, suggesting its potential as a therapeutic agent for diabetic retinopathy.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"134-141"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286001","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 and histopathological characteristics of adenomas and adenocarcinomas of Meibomian glands in dogs.","authors":"Rafal Ciaputa, Adam Szymerowski, Kacper Zebrowski, Stanislaw Dzimira, Izabela Janus-Ziolkowska, Malgorzata Kandefer-Gola, Marcin Nowak","doi":"10.5603/fhc.108299","DOIUrl":"10.5603/fhc.108299","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to provide a comprehensive histopathological and immunohistochemical analysis of Meibomian adenomas and adenocarcinomas.</p><p><strong>Material and methods: </strong>A total of 80 tumours were included in the study: 33 adenomas and 47 Meibomian adenocarcinomas. Ki-67, cytokeratin-7 and von Willebrand factor antibodies were used for the immunohistochemical staining.</p><p><strong>Results: </strong>Detailed characteristics of inflammatory infiltration depending on tumor type and damage to surrounding tissue by tumour cells are presented. A close correlation was found between the structure and intensity of blood vessel proliferation and the level of factor VIII expression.</p><p><strong>Conclusions: </strong>The presented detailed histopathological analysis, combined with the results of immunohistochemical studies, now allows for better treatment planning and prognosis assessment for patients.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"142-148"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286006","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":"Electroacupuncture stimulation inhibited astrogliosis and microglia polarisation to alleviate spinal cord injury via Janus kinase 2/signal transducer and activator of transcription 3 signalling pathway.","authors":"Jianuo Li, Yuhuai Guo, Xiangxin Zeng, Hongzhao Tian, Yapeng Han, Shuo Cai, Min Sun","doi":"10.5603/fhc.104273","DOIUrl":"https://doi.org/10.5603/fhc.104273","url":null,"abstract":"<p><strong>Introduction: </strong>The aberrant activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signalling pathway is involved in spinal cord injury (SCI) progression. Electroacupuncture (EA) stimulation is effective in alleviating SCI, but the mechanism is poorly understood.</p><p><strong>Material and methods: </strong>An SCI model was constructed by cord contusion at T10, and AG490 (a JAK2 inhibitor) served as a positive control in this study. We evaluated the effects of EA on locomotor activity and spinal damage in SCI rats. The effects of EA on astrocytes and microglia and on the JAK2/STAT3 signalling pathway in the cells were investigated.</p><p><strong>Results: </strong>Behavioural tests showed that hind limb motor function of rats was improved after EA stimulation. The therapeutic effects of EA stimulation in restoring motor function, alleviating injured spinal cords, and inhibiting spinal cord neuronal apoptosis in SCI rats, were similar to those of AG490. Increased STAT3 activation was observed in astrocytes and microglia in the spinal cord of SCI rats, and this was reversed by EA stimulation. EA alleviated astrogliosis and inhibited microglia M1 polarisation in SCI rat spinal cords. In addition, RNA expression levels of pro-inflammatory factors IL-6, CXCL1, and TNF-α in rat spinal cords were suppressed by EA stimulation, while the expression level of the anti-inflammatory factor heme oxygenase 1 was increased. Meanwhile, the expression of p-JAK2, p-STAT3, and JAK2/STAT3 downstream targets SOCS3 and COX-2 in the spinal cord of SCI rats was inhibited by EA stimulation. Interestingly, the observed effects were comparable to those treated with EA.</p><p><strong>Conclusions: </strong>Our findings demonstrate that EA stimulation ameliorates SCI in rats and exerts an inhibitory effect on the JAK2/STAT3 signalling pathway.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"63 1","pages":"28-40"},"PeriodicalIF":1.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149840","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":"Nootkatone mitigates periodontal inflammation and reduces alveolar bone loss via Nrf2/HO-1 and NF-κB pathways in rat model of periodontitis.","authors":"Ye Yin, Zeyu Ma, Peiliang Shi","doi":"10.5603/fhc.101862","DOIUrl":"10.5603/fhc.101862","url":null,"abstract":"<p><strong>Introduction: </strong>Periodontitis (PD) is a chronic inflammatory disease leading to alveolar bone loss. This study investigated the effect of nootkatone and regulatory mechanism in reducing periodontal inflammation and alveolar bone loss in a rat model.</p><p><strong>Material and methods: </strong>Twenty male Sprague-Dawley rats were divided into control, periodontitis, and nootkatone-treated groups (45 or 90 mg/kg). Ligature induction method was adopted to establish the PD model. After 21 days, rats received daily gavage of either saline or nootkatone for 10 days. Alveolar bone loss was assessed using micro-CT. Histological analyses included hematoxylin and eosin (H&E), tartrate-resistant acid phosphatase (TRAP), and Masson's trichrome stainings. Immunohistochemistry for heme oxygenase 1 (HO-1) and nuclear factor erythroid-2 related factor 2 (Nrf2) were performed in periodontal tissues. Content of inflammatory cytokines IL-1β, IL-6, and TNF-α in gingival tissues around ligature were assessed using ELISA kits. Malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were analyzed and Western blot for NF-κB expression in gingival tissues were performed.</p><p><strong>Results: </strong>Nootkatone significantly reduced the distance from cementoenamel junction to alveolar bone crest (CEJ-ABC), enhanced bone mineral density (BMD), bone volume (BV), and BV/total volume (TV) ratio in ligature-induced rats. Higher dose of nootkatone (90 mg/kg) did not show more significant therapeutic effect than lower dose (45 mg/kg). Histological staining showed decreased osteoclasts' number and improved bone architecture in the nootkatone group. Content of IL-1β, IL-6, and TNF-α and inflammatory cell infiltration level in gingival tissues around the ligature were decreased in the nootkatone-treatment rats. Nootkatone increased Nrf2 and HO-1 protein expression and decreased NF-κB protein level, suppressing MDA levels and enhancing SOD activity.</p><p><strong>Conclusions: </strong>In a rat model, nootkatone effectively mitigates periodontal inflammation and alveolar bone loss through the Nrf2/HO-1 and NF-κB pathways. These findings suggest nootkatone as a promising therapeutic agent for the treatment of periodontitis.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"145-153"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079880","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":"CCL19 promotes TNF-alpha/IFN-gamma-induced production of cytokines by targeting CCR7/NF-κB signalling in HaCaT cells.","authors":"Ying Zeng, Xiaoqi Nie, Yunhua Deng","doi":"10.5603/fhc.104038","DOIUrl":"https://doi.org/10.5603/fhc.104038","url":null,"abstract":"<p><strong>Introduction: </strong>Atopic dermatitis (AD) is the most common allergic skin disease. The dysfunction of keratinocytes is closely associated with AD progression. Nevertheless, the specific functions of CC chemokine ligand 19 (CCL19) and its receptor CC chemokine receptor 7 (CCR7) in human HaCaT keratinocytes are still unclear.</p><p><strong>Material and methods: </strong>AD cell models in vitro were established by treating HaCaT cells with TNF-alpha (TNF-α, 10 ng/mL) and IFN-gamma (IFN-γ, 10 ng/mL). Cell viability was estimated by MTT assay. The protein levels of CCL19 and CCR7 were tested via Western blotting. The expression of CCL19 protein was knocked down by transfecting si-CCL19 into HaCaT cells. The contents of inflammatory factors i.e. thymus and activation-regulated chemokine (TARC), interleukin 6 (IL-6), and prostaglandin E2 were measured by ELISA, and the nitric oxide content was detected by Griess reagent. The protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) were tested via Western blotting.</p><p><strong>Results: </strong>TNF-α and IFN-γ induced cytotoxicity and upregulated the expression of CCL19 and CCR7 in HaCaT cells. CCL19 knockdown alleviated cytokines-induced cytotoxicity and the release of TARC, IL-6, PGE2 and nitric oxide in TNF-α + IFN-γ-treated HaCaT cells. Furthermore, the protein levels of iNOS and COX-2 were also repressed by CCL19 knockdown. In addition, knockdown of CCL19 decreased CCR7 protein content and inhibited the phosphorylation of IκBα and p65, implying that knockdown of CCL19 inactivated CCR7/NF-κB signalling in HaCaT cells. Rescue assays validated that CCR7 overexpression reversed the effects of CCL19 silencing on the viability and levels of inflammatory factors in TNF-α + IFN-γ-induced HaCaT cells.</p><p><strong>Conclusions: </strong>This study proves that CCL19 can promote TNF-α + IFN-γ-induced skin inflammatory responses by targeting CCR7/NF-κB pathway in HaCaT cells.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"62 4","pages":"203-211"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381987","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":"Anti-atherosclerotic effects of LncRNA NEXN-AS1 by regulation of canonical inflammasome pathway of pyroptosis via NEXN.","authors":"Fei Chen, Yun-Yong Lin, Rui Chen, Wen-Jie Lu, Yi-Wen Wu, Shaodong Qiu, Limei Wu","doi":"10.5603/fhc.102206","DOIUrl":"10.5603/fhc.102206","url":null,"abstract":"<p><strong>Introduction: </strong>Pyroptosis is closely related to many chronic diseases including atherosclerosis, but the potential pathomechanisms are still unclear. This study was aimed at exploring how lncRNAs may contribute to pyroptosis and the potential mechanisms.</p><p><strong>Material and methods: </strong>We performed in vitro assays to investigate the effects of a relatively newly discovered lncRNA, NEXN-AS1, on pyroptosis. Two types of vascular wall cells, i.e. human vascular smooth muscle cells (VSMCs) and endothelial cells (ECs), were used as cell models in this study. A previously constructed lentivirus vector was used to overexpress lncRNA NEXN-AS1 and a small interfering RNA (siRNA) mimic against NEXN to knockdown NEXN. The mRNA and protein levels of molecules of pyroptosis in the canonical inflammasome pathway, including nucleotide-binding oligomerisation segment-like receptor family 3 (NLRP3), caspase-1, gasdermin D (GSDMD), interleukin-1β (IL-1β), and interleukin-18 (IL-18) were detected using quantitative real-time PCR and Western blot analysis, respectively.</p><p><strong>Results: </strong>We found that lentivirus-mediated overexpression of lncRNA NEXN-AS1 increased the expression levels of NEXN and markedly reduced the expression of critical molecules involved in pyroptosis, including NLRP3, caspase-1, GSDMD, IL-1β, and IL-18, in both VSMCs and ECs. Furthermore, NEXN knockdown could reverse the effects of lncRNA NEXN-AS1 overexpression on pyroptosis.</p><p><strong>Conclusions: </strong>lncRNA NEXN-AS1 could act as a target for maintaining endothelium homeostasis, increasing plaque stability, and delaying the progression of atherosclerosis.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"191-202"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970112","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":"Inhibition of IGF2BP1 attenuates the progression of endometriosis through PTBP1.","authors":"Yanlin Su, Wencai Tian, Li Cheng, Ling Yin, Xiaoxia He, Xin Wei","doi":"10.5603/fhc.98213","DOIUrl":"10.5603/fhc.98213","url":null,"abstract":"<p><strong>Introduction: </strong>Endometriosis (EMs), manifested by pain and infertility, is a chronic inflammatory disease. The precise pathophysiology of this disease remains uncertain. Insulin-like growth factor-2 mRNA-binding protein 1 (IGF2BP1) and polypyrimidine tract-binding protein 1 (PTBP1) have both been found to regulate proliferation, apoptosis, and invasion. This study aimed to investigate the effects of IGF2BP1/PTBP1 in treating EMs.</p><p><strong>Materials and methods: </strong>qRT-PCR and western blotting were employed to quantify IGF2BP1 and PTBP1 expression in six patients with EMs (mean age 33.83 years). The correlation analysis, STRING database prediction, and RNA immunoprecipitation were utilized to identify the relationship between IGF2BP1 and PTBP1. Ectopic endometrial volume, weight, HE staining, and IGF2BP1 silencing were utilized to estimate the effects of IGF2BP1 in EMs model rats. qRT-PCR, CCK-8, 5-ethynyl-2'-deoxyuridine (EDU) labeling, Transwell assay, and flow cytometry were utilized to assess the effects of IGF2BP1/PTBP1 on the proliferation, migration, invasion, and apoptosis of ectopic endometrial stromal cells (eESCs). Furthermore, western blotting was employed to evaluate expressions of PCNA, VEGF, and E-cadherin in EMs rats and eESCs.</p><p><strong>Results: </strong>The mRNA and protein levels of IGF2BP1 and PTBP1 in the ectopic and eutopic endometrium of EMs patients were significantly increased. RNA immunoprecipitation revealed a close interaction of IGF2BP1 with PTBP1. Additionally, the endometrial volume, weight, and histopathologic scores in rats were significantly reduced after IGF2BP1 silencing. IGF2BP1 silencing also decreased the expression of PCNA and VEGF, and increased E-cadherin expression in endometrial tissues of EMs rats. Moreover, IGF2BP1 silencing inhibited proliferation, migration, and invasion and promoted apoptosis through PTBP1 in eESCs.</p><p><strong>Conclusions: </strong>IGF2BP1 exhibits potential beneficial properties in the management of EMs by interacting with PTBP1, thereby highlighting IGF2BP1 as a promising therapeutic target for EMs.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"25-36"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140335338","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}