Folia histochemica et cytobiologica最新文献

{"title":"Diosmetin ameliorates osteoarthritic inflammation in vivo and ECM macromolecules degradation in interleukin-1β-stimulated murine chondrocytes through the Nrf2/NF-κB pathway.","authors":"Liang Qian, Chuang Li, Hong Liu, Hui Zhou, Tao Tan","doi":"10.5603/fhc.100071","DOIUrl":"10.5603/fhc.100071","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoarthritis (OA) is a prevailing degenerative disease in elderly population and can lead to severe joint dysfunction. Studies have revealed various pharmacological activities of diosmetin, including the anti-OA efficacy. The present study further investigated its effect on interleukin (IL)-1β-induced OA in chondrocytes.</p><p><strong>Material and methods: </strong>Primary chondrocytes were isolated from young mice, stimulated with IL-1β (10 ng/mL), and pretreated with diosmetin (10 and 20 μM) to conduct the in vitro assays. CCK-8 assay assessed the cytotoxicity of diosmetin whereas the levels of inflammatory factors (PGE2, nitrite, TNF-α, and IL-6) in homogenized cells were evaluated by ELISA. The levels of inflammatory cytokines, content of extracellular matrix (ECM), and signaling-related proteins (Nrf2, HO-1, and NF-κB p65) were assessed by western blotting. Expression of collagen II, p65, and Nrf2 in the chondrocytes was confirmed by immunofluorescence staining. The chondrocytes treated with IL-1β and diosmetin were transfected with Nrf2 knockdown plasmid (si-Nrf2) to investigate the role of Nrf2. In vivo OA mouse model was induced by surgically destabilizing the medial meniscus (DMM). Safranin O staining was conducted to assess the OA severity in the knee-joint tissue.</p><p><strong>Results: </strong>Diosmetin suppressed the expression of iNOS, COX-2, PGE2, nitrite, TNF-α, IL-6, MMP-13, and ADAMTS-5 induced by IL-1β in chondrocytes. The expression of p-p65, p-IκBα, and nuclear p65 was decreased whereas that of Nrf2 and HO-1 increased by diosmetin treatment in IL-1β-treated chondrocytes. Nrf2 knockdown by siRNA reversed the inhibitory effect of diosmetin on IL-1β-induced degradation of ECM proteins and inflammatory factors in cultured chondrocytes. In the DMM-induced model of OA, diosmetin alleviated cartilage degeneration and decreased the Osteoarthritis Research Society International score.</p><p><strong>Conclusions: </strong>Diosmetin ameliorates expression of inflammation biomarkers and ECM macromolecules degradation in cultured murine chondrocytes via inactivation of NF-κB signaling by activating Nrf2/HO-1 signaling pathway.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"99-109"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442409","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":"Mitofusin 2 inhibits high glucose-induced apoptosis of human lens epithelial cells via modulating mitochondrial function and autophagy.","authors":"Yuan-Yi Guo, Jiang-Yue Zhao, Han-Rong Li, Zhuo Guo, Hao-Yue Shen","doi":"10.5603/fhc.98875","DOIUrl":"10.5603/fhc.98875","url":null,"abstract":"<p><strong>Introduction: </strong>Diabetic cataract (DC) is a common ocular complication of diabetes. Mitofusin 2 (MFN2), a mitochondrial fusion protein, is involved in the pathogenesis of cataract and diabetic complications. However, its role and molecular mechanisms in DC remain unclear.</p><p><strong>Materials and methods: </strong>DC models in rats were induced by intraperitoneal injection of streptozocin (STZ) for 12 weeks. We measured the body weight of rats, blood glucose concentrations, sorbitol dehydrogenase (SDH) activity and advanced glycation end products (AGE) content in the lenses of rats. MFN2 mRNA and protein expression levels in the lenses were detected by RT-qPCR and western blot assays. In vitro, human lens epithelial (HLE) B3 cells were treated for 48 h with 25 mM glucose (high glucose, HG) to induce cell damage. To determine the role of MFN2 in HG-induced cell damage, HLE-B3 cells were transfected with lentivirus loaded with MFN2 overexpression plasmid or short hairpin RNA (shRNA) to overexpress or knock down MFN2 expression, followed by HG exposure. Cell viability was assessed by CCK-8 assay. Flow cytometry was used to detect cell apoptosis and reactive oxygen species (ROS) level. JC-1 staining showed the changes in mitochondrial membrane potential (Δψm). The mediators related to apoptosis, mitochondrial damage, and autophagy were determined.</p><p><strong>Results: </strong>STZ-administrated rats showed reduced body weight, increased blood glucose levels, elevated SDH activity and AGE content, suggesting successful establishment of the DC rat model. Interestingly, MFN2 expression was significantly downregulated in DC rat lens and HG-induced HLE-B3 cells. Further analysis showed that under HG conditions, MFN2 overexpression enhanced cell viability and inhibited apoptosis accompanied by decreased Bax, cleaved caspase-9 and increased Bcl-2 expression in HLE-B3 cells. MFN2 overexpression also suppressed the mitochondrial damage elicited by HG as manifested by reduced ROS production, recovered Δψm and increased mitochondrial cytochrome c (Cyto c) level. Moreover, MFN2 overexpression increased LC3BⅡ/LC3BⅠ ratio and Beclin-1 expression, but decreased p62 level, and blocked the phosphorylation of mTOR in HG-treated HLE-B3 cells. In contrast, MFN2 silencing exerted opposite effects.</p><p><strong>Conclusions: </strong>Presented findings indicate that MFN2 expression may be essential for preventing lens epithelial cell apoptosis during development of diabetic cataract.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"76-86"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442410","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":"Platelet-rich plasma ameliorates cartilage degradation in rat models of osteoarthritis via the OPG/RANKL/RANK system.","authors":"Qun Wu, Xianbao Yao, Nan Shan, Yi Cai, Yongzhi Fan","doi":"10.5603/fhc.100179","DOIUrl":"10.5603/fhc.100179","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoarthritis (OA) is one of the most common degenerative joint diseases in the elderly, which is featured by the degradation of articular cartilage. Recently, platelet-rich plasma (PRP) injection into the affected joint has become one biological therapy for OA treatment. The OPG/RANKL/ RANK signalling has been reported to mediate OA progression. Our study aimed to confirm whether PRP injection retards OA development through the regulation of the OPG/RANKL/RANK system.</p><p><strong>Material and methods: </strong>The OA rat models were induced by medial menisci resection combined with anterior cruciate ligament transection. Four weeks after surgery, OA-induced rats received intra- articular injection with 50 μL PRP once a week for 6 weeks. Rats were euthanised one week after the 6th injection. Rat knee joints were subjected to histopathological examination by haematoxylin- eosin (H&E) and safranin O staining. Osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (RANK), and RANK ligand (RANKL) in the articular cartilage of rats were tested through immunofluorescence staining and western blotting. Serum interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels were measured by enzyme-linked immunosorbent assay (ELISA). Matrix metalloproteinase- 13 (MMP-13), aggrecan, collagen α, IL-1β, IL-6, tumour necrosis factor-alpha (TNF-α), and nuclear factor kappa-B (NF-κB) mRNA and protein expression in rat articular cartilage were examined by real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively.</p><p><strong>Results: </strong>Intra-articular injections of PRP significantly improved the structural integrity of the articular cartilage and enhanced the synthesis of glycosaminoglycans. PRP reduced MMP-13 protein level but increased aggrecan and collagen α protein levels in articular cartilage of OA rats. OA-induced increase in serum IL-1β, IL-6, and TNF-α concentrations as well as increased MMP-13, and decreased collagen II mRNA levels were reversed by the administration of PRP. OA increased IL-1β, TNF-α, and NF-κB mRNA expression in rat articular cartilage whereas PRP administration ameliorated these changes. Moreover, in the articular tissue of OA-induced rats the increased OPG protein level was further elevated by PRP injections whereas the protein level of RANK did not change. The increase in the protein level of RANKL in OA-induced articular tissue was offset by PRP administration. PRP elevated OPG mRNA expression and the OPG/RANKL mRNA ratio, but reduced RANKL mRNA expression and the RANKL/RANK mRNA ratio in the articular tissue of OA-induced rats.</p><p><strong>Conclusions: </strong>PRP mitigates cartilage degradation and inflammation in experimental knee OA by regulating the OPG/RANKL/RANK signalling system.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"154-164"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141999708","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":"Digital morphology network for effective teaching of cytology, histology and histopathology for medical and biology curriculum. VM3.0 Erasmus+ project.","authors":"Cornelia Amalinei, Andrei Daniel Timofte, Irina Draga Căruntu, Piotr M Wierzbicki, Michal A Żmijewski, Spiros Sirmakessis, Jose L Girela, Noemí Martínez-Ruiz, M Flores Vizcaya-Moreno, Rosa M Pérez-Cañaveras, Zdravka Harizanova, Ferihan Popova, Cintia Colibaba, Zbigniew Kmieć","doi":"10.5603/fhc.100875","DOIUrl":"10.5603/fhc.100875","url":null,"abstract":"<p><strong>Introduction: </strong>Digital microscopy transformation, the basis for the virtual microscopy applications, is a challenge but also a requirement in modern Medical Education. This paper presents the scope, background, methods, and results of the project \"Digital Transformation of Histology and Histopathology by Virtual Microscopy (VM) for an Innovative Medical School Curriculum\", VM3.0, funded by the European Union under the Erasmus+ framework (ref.no.2022-1- RO01-KA220-HED-000089017). The project was initiated at Grigore T. Popa University of Medicine and Pharmacy, Iași, Romania, with the support of Euroed Foundation, Iași, and cooperation of University partners from Gdansk (Poland), Plovdiv (Bulgaria), Alicante (Spain), and Patras (Greece) aimed to implement digital histology and histopathology teaching in a common network.</p><p><strong>Materials and methods: </strong>The backbone of the project was the development of a Digital Slide Platform based on the scans of histological slides collected from all the partners of the participating universities and the creation of a simple and fast digital/internet communication tool that could be used to improve histology and histopathology teaching of medical and natural sciences students. The construction of a Virtual Microscopy Library (VML) has been based on the acquisition of whole scans of high-quality histological slides stained by hematoxylin and eosin (H&E) and other classical staining methods and description of various organs' details in English as well as respective languages of the project's partners. The VML can be used for different approches, both for students' instruction in classes as well as for individual students' work and self-testing. Universities from other countries could use the modal structure of the developed VML system on the condition that more slides are provided and the implementation of national language(s) is implemented.</p><p><strong>Conclusions: </strong>The combined efforts of all university partners allowed to establish the dynamic low-cost virtual microscopy educational system. The VM system could help unify the standards of cytology, histology, and histopathology teaching in a quest for the digital transformation of the European educational system.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"61-75"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442408","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":"Changes in early endosomes in rat hippocampal CA1 neurons after transient global cerebral ischaemia.","authors":"Min Qiang, Bai-Hong Tan, De-Sheng Huo, Shu-Lei Li, Zi-Zhen Fan, Ze-Qun Zhou, Rong-Yu Wang, Yanchao Li","doi":"10.5603/fhc.101592","DOIUrl":"10.5603/fhc.101592","url":null,"abstract":"<p><strong>Introduction: </strong>Transient global ischaemia in rodents causes selective loss of hippocampal CA1neurons, but the potential involvement of endocytic pathways has not been fully explored. The aim of this study was to investigate the changes in early endosomes in the CA1 subfield after ischaemia and reperfusion.</p><p><strong>Materials and methods: </strong>A four-vessel occlusion (4-VO) model was established in Wistar rats to induce 13 minutes of global cerebral ischaemia. Neuronal death was detected by Fluoro-Jade B (FJ-B) staining at various intervals after reperfusion, and intracellular membrane changes in ischaemic neurons were revealed using DiOC6(3), a lipophilic fluorescent probe. Ras-related protein Rab5 (Rab5) immunostaining was performed to detect changes in early endosomes in ischaemic neurons. Western blot analysis was used to confirm the morphological observations on Rab5 in the CA1 hippocampal subfield.</p><p><strong>Results: </strong>FJ-B staining confirmed progressive neuronal death in the CA1 subfield in ischaemic rats after reperfusion. DiOC6(3) staining revealed abnormally increased membranous components in ischaemic CA1 neurons. Specifically, early endosomes, as labelled by Rab5 immunostaining, significantly increased in number and size in CA1 neurons at 1.5 and 2 days post-reperfusion, followed by rupture at day 3 and a decrease in staining intensity at day 7 post-reperfusion. Western blot analysis confirmed a significant upregulation of Rab5 protein levels at day 2, which returned to near control levels by day 7.</p><p><strong>Conclusions: </strong>Our study revealed significant changes in the dynamics of early endosomes in CA1 neurons after ischaemia-reperfusion injury. The initial increase in the area fraction of early endosomes in CA1 neurons may reflect an upregulation of endocytic activity, whereas the fragmentation and reduction of early endosomes at the later stage may indicate a failure of adaptive mechanisms of ischaemic neurons against ischaemia-induced death. Understanding the temporal dynamics of early endosomes provides critical insights into the cellular mechanisms that govern fate of CA1 hippocampal neuronsl after ischaemia/reperfusion.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"123-132"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344466","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":"Simvastatin suppresses ethanol effects on the kidney of adolescent mice.","authors":"Makgotso Nchodu, Robin du Preez, Alice Efuntayo, Oladiran I Olateju","doi":"10.5603/fhc.95685","DOIUrl":"10.5603/fhc.95685","url":null,"abstract":"<p><strong>Introduction: </strong>Adolescents tend to experiment with ethanol which often results in heavy episodic drinking patterns leading to serious health concerns later in life. Chronic ethanol use damages renal tissue, promotes collagen deposition, and induces renal inflammation, thereby causing renal dysfunction. Therefore, an intervention such as simvastatin (a blood cholesterol-lowering drug) that could suppress the effects of ethanol on the kidney may be beneficial. This study explored the impact of simvastatin against the onset of renal morphological damage, fibrosis, and inflammation caused by ethanol exposure in mice.</p><p><strong>Materials and methods: </strong>Ten four-week old C57BL/6J mice (F = 5; M = 5) were assigned to each experimental group: (I) NT; no administration of ethanol or simvastatin; (II) EtOH; 2.5 g/kg/day of 20% ethanol, intraperitoneal injection (i.p.); (III) SIM; 5 mg/kg/day of simvastatin, orally; (IV) EtOH + SIM5; 5 mg/kg/day of simvastatin, orally, followed by 2.5 g/kg/day of 20% ethanol, i.p.; and (V) EtOH + SIM15; 15 mg/kg/day of simvastatin, orally, followed by 2.5 g/kg/day of 20% ethanol, i.p. After the 28-day treatment period, the right kidney was removed and processed for haematoxylin and eosin staining, Masson's trichrome staining, or tumour necrosis factor-alpha (TNF-α) immunohistochemistry. The renal corpuscular area, glomerular area, and urinary space area were measured and the area of collagen or TNF-α expression was quantified using ImageJ software.</p><p><strong>Results: </strong>Ethanol administration significantly increased the renal corpuscular area, the glomerular area, the area of collagen, and the area of tissue with TNF-α immunoreactivity but decreased the area of urinary space. Simvastatin generally suppressed the ethanol effects in both sexes, although to varying degrees.</p><p><strong>Conclusions: </strong>Simvastatin proved to suppress collagen deposition and the TNF-α production induced by ethanol in the kidney of mice thus indicating its effectiveness in the treatment of ethanol-related renal diseases.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"87-98"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141442411","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":"Diagnostic utility of immunocytochemistry by using liquid-based cytology (LBC) slides.","authors":"Ozben Yalcin, Senay Erdogan-Durmus, Enver Yarikkaya","doi":"10.5603/fhc.97937","DOIUrl":"10.5603/fhc.97937","url":null,"abstract":"<p><strong>Introduction: </strong>Cytological specimens, such as fine needle aspirations (FNAs) and exfoliative cytology samples, are minimally invasive options for diagnostic purposes. Liquid-based cytology (LBC), originally designed for cervical cytology, has gained prominence as an alternative technique for non-gynecological cytology. Immunocytochemistry (ICC) is an ancillary method used when diagnosis becomes challenging due to morphological overlap or the need for cellular origin clarification. This study aims to assess the diagnostic utility of ICC when applied to LBC slides and evaluate its effectiveness in relation to the waiting (lag) time of residual material.</p><p><strong>Materials and methods: </strong>A total of 74 cases in which ICC was applied to LBC slides were studied over one year in a reference pathology laboratory (Prof. Dr. Cemil Tascioglu, Pathology Laboratory, City Hospital, Istanbul, Turkey). Cases in which immunohistochemistry (IHC) was performed on formalin-fixed paraffin-embedded cell blocks were excluded. The SurePath PAP method was used for the main LBC cytology slides. For the ICC study, 1-4 PAP-stained LBC slides were obtained from each case's residual material and stained with a primary antibody.</p><p><strong>Results: </strong>The positive immunostaining was obtained in 81% of cases. The samples were categorized into groups based on the waiting time of residual LBC material for ICC analysis: 1-5 days, 6-10 days, 11-20 days, and 21-38 days. Comparative analysis revealed a decline in ICC efficacy as the waiting (lag) time increased. Additionally, a statistically significant difference was observed between the 11-20 days and 21-38 days groups (P < 0.05). An analysis of 142 LBC slides stained by ICC revealed that nuclear markers exhibited higher positivity compared to non-nuclear markers, although no significant difference was detected between the two groups.</p><p><strong>Conclusions: </strong>High positivity rates can be obtained in ICC studies performed on additional slides obtained from residual LBC material within the first 20 days. ICC applied to LBC slides is an important and useful alternative for diagnostic and prognostic markers in cases without a cell block or with a cell block without sufficient number of cells.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"1-12"},"PeriodicalIF":1.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971558","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":"Dioscin attenuates lupus nephritis in NZB/W F1 mice by decreasing NF-κB activation and NLRP3 inflammasome.","authors":"Yaling Xu, Han Li","doi":"10.5603/fhc.100604","DOIUrl":"10.5603/fhc.100604","url":null,"abstract":"<p><strong>Introduction: </strong>Dioscin, a natural steroid saponin, has anticancer, anti-inflammatory, anti-hyperlipidemic, and glycemic capabilities. This study focused on dioscin roles and its related mechanisms in experimental lupus nephritis.</p><p><strong>Materials and methods: </strong>Lupus-prone NZB/W F1 mice were intragastrically administered with dioscin, prednisone or vehicle, and kidney, urine and blood samples were harvested after the mice were sacrificed. Proteinuria, blood urea nitrogen (BUN), creatinine, anti-dsDNA, IL-1β, and IL-18 levels in serum as well as IFN-γ, IL-6, IL-17 and TNF-α levels in kidney tissues were assessed. Renal histopathology was examined through hematoxylin-eosin staining. IgG and C3 expression in kidney was evaluated using immunofluorescence staining. The number of glomerular F4/80-positive cells and NLRP3-positive cells was determined by immunohistochemical staining. The protein expression was examined by western blotting.</p><p><strong>Results: </strong>Dioscin alleviated lupus nephritis in NZB/W F1 mice. Dioscin declined serum anti-dsDNA level, prevented deposition of immune complexes in renal glomeruli, and inhibited the inflammatory response and infiltration of macrophages into mouse kidneys. Dioscin inhibited NF-κB and NLRP3 inflammasome in NZB/W F1 mice.</p><p><strong>Conclusions: </strong>Dioscin ameliorates lupus nephritis through inhibition of NLRP3 inflammasome and NF-κB signaling.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"110-121"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747890","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":"Long non-coding RNA HOTAIR promotes tumourigenesis by affecting proliferation, invasion, migration, and apoptosis of liver cancer cells.","authors":"Xinzi Zheng, Renyin Cui, Yan Jiao, Dongxia Chu, Bingrong Wang, Na Li","doi":"10.5603/fhc.100686","DOIUrl":"10.5603/fhc.100686","url":null,"abstract":"<p><strong>Introduction: </strong>Increasing evidence shows that Hox transcript antisense RNA (HOTAIR) plays a vital role in liver cancer initiation and progression by affecting the proliferation, invasion, migration, and apoptosis of liver cancer cells. However, the underlying mechanism of how HOTAIR exerts its functions in liver cancer cells remains unclear. Previous studies have shown that HOTAIR affects the invasion and migration of liver cancer cells by regulating the expression of E-cadherin. Snail2, a transcription factor involved in epithelial-mesenchymal transition, directly binds to the E-boxes of the E-cadherin promoter to repress its transcription. The aim of the study was to examine the correlation between HOTAIR and Snail2 in the HOTAIR/Snail2/E-cadherin signal pathway and explore the role of HOTAIR in the proliferation, invasion, migration, and apoptosis of liver cancer cells.</p><p><strong>Materials and methods: </strong>Fifty matched normal liver tissues and 373 liver cancer tissues were analysed and evaluated. HepG2 and SNU-387 cells were cultured and transfected with plasmids knocking down HOTAIR to disrupt HOTAIR expression. Cell scratch and transwell assays were performed to examine the migration and invasion of HepG2 and SNU-387 cells; in addition, the expression of MMP2 and MMP9 was detected by immunoblotting analysis, RT-qPCR analysis, immunofluorescence analysis, and bioinformatics analysis, which elucidated the regulatory relationship between HOTAIR and Snail2. We used flow cytometry and JC-1 probe analysis assays to clarify the function of HOTAIR inliver cancer cell apoptosis.</p><p><strong>Results: </strong>The HOTAIR mRNA was upregulated in liver cancer tissues, which was related to worse overall survival. HOTAIR induced the expression of matrix metalloproteinase-9 (MMP9) and metalloproteinase-2 (MMP2), leading to degradation of extracellular matrix. HOTAIR knockdown significantly reduced the doubling time and inhibited cell migration and invasion of liver cancer cells. Furthermore, HOTAIR depletion induced mitochondrial-related apoptosis in HepG2 and SNU-387 cell lines.</p><p><strong>Conclusions: </strong>In this study, we propose a novel mechanism in which HOTAIR promotes invasion and migration of liver cancer cells by regulating the nuclear localisation of Snail2.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":" ","pages":"165-179"},"PeriodicalIF":1.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715952","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":"Periostin in ovarian carcinoma: from heterogeneity to prognostic value.","authors":"Ludmila Lozneanu,&nbsp;Irina-Draga Caruntu,&nbsp;Cornelia Amalinei,&nbsp;Mihaela Moscalu,&nbsp;Bogdan Gafton,&nbsp;Mihai Vasile Marinca,&nbsp;Andreea Rusu,&nbsp;Raluca Balan,&nbsp;Simona-Eliza Giusca","doi":"10.5603/FHC.a2023.0004","DOIUrl":"https://doi.org/10.5603/FHC.a2023.0004","url":null,"abstract":"<p><strong>Introduction: </strong>Periostin (POSTN), an extracellular matrix protein, is involved in tumor-associated extracellular matrix (ECM) remodeling. However, its potential value as a prognostic and/or predictive factor has not yet been confirmed. The present study aims to assess POSTN expression separately in tumor cells and stroma of different ovarian carcinoma (OC) histological types, and its relationship with clinicopathological features.</p><p><strong>Material and methods: </strong>102 cases of different histological OC subtypes were immunohistochemically investigated, for POSTN expression assessment in both epithelial tumor cells and tumor stroma. Statistical analysis was performed to correlate POSTN profile with clinicopathological characteristics, therapeutic response, and survival.</p><p><strong>Results: </strong>POSTN expression in epithelial tumor cells was significantly correlated with POSTN expression in tumor stroma. The expression of POSTN in tumor cells was associated with histological type, tumor type (type I and II), tumor recurrence, progression-free survival (PFS), and overall survival (OS), whereas stromal POSTN expression was significantly correlated with age, histological type, tumor type, grade, and stage, residual disease, tumor recurrence, response to chemotherapy, and OS. Survival analysis revealed significant differences of PFS and OS in patients with high POSTN expression in tumor cells and negative stromal POSTN expression compared to patients with low POSTN expression in tumor cells and positive stromal POSTN expression (PFS: hazard ratio (HR) = 2.11, 95% confidence interval (CI): 1.33-3.37, P = 0.002; OS: HR = 1.78, 95% CI: 1.09-2.89, P = 0.019).</p><p><strong>Conclusions: </strong>The comparative assessment of POSTN immunoexpression in two tumor compartments: in tumor cells and stroma, by use of different scoring systems revealed that higher stromal POSTN levels are evidently correlated with unfavorable clinical features and poorer prognosis, while POSTN expression in tumor cells seems to be associated with a better patient outcome.</p>","PeriodicalId":12322,"journal":{"name":"Folia histochemica et cytobiologica","volume":"61 1","pages":"1-16"},"PeriodicalIF":1.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9201845","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}