Folia Biologica最新文献

{"title":"Gallic Acid Alleviates Psoriasis Keratinization and Inflammation by Regulating BRD4 Expression.","authors":"Li Zhang, Qiaoyuan Ye, Saiyang Gan, Huan Liu, Qing Zhang, Shuangshuang Wang, Can Cheng","doi":"10.14712/fb2024070010053","DOIUrl":"10.14712/fb2024070010053","url":null,"abstract":"<p><p>Psoriasis is a chronic non-contagious autoimmune disease. Gallic acid is a natural compound with potential health benefits, including antioxidant, anticancer, antiviral and antibacterial properties. Nevertheless, the influence of gallic acid on psoriasis has not been fully determined. This investigation aimed to discover the effect of gallic acid on psoriasis. Thirty-one pairs of psoriatic skin tissues and healthy adult human skin tissues were collected. Human keratinocytes (HaCaT cells) were transfected with interleukin 17A (IL-17A) to create the psoriatic keratinocyte model. The content of bromodomain-containing protein 4 (BRD4) microRNA was assessed using qRT-PCR testing. The content of BRD4 was detected by Western blotting. Cell migration was evaluated by conducting a wound healing assay. Cell proliferation was determined using an EdU assay. Apoptosis was detected by the TUNEL assay. The contents of interferon gamma (IFN-γ), IL-6, IL-8 and IL-17 were detected by ELISA. BRD4 was up-regulated in psoriatic skin tissues and in the IL-17A group compared to the healthy adult human skin tissues and the control group. Silencing BRD4 inhibited cell migration, proliferation and inflammatory response but induced apoptosis in IL-17A-treated HaCaT cells. Conversely, BRD4 over-expression promoted cell migration, proliferation and inflammatory response but suppressed apoptosis in IL-17A-treated HaCaT cells. Gallic acid repressed cell migration, proliferation and inflammatory response but indu-ced apoptosis in HaCaT cells transfected with IL-17A by down-regulating BRD4. Gallic acid represses cell migration, proliferation and inflammatory response but induces apoptosis in IL-17A-transfected HaCaT cells by down-regulating BRD4.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"70 1","pages":"53-61"},"PeriodicalIF":0.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141237162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-325 Supresses Cell Proliferation and Migration in Non-Small Cell Lung Cancer via Targeting DNA Ligase 1 (LIG1).","authors":"Maixia Yu, Linchan Li, Peng Xu","doi":"10.14712/fb2024070020095","DOIUrl":"10.14712/fb2024070020095","url":null,"abstract":"<p><p>DNA ligase 1 (LIG1) plays a key role in DNA synthesis and DNA damage repair pathways. LIG1 has been shown to be up-regulated in human non-small cell lung cancer (NSCLC); however, its role and molecular regulatory mechanism in NSCLC cell proliferation are still not fully understand. In this study, we aimed to explore the role of LIG1 and post-transcripional regulators in NSCLC. Utilizing bioinformatic tools and qRT-PCR, our investigation substantiated the up-regulation of LIG1 within NSCLC cell lines and tumour tissues. Remarkably, individuals exhibiting elevated levels of LIG1 had diminished survival rates. Functionally, the depletion of LIG1 inhibited cell proliferation and migration, contrasting with the increased proliferation and migration upon LIG1 over-expression. Prediction from the TargetScanHuman database and results of dual luciferase reporter assays indicated that miR-325 could directly bind to and negatively regulate LIG1. Moreover, our findings demonstrated that the mimicry of miR-325 decreased cell viability, whereas its inhibition correspondingly increased viability, indicative of the tumour-suppressive role of miR-325 through the down-regulation of LIG1. Collectively, our findings show that LIG1 could promote tumour progression and knockdown of LIG1 could exert suppressive effects on NSCLC. As the post-transcriptional factor of LIG1, miR-325 could negatively regulate the expression of LIG1 to inhibit tumour progression in vitro. These findings suggest that LIG1 and miR-325 might be potential therapeutic targets for NSCLC treatment.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"70 2","pages":"95-103"},"PeriodicalIF":1.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Predisposition to Male Breast Cancer.","authors":"Markéta Janatová, Marianna Borecká, Petra Zemánková, Kateřina Matějková, Petr Nehasil, Leona Černá, Marta Černá, Petra Dušková, Taťána Doležalová, Lenka Foretová, Ondřej Havránek, Jana Házová, Klára Horáčková, Milena Hovhannisyan, Lucie Hrušková, Štěpán Chvojka, Mária Janíková, Marta Kalousová, Marcela Kosařová, Monika Koudová, Veronika Krhutová, Veronika Krulišová, Eva Macháčková, Renáta Michalovská, Barbora Němcová, Jan Novotný, Markéta Šafaříková, Barbora Šťastná, Viktor Stránecký, Ivan Šubrt, Spiros Tavandzis, Zdeňka Vlčková, Michal Vočka, Radek Vrtěl, Tomáš Zima, Jana Soukupová, Petra Kleiblová, Zdeněk Kleibl","doi":"10.14712/fb2024070050274","DOIUrl":"https://doi.org/10.14712/fb2024070050274","url":null,"abstract":"<p><p>Male breast cancer (mBC) is a rare cancer diagnosis that constitutes less than 1 % of all breast cancer cases globally. Genetic factors play an important role in the mBC risk. Germline pathogenic variants (PVs) in cancer predisposition genes could be identified in about 15 % of cases. We performed germline genetic testing in 248 Czech mBC patients and 3,626 non-cancer male controls using next-generation sequencing by the CZECANCA panel (226 genes). We identified 46/248 (18.5 %) carriers of PVs in the established mBC predisposition genes, primarily in BRCA2 (N = 34), less frequently in BRCA1 (N = 7) and PALB2 (N = 5). The presence of a PV in these genes significantly increased the mBC risk (OR 44.04; 5.82; and 8.26, respectively). Additionally, we identified 16 carriers of PVs in candidate mBC genes, but only PVs in CHEK2 were significantly associated with increased mBC risk (OR = 4.98). The significance of 26 germline alterations in 23/192 additionally analysed genes remained uncertain. The carriers of PVs in BRCA1 and CHEK2 were significantly younger (55.8 and 52.6 years, respectively) than non-carriers (64.8 years), and all carriers of PVs in the established genes had more frequently grade G3 tumours and positive family cancer history. Our study underscores the critical role of BRCA2 in mBC predisposition while also highlighting the potential contributions of additional genes that warrant further investigation. Moreover, it supports and justifies universal genetic testing for all mBC patients to generally improve early cancer detection and tailored treatment.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"70 5-6","pages":"274-284"},"PeriodicalIF":1.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alarmins and Related Molecules in Elective Surgery.","authors":"Sabina Strohalmová, Kateřina Levová, Aleš Antonín Kuběna, David Hoskovec, Zdeněk Krška, Tomáš Zima, Marta Kalousová","doi":"10.14712/fb2023069020050","DOIUrl":"https://doi.org/10.14712/fb2023069020050","url":null,"abstract":"<p><p>Surgery is associated with alterations of alarmins' and related molecules' levels. The aim of this study was to investigate which biomarkers are most involved in surgery. The studied group consisted of 58 patients with inguinal or umbilical hernia or cholecystolithiasis and 21 healthy controls for compa-rison. We also added seven acute patients with appendicitis, cholecystitis and incarcerated hernia. Serum concentrations of soluble receptor of advanced glycation end-products (sRAGE), extracellular newly identified receptor for advanced glycation end-products binding protein (EN-RAGE), calprotectin, high mobility group box 1 (HMGB1) and interleukin 6 (IL-6) were analysed by ELISA before and after surgery. Preoperative concentrations of calprotectin were significantly decreased while concentrations of sRAGE were significantly increased in patients compared to controls; the concentrations of EN-RAGE and HMGB1 did not differ significantly. IL-6 levels were undetectable in elective patients preoperatively and in controls. Postoperatively, there was a significant increase of EN-RAGE, calprotectin, HMGB1, and IL-6 and a significant decrease of sRAGE compared to preoperative levels. In acute patients, all tested molecules except for sRAGE were significantly increased preoperatively, and sRAGE was significantly decreased. In contrast, after surgery, we could observe a further increase in IL-6; the other biomarkers did not differ significantly. We can conclude that the concentrations of all tested biomarkers are significantly influenced by elective surgery. The postoperative levels of all tested molecules increase except for sRAGE, whose level is significantly decreased after surgery. In acute states, these molecules are already increased, and the influence of surgery is, apart from IL-6, insignificant.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 2","pages":"50-58"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138794950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-19a-3p Promotes Aerobic Glycolysis in Ovarian Cancer Cells via IGFBP3/PI3K/AKT Pathway.","authors":"Lijun Du, Kaikai Dou, Dan Zhang, Huidong Xia, Nianhai Liang, Ningping Wang, Jianmin Sun, Ru Bai","doi":"10.14712/fb2023069050163","DOIUrl":"https://doi.org/10.14712/fb2023069050163","url":null,"abstract":"<p><p>Aerobic glycolysis is a prominent feature of cancer. Here, we reported that miR-19a-3p promotes aerobic glycolysis in ovarian cancer cells SKVO3 and ES-2 by increased production of ATP, lactic acid, extracellular acidification (ECAR), and increased expression of PKM2, LDHA, GLUT1 and GLUT3. Further study showed that over-expression of IGFBP3, the target of miR-19a-3p, decreases aerobic glycolysis in ovarian cancer cells, while knockdown of IGFBP3 expression increases aerobic glycolysis. The rescue assay suggested that miR-19a-3p promotes aerobic glycolysis in ovarian cancer cells through targeting IGFBP3. Moreover, over-expression of miR-19a-3p or silencing of IGFBP3 expression promoted activation of AKT, which is important for aerobic glycolysis in cancer cells, indicating that miR-19a-3p promotes aerobic glycolysis in ovarian cancer cells through the IGFBP3/PI3K/AKT pathway. This suggests that miR-19a-3p and IGFBP3 may serve as potential treatment targets of ovarian cancer.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 5-6","pages":"163-172"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140861844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenesis of Collagen-Induced Arthritis: Role of Immune Cells with Associated Cytokines and Antibodies, Comparison with Rheumatoid Arthritis.","authors":"Monika Šteigerová, Martin Šíma, Ondřej Slanař","doi":"10.14712/fb2023069020041","DOIUrl":"https://doi.org/10.14712/fb2023069020041","url":null,"abstract":"<p><p>Collagen-induced arthritis is the most com-mon in vivo model of rheumatoid arthritis used for investigation of new potential therapies in preclinical research. Rheumatoid arthritis is a systemic inflammatory and autoimmune disease affecting joints, accompanied by significant extra-articular symptoms. The pathogenesis of rheumatoid arthritis and collagen-induced arthritis involves a so far properly unexplored network of immune cells, cytokines, antibodies and other factors. These agents trigger the autoimmune response leading to polyarthritis with cell infiltration, bone and cartilage degeneration and synovial cell proliferation. Our review covers the knowledge about cytokines present in the rat collagen-induced arthritis model and the factors affecting them. In addition, we provide a comparison with rheumatoid arthritis and a description of their important effects on the development of both diseases. We discuss the crucial roles of various immune cells (subtypes of T and B lymphocytes, dendritic cells, monocytes, macrophages), fibroblast-like synoviocy-tes, and their related cytokines (TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-17, IL-23, GM-CSF, TGF-β). Finally, we also focus on key antibodies (rheu-matoid factor, anti-citrullinated protein antibodies, anti-collagen II antibodies) and tissue-degrading enzymes (matrix metalloproteinases).</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 2","pages":"41-49"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138795230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of Dihydropyrimidinase-like 3 Gene Expression by MicroRNAs in PC12 Cells with Induced Ischaemia and Hypothermia.","authors":"Kisang Kwon, Ji-Hye Song, Hyewon Park, O-Yu Kwon, Seung-Whan Kim","doi":"10.14712/fb2023069020069","DOIUrl":"10.14712/fb2023069020069","url":null,"abstract":"<p><p>Although hypothermic treatment has been reported to have some beneficial effects on ischaemia at the clinical level, the mechanism of ischaemia suppression by hypothermia remains unclear due to a lack of mechanism understanding and insufficient data. The aim of this study was to isolate and characterize microRNAs specifically expressed in ischaemia-hypothermia for the dihydropyrimidinase-like 3 (Dpysl3) gene. PC12 cells were induced with CoCl2 for chemical ischaemia and incubated at 32 ℃ for hypothermia. In ischaemia-hypothermia, four types of microRNAs (miR-106b-5p, miR-194-5p, miR-326-5p, and miR-497-5p) were highly related to the Dpysl3 gene based on exosomal microRNA analysis. Dpysl3 gene expression was up-regulated by miR-497-5p but down-regulated by miR-106b-5p, miR-194-5p and miR-326-5p. Our results suggest that these four microRNAs are involved in the regulation of Dpysl3 gene expression. These findings provide valuable clues that exosomal microRNAs could be used as therapeutic targets for effective treatment of ischaemia.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 2","pages":"69-73"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138795346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum - Tri-Lineage Differentiation of NTERA2 Clone D1 Cells towards Neural, Hepatic and Osteogenic Lineages in Vitro.","authors":"Balázs Szeky, B Mayer, M Gyongy, A Hajdara, S Barsi, S Karpati, K Nemeth","doi":"10.14712/fb2023069010040","DOIUrl":"10.14712/fb2023069010040","url":null,"abstract":"<p><p>The images in Fig. 4 were not presented correctly. The correct version of Fig. 4: see the last page of pdf. The original article was published in Folia Biologica (Praha) Volume 67, No. 5-6 (2021), 174-182. https://doi.org/10.14712/fb2021067050174.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 1","pages":"40"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92153418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Technical Note Cell Dysplasia - Cell Dysplastic Features (A Morphological Note).","authors":"Karel Smetana, Dana Mikulenková, Hana Klamová, Josef Karban, Marek Trněný","doi":"10.14712/fb2023069010034","DOIUrl":"10.14712/fb2023069010034","url":null,"abstract":"<p><p>Cell dysplasia is a currently used term describing various cellular developmental abnormalities visible by microscopy. However, detailed description of these developmental abnormalities might provide useful information not only on the cell state but also on the abnormal developmental steps of cell lineages, tissues and organs. The frequently noted visualized cell dysplastic features reflect nuclear- or nucleolar-cytoplasmic anarchy (asynchrony), premature heterochromatin condensation state, marked aneuploidy, abnormal nucleus-cytoplasm ratio, abnormality of cell organelles including mitochondria, abnormal presence or absence of cell lineage-specific granules, and formation of peripheral buds or blebbing on the cell surface. The description of these frequently occurring cell dysplastic features might also be helpful in recognizing and studying defined specific disorders of the \"whole macro-body\" expressed as a disease.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 1","pages":"34-39"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92153421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox Status of Erythrocytes as an Important Factor in Eryptosis and Erythronecroptosis.","authors":"Anton Tkachenko, Ondřej Havránek","doi":"10.14712/fb2023069040116","DOIUrl":"10.14712/fb2023069040116","url":null,"abstract":"<p><p>Overall, reactive oxygen species (ROS) signalling significantly contributes to initiation and mo-dulation of multiple regulated cell death (RCD) pathways. Lately, more information has become available about RCD modalities of erythrocytes, including the role of ROS. ROS accumulation has therefore been increasingly recognized as a critical factor involved in eryptosis (apoptosis of erythrocytes) and erythro-necroptosis (necroptosis of erythrocytes). Eryptosis is a Ca2+-dependent apoptosis-like RCD of erythrocytes that occurs in response to oxidative stress, hyperosmolarity, ATP depletion, and a wide range of xenobiotics. Moreover, eryptosis seems to be involved in the pathogenesis of multiple human diseases and pathological processes. Several studies have reported that erythrocytes can also undergo necroptosis, a lytic RIPK1/RIPK3/MLKL-mediated RCD. As an example, erythronecroptosis can occur in response to CD59-specific pore-forming toxins. We have systematically summarized available studies regarding the involvement of ROS and oxidative stress in these two distinct RCDs of erythrocytes. We have focused specifically on cellular signalling pathways involved in ROS-mediated cell death decisions in erythrocytes. Furthermore, we have summarized dysregulation of related erythrocytic antioxidant defence systems. The general concept of the ROS role in eryptotic and necroptotic cell death pathways in erythrocytes seems to be established. However, further studies are required to uncover the complex role of ROS in the crosstalk and interplay between the survival and RCDs of erythrocytes.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 4","pages":"116-126"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139971525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}