Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069020041
Monika Šteigerová, Martin Šíma, Ondřej Slanař
{"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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069020069
Kisang Kwon, Ji-Hye Song, Hyewon Park, O-Yu Kwon, Seung-Whan Kim
{"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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069010040
Balázs Szeky, B Mayer, M Gyongy, A Hajdara, S Barsi, S Karpati, K Nemeth
{"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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069010034
Karel Smetana, Dana Mikulenková, Hana Klamová, Josef Karban, Marek Trněný
{"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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069040116
Anton Tkachenko, Ondřej Havránek
{"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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069050186
Guangyu Wang, Xu Tian, Lintao Liu, Jingming Dong
{"title":"Astaxanthin Induces Apoptosis in Human Osteosarcoma MG-63 Cells.","authors":"Guangyu Wang, Xu Tian, Lintao Liu, Jingming Dong","doi":"10.14712/fb2023069050186","DOIUrl":"https://doi.org/10.14712/fb2023069050186","url":null,"abstract":"<p><p>We explored the mechanism of human osteosarcoma MG-63 cell apoptosis induced by asta-xanthin. The MTT assay was used to detect the effect of astaxanthin on cell viability. Morphological changes associated with apoptosis were observed after DAPI staining. Early and late stages of apoptosis were detected by flow cytometry with annexin V-FITC/PI staining. Activation of caspases-8, -9 and -3 was detected by enzyme activity in vitro. Changes in the mitochondrial membrane potential were detected by MitoCapture staining. Western blot was used to detect the cleavage of PARP, which is a caspase-3 substrate, the release of cytochrome c and Smac into the cytosol, the translocation of pro-apoptotic proteins Bax and Bak, and the expression of mitochondrial pathway-related proteins. The translocation of Bax was also detected by immunofluorescence assay. Astaxanthin significantly inhibited the viability of human osteosarcoma MG-63 cells with an IC50 value of 12.36 μg/ml. The DAPI-stained cells showed characteristic apoptotic morphological changes - cell shrinkage, cell membrane blebbing, nuclear condensation, and apoptotic body formation. Cytochrome c and Smac were released from mitochondria to the cytosol. Pro-apoptotic proteins Bax and Bak were rapidly translocated to mitochondria after six hours of astaxanthin action. Caspases-9 and -3 were activated and PARP was cleaved. The expression of anti-apoptotic proteins Bcl-2, Bcl-xL and XIAP was significantly decreased. Astaxanthin induced human osteosarcoma MG-63 cell apoptosis through the mitochondria-mediated endogenous apoptosis pathway.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 5-6","pages":"186-193"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140853049","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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069050149
Ondřej Vít, Jiří Petrák
{"title":"Autotaxin and Lysophosphatidic Acid Signalling: the Pleiotropic Regulatory Network in Cancer.","authors":"Ondřej Vít, Jiří Petrák","doi":"10.14712/fb2023069050149","DOIUrl":"https://doi.org/10.14712/fb2023069050149","url":null,"abstract":"<p><p>Autotaxin, also known as ecto-nucleotide pyrophosphatase/phosphodiesterase family member 2, is a secreted glycoprotein that plays multiple roles in human physiology and cancer pathology. This protein, by converting lysophosphatidylcholine into lysophosphatidic acid, initiates a complex signalling cascade with significant biological implications. The article outlines the autotaxin gene and protein structure, expression regulation and physiological functions, but focuses mainly on the role of autotaxin in cancer development and progression. Autotaxin and lysophosphatidic acid signalling influence several aspects of cancer, including cell proliferation, migration, metastasis, therapy resistance, and interactions with the immune system. The potential of autotaxin as a diagnostic biomarker and promising drug target is also examined.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 5-6","pages":"149-162"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847825","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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069050194
Libor Macůrek
{"title":"Many Ways to the Cell Cycle Exit after Inhibition of CDK4/6.","authors":"Libor Macůrek","doi":"10.14712/fb2023069050194","DOIUrl":"https://doi.org/10.14712/fb2023069050194","url":null,"abstract":"<p><p>Cyclin-dependent kinases (CDKs) are master regulators of proliferation, and therefore they represent attractive targets for cancer therapy. Deve-lopment of selective CDK4/6 inhibitors including palbociclib revolutionized the treatment of advanced HR+/HER2- breast cancer. Inhibition of CDK4/6 leads to cell cycle arrest in G0/G1 phase and eventually to a permanent cell cycle exit called senescence. One of the main features of the senescence is an increased cell size. For many years, it was believed that the non-dividing cells simply continue to grow and as a result, they become excessively large. There is now emerging evidence that the increased cell size is a cause rather than consequence of the cell cycle arrest. This review aims to summarize recent advances in our understanding of senescence induction, in particular that resulting from treatment with CDK4/6 inhibitors.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 5-6","pages":"194-196"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140850107","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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069030081
Munki Jeong, Euitaek Jung, Sukjin Oh, Soon Young Shin
{"title":"Homeobox Protein PROX1 Expression is Negatively Regulated by Histone Deacetylase 1 and c-JUN Complex in MDA-MB-231 Human Breast Cancer Cells.","authors":"Munki Jeong, Euitaek Jung, Sukjin Oh, Soon Young Shin","doi":"10.14712/fb2023069030081","DOIUrl":"10.14712/fb2023069030081","url":null,"abstract":"<p><p>Prospero homeobox 1 (PROX1) is a member of the homeobox transcription factor family that plays a critical role in the development of multiple tissues and specification of cell fate. PROX1 expression is differentially regulated based on the cellular context and plays an antagonistic role as a tumour promoter or suppressor in different tumour types. In human breast cancer, PROX1 expression is suppress-ed; however, the molecular mechanism by which it is down-regulated remains poorly understood. Here, we show that ectopic expression of PROX1 reduces the motility and invasiveness of MDA-MB-231 human breast cancer cells, suggesting that PROX1 functions as a negative regulator of tumour invasion in MDA-MB-231 cells. Treatment with histone deacetylase (HDAC) inhibitors up-regulates PROX1 mRNA and protein expression levels. Knockdown of HDAC1 using short hairpin RNA also up-regulates PROX1 mRNA and protein expression levels. We found that HDAC1 interacted with c-JUN at the activator protein (AP)-1-binding site located at -734 to -710 in the PROX1 promoter region to suppress PROX1 expression. In addition, c-JUN N-terminal kinase-mediated c-JUN phosphorylation was found to be crucial for silencing PROX1 expression. In conclusion, PROX1 expression can be silenced by the epigenetic mechanism involved in the complex formation of HDAC1 and c-JUN at the AP-1 site in the PROX1 promoter region in MDA-MB-231 human breast cancer cells. Therefore, this study revealed the epigenetic regulatory mechanism involved in the suppression of PROX1 expression in breast cancer cells.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 3","pages":"81-90"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139424547","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}
Folia BiologicaPub Date : 2023-01-01DOI: 10.14712/fb2023069030091
Soňa Argalácsová, Ľudmila Křížová, Martin Matějů, Dominika Svobodová, Michal Vočka
{"title":"Radiation-Induced Lymphopoenia and Treatment Outcome in Hereditary Breast Cancer Patients.","authors":"Soňa Argalácsová, Ľudmila Křížová, Martin Matějů, Dominika Svobodová, Michal Vočka","doi":"10.14712/fb2023069030091","DOIUrl":"10.14712/fb2023069030091","url":null,"abstract":"<p><p>Many breast cancer (BC) predisposition genes encode proteins involved in DNA damage repair (DDR). Identification of germline pathogenic va-riants (PV) in DDR genes raises the question whether their presence can influence the treatment outcomes and potential radiation-induced toxicity in their carriers treated by adjuvant radiotherapy, which has not yet been answered conclusively. We retrospectively examined records of 213 BC patients treated by adjuvant radiotherapy, including 39 (18.3 %) BRCA1/2 PV carriers, 25 carriers (11.7 %) of PV in other breast cancer-predisposing genes, and 149 (70 %) non-carriers. Our goal was to examine 5-year disease-free survival (5y DFS) rates among the study groups and determine the impact of radiotherapy-induced lymphopoenia (RIL) on this outcome. While we found no significant difference in 5y DFS between non-carriers and carriers of BRCA mutations (86.4 % vs 78.4 % P = 0.24) or between non-carriers and other studied mutations (86.4 % vs 93.3 %; P = 0.27), respectively, we observed that the entire group of PV carriers had a significantly lower proportion of patients without RIL (P = 0.04) than the non-carriers. In contrast, subsequent analyses indicated a non-significant trend toward an increased 5y DFS in PV carriers with RIL. Our single-centre study indicated that the presence of PV in BC patients has an insignificant impact on DFS but can reduce the risk of RIL associated with adjuvant radiotherapy. It remains unclear whether this may result from the paradoxical activation of anti-tumour immunity in PV carriers with higher lymphocyte consumption resulting from higher immune effectiveness.</p>","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"69 3","pages":"91-98"},"PeriodicalIF":0.6,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139424548","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}