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  1. AU="Králiková, Lucie"
  2. AU="Burton, Thomas D"

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  1. Article ; Online: Tick-borne encephalitis virus modulates sphingolipid and phospholipid metabolism in infected human neuronal cells.

    Šimečková, Pavlína / Slavík, Josef / Fořtová, Andrea / Huvarová, Ivana / Králiková, Lucie / Stefanik, Michal / Svoboda, Pavel / Ruzek, Daniel / Machala, Miroslav

    Microbes and infection

    2024  , Page(s) 105303

    Abstract: The life cycle of enveloped viruses is closely linked to host-cell lipids. However, changes in lipid metabolism during infections with the tick-borne encephalitis virus (TBEV) have not been described. TBEV is a medically important orthoflavivirus, which ... ...

    Abstract The life cycle of enveloped viruses is closely linked to host-cell lipids. However, changes in lipid metabolism during infections with the tick-borne encephalitis virus (TBEV) have not been described. TBEV is a medically important orthoflavivirus, which is endemic to many parts of Europe and Asia. In the present study, we performed targeted lipidomics with HPLC-MS/MS to evaluate changes in phospholipid and sphingolipid concentrations in TBEV-infected human neuronal SK-N-SH cells. TBEV infections significantly increased phosphatidylcholine, phosphatidylinositol, and phosphatidylserine levels within 48 h post-infection (hpi). Sphingolipids were slightly increased in dihydroceramides within 24 hpi. Later, at 48 hpi, the contents of sphinganine, dihydroceramides, ceramides, glucosylceramides, and ganglioside GD3 were elevated. On the other hand, sphingosine-1-phosphate content was slightly reduced in TBEV-infected cells. Changes in sphingolipid concentrations were accompanied by suppressed expression of a majority of the genes linked to sphingolipid and glycosphingolipid metabolism. Furthermore, we found that a pharmacological inhibitor of sphingolipid synthesis, fenretinide (4-HPR), inhibited TBEV infections in SK-N-SH cells. Taken together, our results suggested that both structural and signaling functions of lipids could be affected during TBEV infections. These changes might be connected to virus propagation and/or host-cell defense.
    Language English
    Publishing date 2024-01-24
    Publishing country France
    Document type Journal Article
    ZDB-ID 1465093-9
    ISSN 1769-714X ; 1286-4579
    ISSN (online) 1769-714X
    ISSN 1286-4579
    DOI 10.1016/j.micinf.2024.105303
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Screening of Cellular Stress Responses Induced by Ambient Aerosol Ultrafine Particle Fraction PM0.5 in A549 Cells.

    Šimečková, Pavlína / Marvanová, Soňa / Kulich, Pavel / Králiková, Lucie / Neča, Jiří / Procházková, Jiřina / Machala, Miroslav

    International journal of molecular sciences

    2019  Volume 20, Issue 24

    Abstract: Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various ... ...

    Abstract Effects of airborne particles on the expression status of markers of cellular toxic stress and on the release of eicosanoids, linked with inflammation and oxidative damage, remain poorly characterized. Therefore, we proposed a set of various methodological approaches in order to address complexity of PM0.5-induced toxicity. For this purpose, we used a well-characterized model of A549 pulmonary epithelial cells exposed to a non-cytotoxic concentration of ambient aerosol particle fraction PM0.5 for 24 h. Electron microscopy confirmed accumulation of PM0.5 within A549 cells, yet, autophagy was not induced. Expression profiles of various cellular stress response genes that have been previously shown to be involved in early stress responses, namely unfolded protein response, DNA damage response, and in aryl hydrocarbon receptor (AhR) and p53 signaling, were analyzed. This analysis revealed induction of GREM1, EGR1, CYP1A1, CDK1A, PUMA, NOXA and GDF15 and suppression of SOX9 in response to PM0.5 exposure. Analysis of eicosanoids showed no oxidative damage and only a weak anti-inflammatory response. In conclusion, this study helps to identify novel gene markers, GREM1, EGR1, GDF15 and SOX9, that may represent a valuable tool for routine testing of PM0.5-induced in vitro toxicity in lung epithelial cells.
    MeSH term(s) A549 Cells ; Aerosols ; Air Pollutants/toxicity ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Expression Regulation/drug effects ; Humans ; Lung/metabolism ; Lung/pathology ; Particulate Matter/toxicity ; Signal Transduction/drug effects
    Chemical Substances Aerosols ; Air Pollutants ; Particulate Matter
    Language English
    Publishing date 2019-12-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20246310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Colon Cancer and Perturbations of the Sphingolipid Metabolism.

    Machala, Miroslav / Procházková, Jiřina / Hofmanová, Jiřina / Králiková, Lucie / Slavík, Josef / Tylichová, Zuzana / Ovesná, Petra / Kozubík, Alois / Vondráček, Jan

    International journal of molecular sciences

    2019  Volume 20, Issue 23

    Abstract: The development and progression of colorectal cancer (CRC), a major cause of cancer-related death in the western world, is accompanied with alterations of sphingolipid (SL) composition in colon tumors. A number of enzymes involved in the SL metabolism ... ...

    Abstract The development and progression of colorectal cancer (CRC), a major cause of cancer-related death in the western world, is accompanied with alterations of sphingolipid (SL) composition in colon tumors. A number of enzymes involved in the SL metabolism have been found to be deregulated in human colon tumors, in experimental rodent studies, and in human colon cancer cells in vitro. Therefore, the enzymatic pathways that modulate SL levels have received a significant attention, due to their possible contribution to CRC development, or as potential therapeutic targets. Many of these enzymes are associated with an increased sphingosine-1-phosphate/ceramide ratio, which is in turn linked with increased colon cancer cell survival, proliferation and cancer progression. Nevertheless, more attention should also be paid to the more complex SLs, including specific glycosphingolipids, such as lactosylceramides, which can be also deregulated during CRC development. In this review, we focus on the potential roles of individual SLs/SL metabolism enzymes in colon cancer, as well as on the pros and cons of employing the current in vitro models of colon cancer cells for lipidomic studies investigating the SL metabolism in CRC.
    MeSH term(s) Acid Ceramidase/genetics ; Acid Ceramidase/metabolism ; Alkaline Ceramidase/genetics ; Alkaline Ceramidase/metabolism ; Animals ; Ceramides/metabolism ; Colonic Neoplasms/enzymology ; Colonic Neoplasms/genetics ; Colonic Neoplasms/pathology ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Humans ; Lactosylceramides/metabolism ; Lipid Metabolism/genetics ; Lysophospholipids/metabolism ; Neutral Ceramidase/genetics ; Neutral Ceramidase/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Sphingolipids/metabolism ; Sphingosine/analogs & derivatives ; Sphingosine/metabolism ; Sphingosine N-Acyltransferase/genetics ; Sphingosine N-Acyltransferase/metabolism ; Tumor Cells, Cultured
    Chemical Substances Ceramides ; Lactosylceramides ; Lysophospholipids ; Sphingolipids ; ceramide 1-phosphate ; sphingosine 1-phosphate (26993-30-6) ; Sphingosine N-Acyltransferase (EC 2.3.1.24) ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; sphingosine kinase (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; ACER2 protein, human (EC 3.5.1.23) ; ASAH1 protein, human (EC 3.5.1.23) ; ASAH2 protein, human (EC 3.5.1.23) ; Acid Ceramidase (EC 3.5.1.23) ; Alkaline Ceramidase (EC 3.5.1.23) ; Neutral Ceramidase (EC 3.5.1.23) ; Sphingosine (NGZ37HRE42)
    Language English
    Publishing date 2019-11-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20236051
    Database MEDical Literature Analysis and Retrieval System OnLINE

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