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  1. Artikel ; Online: Spike Protein Impairs Mitochondrial Function in Human Cardiomyocytes: Mechanisms Underlying Cardiac Injury in COVID-19.

    Huynh, Tin Van / Rethi, Lekha / Lee, Ting-Wei / Higa, Satoshi / Kao, Yu-Hsun / Chen, Yi-Jen

    Cells

    2023  Band 12, Heft 6

    Abstract: Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key ... ...

    Abstract Background: COVID-19 has a major impact on cardiovascular diseases and may lead to myocarditis or cardiac failure. The clove-like spike (S) protein of SARS-CoV-2 facilitates its transmission and pathogenesis. Cardiac mitochondria produce energy for key heart functions. We hypothesized that S1 would directly impair the functions of cardiomyocyte mitochondria, thus causing cardiac dysfunction.
    Methods: Through the Seahorse Mito Stress Test and real-time ATP rate assays, we explored the mitochondrial bioenergetics in human cardiomyocytes (AC16). The cells were treated without (control) or with S1 (1 nM) for 24, 48, and 72 h and we observed the mitochondrial morphology using transmission electron microscopy and confocal fluorescence microscopy. Western blotting, XRhod-1, and MitoSOX Red staining were performed to evaluate the expression of proteins related to energetic metabolism and relevant signaling cascades, mitochondrial Ca
    Results: The 24 h S1 treatment increased ATP production and mitochondrial respiration by increasing the expression of fatty-acid-transporting regulators and inducing more negative mitochondrial membrane potential (Δψm). The 72 h S1 treatment decreased mitochondrial respiration rates and Δψm, but increased levels of reactive oxygen species (ROS), mCa
    Conclusion: S1 might impair mitochondrial function in human cardiomyocytes by altering Δψm, mCa
    Mesh-Begriff(e) Rats ; Animals ; Humans ; Myocytes, Cardiac/metabolism ; Reactive Oxygen Species/metabolism ; Rats, Sprague-Dawley ; Angiotensin-Converting Enzyme 2/metabolism ; Spike Glycoprotein, Coronavirus/metabolism ; COVID-19/metabolism ; SARS-CoV-2/metabolism ; Mitochondria, Heart/metabolism ; Adenosine Triphosphate/metabolism
    Chemische Substanzen Reactive Oxygen Species ; spike protein, SARS-CoV-2 ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Spike Glycoprotein, Coronavirus ; Adenosine Triphosphate (8L70Q75FXE)
    Sprache Englisch
    Erscheinungsdatum 2023-03-11
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12060877
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Lithium downregulates phosphorylated acetyl‑CoA carboxylase 2 and attenuates mitochondrial fatty acid utilization and oxidative stress in cardiomyocytes.

    Chen, Pao-Huan / Lee, Ting-Wei / Liu, Shuen-Hsin / Huynh, Tin Van / Chung, Cheng-Chih / Yeh, Yung-Hsin / Kao, Yu-Hsun / Chen, Yi-Jen

    Experimental and therapeutic medicine

    2024  Band 27, Heft 4, Seite(n) 126

    Abstract: Acetyl-CoA carboxylase 2 plays a crucial role in regulating mitochondrial fatty acid oxidation in cardiomyocytes. Lithium, a monovalent cation known for its cardioprotective potential, has been investigated for its influence on mitochondrial ... ...

    Abstract Acetyl-CoA carboxylase 2 plays a crucial role in regulating mitochondrial fatty acid oxidation in cardiomyocytes. Lithium, a monovalent cation known for its cardioprotective potential, has been investigated for its influence on mitochondrial bioenergetics. The present study explored whether lithium modulated acetyl-CoA carboxylase 2 and mitochondrial fatty acid metabolism in cardiomyocytes and the potential therapeutic applications of lithium in alleviating metabolic stress. Mitochondrial bioenergetic function, fatty acid oxidation, reactive oxygen species production, membrane potential and the expression of proteins involved in fatty acid metabolism in H9c2 cardiomyocytes treated with LiCl for 48 h was measured by using a Seahorse extracellular flux analyzer, fluorescence microscopy and western blotting. Small interfering RNA against glucose transporter type 4 was transfected into H9c2 cardiomyocytes for 48 h to induce metabolic stress mimicking insulin resistance. The results revealed that LiCl at a concentration of 0.3 mM (but not at a concentration of 0.1 or 1.0 mM) upregulated the expression of phosphorylated (p-)glycogen synthase kinase-3 beta and downregulated the expression of p-acetyl-CoA carboxylase 2 but did not affect the expression of adenosine monophosphate-activated protein kinase or calcineurin. Cotreatment with TWS119 (8 µM) and LiCl (0.3 mM) downregulated p-acetyl-CoA carboxylase 2 expression to a similar extent as did treatment with TWS119 (8 µM) alone. Moreover, LiCl (0.3 mM) inhibited mitochondrial fatty acid oxidation, improved coupling efficiency and the cellular respiratory control ratio, hindered reactive oxygen species production and proton leakage and restored mitochondrial membrane potential in glucose transporter type 4 knockdown-H9c2 cardiomyocytes. These findings suggested that low therapeutic levels of lithium can downregulate p-acetyl-CoA carboxylase 2, thus reducing mitochondrial fatty acid oxidation and oxidative stress in cardiomyocytes.
    Sprache Englisch
    Erscheinungsdatum 2024-02-05
    Erscheinungsland Greece
    Dokumenttyp Journal Article
    ZDB-ID 2683844-8
    ISSN 1792-1015 ; 1792-0981
    ISSN (online) 1792-1015
    ISSN 1792-0981
    DOI 10.3892/etm.2024.12413
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: BANANA at WNUT-2020 Task 2: Identifying COVID-19 Information on Twitter by Combining Deep Learning and Transfer Learning Models

    Huynh, Tin Van / Nguyen, Luan Thanh / Luu, Son T.

    Abstract: The outbreak COVID-19 virus caused a significant impact on the health of people all over the world. Therefore, it is essential to have a piece of constant and accurate information about the disease with everyone. This paper describes our prediction ... ...

    Abstract The outbreak COVID-19 virus caused a significant impact on the health of people all over the world. Therefore, it is essential to have a piece of constant and accurate information about the disease with everyone. This paper describes our prediction system for WNUT-2020 Task 2: Identification of Informative COVID-19 English Tweets. The dataset for this task contains size 10,000 tweets in English labeled by humans. The ensemble model from our three transformer and deep learning models is used for the final prediction. The experimental result indicates that we have achieved F1 for the INFORMATIVE label on our systems at 88.81% on the test set.
    Schlagwörter covid19
    Verlag ArXiv
    Dokumenttyp Artikel
    Datenquelle COVID19

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  4. Artikel ; Online: Class I HDAC modulates angiotensin II-induced fibroblast migration and mitochondrial overactivity.

    Huynh, Tin Van / Rethi, Lekha / Chung, Cheng-Chih / Yeh, Yung-Hsin / Kao, Yu-Hsun / Chen, Yi-Jen

    European journal of clinical investigation

    2021  Band 52, Heft 4, Seite(n) e13712

    Abstract: Background: Inhibition of histone deacetylases (HDACs) attenuates cardiac fibrosis. In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its ... ...

    Abstract Background: Inhibition of histone deacetylases (HDACs) attenuates cardiac fibrosis. In this study, we evaluated whether the inhibition of class I HDACs can attenuate angiotensin II (ANG II)-induced fibrogenesis and mitochondrial malfunction through its effects on reactive oxygen species (ROS) and calcium dysregulation in human cardiac fibroblasts (CFs).
    Methods: Seahorse XF24 extracellular flux analyser, fluorescence staining, Western blotting, HDAC activity assays and Transwell migration assay were used to study mitochondrial respiration, adenosine triphosphate (ATP) production, mitochondrial calcium uptake and ROS, HDAC expression and activity and fibroblast activity in CFs without (control) or with ANG II (100 nM) and/or MS-275 (HDAC class 1 inhibitor, 10 μM) for 24 h.
    Results: ANG II increased HDAC activity without changing protein expression in CFs. Compared with controls, ANG II-treated CFs had greater migration activity, higher ATP production, maximal respiration and spare capacity with higher mitochondrial Ca
    Conclusions: Modulating mitochondrial function by regulation of HDAC may be a novel strategy for controlling CF activity.
    Mesh-Begriff(e) Angiotensin II/drug effects ; Angiotensin II/physiology ; Calcium/metabolism ; Cell Movement/physiology ; Cells, Cultured ; Fibroblasts/physiology ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/physiology ; Humans ; Mitochondria/drug effects ; Mitochondria/physiology ; Myocardium/cytology ; Reactive Oxygen Species/metabolism
    Chemische Substanzen Histone Deacetylase Inhibitors ; Reactive Oxygen Species ; Angiotensin II (11128-99-7) ; Histone Deacetylases (EC 3.5.1.98) ; Calcium (SY7Q814VUP)
    Sprache Englisch
    Erscheinungsdatum 2021-11-27
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 186196-7
    ISSN 1365-2362 ; 0014-2972 ; 0960-135X
    ISSN (online) 1365-2362
    ISSN 0014-2972 ; 0960-135X
    DOI 10.1111/eci.13712
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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