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  1. Article: Cardiac Exosomes in Ischemic Heart Disease- A Narrative Review.

    Røsand, Øystein / Høydal, Morten Andre

    Diagnostics (Basel, Switzerland)

    2021  Volume 11, Issue 2

    Abstract: Ischemic heart disease (IHD) is the primary cause of death globally. IHD is associated with the disruption of blood supply to the heart muscles, which often results in myocardial infarction (MI) that further may progress to heart failure (HF). Exosomes ... ...

    Abstract Ischemic heart disease (IHD) is the primary cause of death globally. IHD is associated with the disruption of blood supply to the heart muscles, which often results in myocardial infarction (MI) that further may progress to heart failure (HF). Exosomes are a subgroup of extracellular vesicles that can be secreted by virtually all types of cells, including cardiomyocytes, cardiac fibroblasts, endothelial cells, and stem and progenitor cells. Exosomes represent an important means of cell-cell communication through the transport of proteins, coding and non-coding RNA, and other bioactive molecules. Several studies show that exosomes play an important role in the progression of IHD, including endothelial dysfunction, the development of arterial atherosclerosis, ischemic reperfusion injury, and HF development. Recently, promising data have been shown that designates exosomes as carriers of cardioprotective molecules that enhance the survival of recipient cells undergoing ischemia. In this review, we summarize the functional involvement of exosomes regarding IHD. We also highlight the cardioprotective effects of native and bioengineered exosomes to IHD, as well as the possibility of using exosomes as natural biomarkers of cardiovascular diseases. Lastly, we discuss the opportunities and challenges that need to be addressed before exosomes can be used in clinical applications.
    Language English
    Publishing date 2021-02-09
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2662336-5
    ISSN 2075-4418
    ISSN 2075-4418
    DOI 10.3390/diagnostics11020269
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: GSK3β Inhibition Is the Molecular Pivot That Underlies the Mir-210-Induced Attenuation of Intrinsic Apoptosis Cascade during Hypoxia.

    Marwarha, Gurdeep / Røsand, Øystein / Slagsvold, Katrine Hordnes / Høydal, Morten Andre

    International journal of molecular sciences

    2022  Volume 23, Issue 16

    Abstract: Apoptotic cell death is a deleterious consequence of hypoxia-induced cellular stress. The ... ...

    Abstract Apoptotic cell death is a deleterious consequence of hypoxia-induced cellular stress. The master
    MeSH term(s) Apoptosis/genetics ; Glycogen Synthase Kinase 3 beta/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Hypoxia/genetics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Signal Transduction
    Chemical Substances MIRN210 microRNA, human ; MicroRNAs ; GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
    Language English
    Publishing date 2022-08-19
    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/ijms23169375
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Overexpression of Neuron-Derived Orphan Receptor 1 (NOR-1) Rescues Cardiomyocytes from Cell Death and Improves Viability after Doxorubicin Induced Stress.

    Berg, Per-Christian / Hansson, Åse Mari Larsen / Røsand, Øystein / Marwarha, Gurdeep / Høydal, Morten Andre

    Biomedicines

    2021  Volume 9, Issue 9

    Abstract: Following myocardial infarction, reperfusion injury (RI) is commonly observed due to the excessive formation of, e.g., reactive oxygen species (ROS). Doxorubicin (DOX), a widely used anti-cancer drug, is also known to cause cardiotoxicity due to ... ...

    Abstract Following myocardial infarction, reperfusion injury (RI) is commonly observed due to the excessive formation of, e.g., reactive oxygen species (ROS). Doxorubicin (DOX), a widely used anti-cancer drug, is also known to cause cardiotoxicity due to excessive ROS production. Exercise training has been shown to protect the heart against both RI- and DOX-induced cardiotoxicity, but the exact mechanism is still unknown. Neuron-derived orphan receptor 1 (NOR-1) is an important exercise-responsive protein in the skeletal muscle which has also been reported to facilitate cellular survival during hypoxia. Therefore, we hypothesized that NOR-1 could protect cardiomyocytes (CMs) against cellular stress induced by DOX. We also hypothesized that NOR-1 is involved in preparing the CMs against a stress situation during nonstimulated conditions by increasing cell viability. To determine the protective effect of NOR-1 in CMs stressed with DOX challenge, we overexpressed NOR-1 in AC16 human CMs treated with 5 µM DOX for 12 h or the respective vehicle control, followed by performing Lactate dehydrogenase (LDH) activity, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and caspase-3 activity assays to measure cell death, cell viability, and apoptosis, respectively. In addition, Western blotting analysis was performed to determine the expression of key proteins involved in cardioprotection. We demonstrated that NOR-1 overexpression decreased cell death (
    Language English
    Publishing date 2021-09-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines9091233
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: miR-210 Regulates Apoptotic Cell Death during Cellular Hypoxia and Reoxygenation in a Diametrically Opposite Manner.

    Marwarha, Gurdeep / Røsand, Øystein / Scrimgeour, Nathan / Slagsvold, Katrine Hordnes / Høydal, Morten Andre

    Biomedicines

    2021  Volume 10, Issue 1

    Abstract: Apoptotic cell death of cardiomyocytes is a characteristic hallmark of ischemia-reperfusion (I/R) injury. The ... ...

    Abstract Apoptotic cell death of cardiomyocytes is a characteristic hallmark of ischemia-reperfusion (I/R) injury. The master
    Language English
    Publishing date 2021-12-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10010042
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Generation of a Mouse Model Lacking the Non-Homologous End-Joining Factor Mri/Cyren.

    Castañeda-Zegarra, Sergio / Huse, Camilla / Røsand, Øystein / Sarno, Antonio / Xing, Mengtan / Gago-Fuentes, Raquel / Zhang, Qindong / Alirezaylavasani, Amin / Werner, Julia / Ji, Ping / Liabakk, Nina-Beate / Wang, Wei / Bjørås, Magnar / Oksenych, Valentyn

    Biomolecules

    2019  Volume 9, Issue 12

    Abstract: Classical non-homologous end joining (NHEJ) is a molecular pathway that detects, processes, and ligates DNA double-strand breaks (DSBs) throughout the cell cycle. Mutations in several NHEJ genes result in neurological abnormalities and immunodeficiency ... ...

    Abstract Classical non-homologous end joining (NHEJ) is a molecular pathway that detects, processes, and ligates DNA double-strand breaks (DSBs) throughout the cell cycle. Mutations in several NHEJ genes result in neurological abnormalities and immunodeficiency both in humans and mice. The NHEJ pathway is required for V(D)J recombination in developing B and T lymphocytes, and for class switch recombination in mature B cells. The Ku heterodimer formed by Ku70 and Ku80 recognizes DSBs and facilitates the recruitment of accessory factors (e.g., DNA-PKcs, Artemis, Paxx and Mri/Cyren) and downstream core factor subunits X-ray repair cross-complementing group 4 (XRCC4), XRCC4-like factor (XLF), and DNA ligase 4 (Lig4). Accessory factors might be dispensable for the process, depending on the genetic background and DNA lesion type. To determine the physiological role of Mri in DNA repair and development, we introduced a frame-shift mutation in the Mri gene in mice. We then analyzed the development of
    MeSH term(s) Animals ; B-Lymphocytes/immunology ; Cell Line ; Cell Proliferation ; DNA End-Joining Repair/genetics ; DNA Repair Enzymes/genetics ; DNA-Binding Proteins/genetics ; Humans ; Immunoglobulin Class Switching ; Immunoglobulin G/immunology ; Mice, Knockout ; Models, Animal ; Stem Cells ; T-Lymphocytes/immunology
    Chemical Substances DNA-Binding Proteins ; Immunoglobulin G ; DNA Repair Enzymes (EC 6.5.1.-)
    Language English
    Publishing date 2019-11-28
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom9120798
    Database MEDical Literature Analysis and Retrieval System OnLINE

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