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Tytuł:
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DJ-1 alleviates anoxia and hypoglycemia injury in cardiac microvascular via AKT and GSH.
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Autorzy:
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Wang J; Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, 110001, China; Department of Nursing, The First Affiliated Hospital of China Medical University, Liaoning, 110001, China.
Zhang H; Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, 110001, China.
Du A; Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, 110001, China.
Li Y; Department of Cardiology, The First Affiliated Hospital of China Medical University, Liaoning, 110001, China. Electronic address: .
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Źródło:
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Molecular and cellular probes [Mol Cell Probes] 2020 Oct; Vol. 53, pp. 101600. Date of Electronic Publication: 2020 May 20.
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: London ; New York : Academic Press, c1987-
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MeSH Terms:
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Hypoglycemia/*pathology
Hypoxia/*pathology
Microvessels/*pathology
Protein Deglycase DJ-1/*genetics
Protein Deglycase DJ-1/*metabolism
Cell Line ; Cell Survival ; Down-Regulation ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Glutathione/metabolism ; Humans ; Hypoglycemia/genetics ; Hypoglycemia/metabolism ; Hypoxia/genetics ; Hypoxia/metabolism ; Microvessels/cytology ; Microvessels/metabolism ; Models, Biological ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species ; Reperfusion Injury
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Contributed Indexing:
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Keywords: A/H injury; AKT; Cardiac microvascular endothelial cells; DJ-1; GSH
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Substance Nomenclature:
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0 (Reactive Oxygen Species)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 3.1.2.- (PARK7 protein, human)
EC 3.1.2.- (Protein Deglycase DJ-1)
GAN16C9B8O (Glutathione)
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Entry Date(s):
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Date Created: 20200524 Date Completed: 20210714 Latest Revision: 20210714
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Update Code:
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20240105
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DOI:
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10.1016/j.mcp.2020.101600
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PMID:
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32445781
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Cardiac microvascular damage, which is often caused by anoxia and hypoglycemia, is associated with the development of cardiac injury. DJ-1 encodes a peptidase C56 protein family related protein, is has been linked to oxidative stress in various cells such as neurons, COPD epithelial cells, and macrophages. However, the effect of DJ-1 towards oxidative stress caused by anoxia and hypoglycemia of cardiac microvascular endothelial cells (CMEC) remains unclear. In this study, we investigated the role and underlying molecular mechanism of DJ-1 in CMEC with anoxia/hypoglycemic (A/H) injury. We found that the mRNA and the protein expression of DJ-1 in CMEC with A/H injury were significantly downregulated. DJ-1 overexpression by pcDNA.3.1-DJ-1 transfection elevated cell viability while it inhibited LDH leakage, cell apoptosis, caspase-3 activity, ROS level, and MDA contents, while knockdown of DJ-1 has the opposite results. In addition, tube formation was increased in DJ-1 overexpression, while it was decreased in DJ-1 knockdown CMEC with A/H injury. In addition, our results indicated that DJ-1 can regulate glutathione (GSH) levels by modulating AKT activity in CMEC with A/H injury. The downregulation of AKT and GSH may remove the protective role of DJ-1 against A/H injury in CMEC. Taken together, this study showed that DJ-1 upregulation protected CMEC against A/H injury via the AKT/GSH signaling pathway.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)