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- W2995514280 endingPage "109503" @default.
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- W2995514280 abstract "Oxidation of membrane cholesterol is a hallmark of many pathological conditions, including cardiovascular diseases. Cholesterol could be oxidized in a result of free radical and enzymatic reactions. Here, we studied the effect of cholesterol oxidation by cholesterol oxidase (ChO) on responses to β-AR stimulation in isolated mouse atria. Acute exposure to ChO led to partial cholesterol oxidation without a significant change in atrial membrane cholesterol content. Pretreatment with ChO itself did not affect contractions and Ca2+ transient amplitude. However, cholesterol oxidation markedly suppressed β-AR-mediated increase in contractility and Ca2+ transient as well as NO levels. At the same time, ChO markedly facilitated β-AR-induced reactive oxygen species (ROS) production. Antioxidant and protein kinase C inhibitor prevented the depressant action of ChO on ISO-dependent contractility, Ca2+ transient and NO production. Similar effects had a selective β2-AR antagonist, which also suppressed the increase in ROS levels after ChO pretreatment. These results suggest that membrane cholesterol oxidation enhances β2-AR-dependent elevation of ROS production, leading to suppression of β-AR-mediated increase in contractility, Ca2+ transient and NO synthesis in mice atria. The oxidative cholesterol modification could contribute to disturbance in β-AR signaling in pathological conditions." @default.
- W2995514280 created "2019-12-26" @default.
- W2995514280 creator A5014271187 @default.
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- W2995514280 date "2020-03-01" @default.
- W2995514280 modified "2023-10-17" @default.
- W2995514280 title "Membrane cholesterol oxidation downregulates atrial β-adrenergic responses in ROS-dependent manner" @default.
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- W2995514280 doi "https://doi.org/10.1016/j.cellsig.2019.109503" @default.
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