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Membrane cholesterol oxidation downregulates atrial $\upbeta$-adrenergic responses in ROS-dependent mannerстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 4 марта 2020 г.
- Авторы: Ursan Roman, Odnoshivkina Ulia G., Petrov Alexey M.
- Журнал: Cellular Signalling
- Том: 67
- Год издания: 2020
- Издательство: Elsevier BV
- Местоположение издательства: Netherlands
- Первая страница: 109503
- DOI: 10.1016/j.cellsig.2019.109503
- Аннотация: 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. © 2019 Elsevier Inc.
- Добавил в систему: Урсан Роман Викторович