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Alpha-synuclein overexpression in SH-SY5Y human neuroblastoma cells leads to the accumulation of thioflavin S-positive aggregates and impairment of glycolysisстатья
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: 10 июня 2020 г.
- Авторы: Melnikova A., Pozdyshev D., Barinova K., Kudryavtseva S., Muronetz V.I.
- Журнал: Biochemistry (Moscow)
- Том: 85
- Номер: 5
- Год издания: 2020
- Издательство: Pleiades Publishing, Ltd
- Местоположение издательства: Road Town, United Kingdom
- Первая страница: 604
- Последняя страница: 613
- DOI: 10.1134/s0006297920050090
- Аннотация: Deterioration of energy metabolism in affected cells is an important feature of synucleinopathies, including Parkinson's disease. Here, we studied the association between α-synuclein accumulation and glycolysis using SH-SY5Y neuroblastoma cell lines stably expressing wild-type α-synuclein or its A53T mutant linked to the autosomal dominant form of the disease. Overexpression of both proteins led to the accumulation of thioflavin S-positive aggregates, more pronounced for α-synuclein A53T. It also caused changes in the cell energy metabolism manifested as a decrease in the lactate accumulation and glucose uptake. Impairments in glycolysis were also accompanied by a decrease in the activity of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). In vitro experiments with purified proteins indicated that GAPDH inactivation might be caused by its binding to the monomeric and oligomeric forms of α-synuclein. Therefore, a decrease in the GAPDH activity induced by its interaction with α-synuclein, might be one of the causes of glucose metabolism deterioration in synucleinopathies.
- Добавил в систему: Мельникова Александра Кирилловна