The Effects of PP2A Disruption on ER-Mitochondria Contact and Mitochondrial Functions in Neuronal-like Cells
4
Issued Date
2023-04-01
Resource Type
eISSN
22279059
Scopus ID
2-s2.0-85153757578
Journal Title
Biomedicines
Volume
11
Issue
4
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomedicines Vol.11 No.4 (2023)
Suggested Citation
Chaiwijit P., Uppakara K., Asavapanumas N., Saengsawang W. The Effects of PP2A Disruption on ER-Mitochondria Contact and Mitochondrial Functions in Neuronal-like Cells. Biomedicines Vol.11 No.4 (2023). doi:10.3390/biomedicines11041011 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/82077
Title
The Effects of PP2A Disruption on ER-Mitochondria Contact and Mitochondrial Functions in Neuronal-like Cells
Author(s)
Other Contributor(s)
Abstract
Mitochondria-associated membranes (MAMs) regulate several cellular processes, including calcium homeostasis and mitochondrial function, and dynamics. While MAMs are upregulated in Alzheimer’s disease (AD), the mechanisms underlying this increase remain unknown. A possible mechanism may include dysregulation of protein phosphatase 2A (PP2A), which is reduced in the AD brain. Furthermore, PP2A has been previously reported to modulate MAM formation in hepatocytes. However, it is unknown whether PP2A and MAMs are linked in neuronal cells. Here, to test the correlation between PP2A and MAMs, we inhibited the activity of PP2A to mimic its low levels in AD brains and observed MAM formation, function, and dynamics. MAMs were significantly increased after PP2A inhibition, which correlated with elevated mitochondrial Ca2+ influx and disrupted mitochondrial membrane potential and mitochondrial fission. This study highlights the essential role PP2A plays in regulating MAM formation and mitochondrial function and dynamics for the first time in neuronal-like cells.