ArticleActa biochimica et biophysica Sinica2015
ACAT1 regulates the dynamics of free cholesterols in plasma membrane which leads to the APP-α-processing alteration.
Article in Acta biochimica et biophysica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Glycolysis-cholesterol metabolic axis in immuno-oncology microenvironment: emerging role in immune cells and immunosuppressive signaling.Cell & bioscience · 2023Review
- Acute ACAT1/SOAT1 Blockade Increases MAM Cholesterol and Strengthens ER-Mitochondria Connectivity.International journal of molecular sciences · 2023Article
- RAR-related orphan receptor alpha and the staggerer mice: a fine molecular story.Frontiers in endocrinology · 2023Review
- Cancer-cell stiffening via cholesterol depletion enhances adoptive T-cell immunotherapy.Nature biomedical engineering · 2021Article
- 27-Hydroxycholesterol Promotes the Transfer of Astrocyte-Derived Cholesterol to Neurons in Co-cultured SH-SY5Y Cells and C6 Cells.Frontiers in cell and developmental biology · 2020Article
- Cellular cholesterol homeostasis and Alzheimer's disease.Journal of lipid research · 2017Review
- Intracellular Cholesterol Trafficking and Impact in Neurodegeneration.Frontiers in molecular neuroscience · 2017Review
- The ACAT2 expression of human leukocytes is responsible for the excretion of lipoproteins containing cholesteryl/steryl esters.Acta biochimica et biophysica Sinica · 2016Article
- Low-level expression of human ACAT2 gene in monocytic cells is regulated by the C/EBP transcription factors.Acta biochimica et biophysica Sinica · 2016Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Acyl-CoA:cholesterol acyltransferase 1 (ACAT1) is a key enzyme exclusively using free cholesterols as the substrates in cell and is involved in the cellular cholesterol homeostasis. In this study, we used human neuroblastoma cell line SK-N-SH as a model and first observed that inhibiting ACAT1 can decrease the amyloid precursor protein (APP)-α-processing. Meanwhile, the transfection experiments using the small interfering RNA and expression plasmid of ACAT1 indicated that ACAT1 can dependently affect the APP-α-processing. Furthermore, inhibiting ACAT1 was found to increase the free cholesterols in plasma membrane (PM-FC), and the increased PM-FC caused by inhibiting ACAT1 can lead to the decrease of the APP-α-processing, indicating that ACAT1 regulates the dynamics of PM-FC, which leads to the alteration of the APP-α-processing. More importantly, further results showed that under the ACAT1 inhibition, the alterations of the PM-FC and the subsequent APP-α-processing are not dependent on the cellular total cholesterol level, confirming that ACAT1 regulates the dynamics of PM-FC. Finally, we revealed that even when the Niemann-Pick-Type C-dependent pathway is blocked, the ACAT1 inhibition still obviously results in the PM-FC increase, suggesting that the ACAT1-dependent pathway is responsible for the shuttling of PM-FC to the intracellular pool. Our data provide a novel insight that ACAT1 which enzymatically regulates the dynamics of PM-FC may play important roles in the human neuronal cells.
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