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Int. J. Mol. Sci. 2014, 15(11), 20876-20899; doi:10.3390/ijms151120876

Palmitic Acid-Induced Neuron Cell Cycle G2/M Arrest and Endoplasmic Reticular Stress through Protein Palmitoylation in SH-SY5Y Human Neuroblastoma Cells

1
Department of School of Nutrition and Health Sciences, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan
2
Department of Nutrition and Health Sciences, Kainan University, No.1 Kainan Road, Luzhu Shiang, Taoyuan 338, Taiwan
*
Author to whom correspondence should be addressed.
Received: 29 August 2014 / Revised: 27 October 2014 / Accepted: 30 October 2014 / Published: 13 November 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Obesity-related neurodegenerative diseases are associated with elevated saturated fatty acids (SFAs) in the brain. An increase in SFAs, especially palmitic acid (PA), triggers neuron cell apoptosis, causing cognitive function to deteriorate. In the present study, we focused on the specific mechanism by which PA triggers SH-SY5Y neuron cell apoptosis. We found that PA induces significant neuron cell cycle arrest in the G2/M phase in SH-SY5Y cells. Our data further showed that G2/M arrest is involved in elevation of endoplasmic reticular (ER) stress according to an increase in p-eukaryotic translation inhibition factor 2α, an ER stress marker. Chronic exposure to PA also accelerates beta-amyloid accumulation, a pathological characteristic of Alzheimer’s disease. Interestingly, SFA-induced ER stress, G2/M arrest and cell apoptosis were reversed by treatment with 2-bromopalmitate, a protein palmitoylation inhibitor. These findings suggest that protein palmitoylation plays a crucial role in SFA-induced neuron cell cycle G2/M arrest, ER stress and apoptosis; this provides a novel strategy for preventing SFA-induced neuron cell dysfunction. View Full-Text
Keywords: obesity; neurodegenerative disease; saturated fatty acids; palmitic acid; cell cycle arrest; endoplasmic reticular stress; neurons; protein palmitoylation obesity; neurodegenerative disease; saturated fatty acids; palmitic acid; cell cycle arrest; endoplasmic reticular stress; neurons; protein palmitoylation
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Hsiao, Y.-H.; Lin, C.-I.; Liao, H.; Chen, Y.-H.; Lin, S.-H. Palmitic Acid-Induced Neuron Cell Cycle G2/M Arrest and Endoplasmic Reticular Stress through Protein Palmitoylation in SH-SY5Y Human Neuroblastoma Cells. Int. J. Mol. Sci. 2014, 15, 20876-20899.

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