Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells

Elevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of long-ch...

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Autores principales:	C. J. Urso, Heping Zhou
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	fatty acid uptake palmitic acid cell cycle CD36 lipotoxicity saturated fatty acids Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/984855d46b2d46458a869795ba50e6e6
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spelling	oai:doaj.org-article:984855d46b2d46458a869795ba50e6e62021-11-25T16:51:56ZRole of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells10.3390/biom111115672218-273Xhttps://doaj.org/article/984855d46b2d46458a869795ba50e6e62021-10-01T00:00:00Zhttps://www.mdpi.com/2218-273X/11/11/1567https://doaj.org/toc/2218-273XElevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of long-chain free fatty acids (FFAs) into cells, serves a fatty acid (FA) sensing function in areas including taste buds and the proximal gut, and acts as a scavenger receptor that binds to many ligands, including FAs, collagen, oxidized low-density lipoproteins, and anionic phospholipids. However, the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells remains unclear. In this study, we examined FA uptake in BSA- and PA-treated N2a cells and investigated the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells. Our data showed that PA treatment promoted FA uptake in N2a cells, and that treatment with sulfo-N-succinimidyl oleate (SSO), a CD36 inhibitor, significantly decreased FA uptake in BSA- and PA-treated N2a cells, and ameliorated PA-induced decrease of cell viability, decrease of diploid cells, and increase of tetraploid cells. We also found that CD36 knockdown significantly decreased FA uptake in both BSA- and PA-treated cells as compared to their corresponding wild-type controls, and dramatically attenuated PA-induced cell cycle defects in N2a cells. Our data suggest that CD36 may play a critical role in FA uptake and PA lipotoxicity in N2a cells. CD36 may therefore represent a regulatory target against pathologies caused by excess FAs.C. J. UrsoHeping ZhouMDPI AGarticlefatty acid uptakepalmitic acidcell cycleCD36lipotoxicitysaturated fatty acidsMicrobiologyQR1-502ENBiomolecules, Vol 11, Iss 1567, p 1567 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	fatty acid uptake palmitic acid cell cycle CD36 lipotoxicity saturated fatty acids Microbiology QR1-502
spellingShingle	fatty acid uptake palmitic acid cell cycle CD36 lipotoxicity saturated fatty acids Microbiology QR1-502 C. J. Urso Heping Zhou Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
description	Elevated level of palmitic acid (PA), a long-chain saturated fatty acid (SFA), is lipotoxic to many different types of cells including Neuro-2a (N2a) neuroblastoma cells. CD36 is a multifunctional membrane glycoprotein that acts as a fatty acid translocase (FAT) facilitating the transport of long-chain free fatty acids (FFAs) into cells, serves a fatty acid (FA) sensing function in areas including taste buds and the proximal gut, and acts as a scavenger receptor that binds to many ligands, including FAs, collagen, oxidized low-density lipoproteins, and anionic phospholipids. However, the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells remains unclear. In this study, we examined FA uptake in BSA- and PA-treated N2a cells and investigated the involvement of CD36 in FA uptake and PA lipotoxicity in N2a cells. Our data showed that PA treatment promoted FA uptake in N2a cells, and that treatment with sulfo-N-succinimidyl oleate (SSO), a CD36 inhibitor, significantly decreased FA uptake in BSA- and PA-treated N2a cells, and ameliorated PA-induced decrease of cell viability, decrease of diploid cells, and increase of tetraploid cells. We also found that CD36 knockdown significantly decreased FA uptake in both BSA- and PA-treated cells as compared to their corresponding wild-type controls, and dramatically attenuated PA-induced cell cycle defects in N2a cells. Our data suggest that CD36 may play a critical role in FA uptake and PA lipotoxicity in N2a cells. CD36 may therefore represent a regulatory target against pathologies caused by excess FAs.
format	article
author	C. J. Urso Heping Zhou
author_facet	C. J. Urso Heping Zhou
author_sort	C. J. Urso
title	Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
title_short	Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
title_full	Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
title_fullStr	Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
title_full_unstemmed	Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells
title_sort	role of cd36 in palmitic acid lipotoxicity in neuro-2a neuroblastoma cells
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/984855d46b2d46458a869795ba50e6e6
work_keys_str_mv	AT cjurso roleofcd36inpalmiticacidlipotoxicityinneuro2aneuroblastomacells AT hepingzhou roleofcd36inpalmiticacidlipotoxicityinneuro2aneuroblastomacells
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Role of CD36 in Palmitic Acid Lipotoxicity in Neuro-2a Neuroblastoma Cells

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