Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells

To investigate the underlying mechanisms of decreased plasmalogens (Pls) levels in neurodegenerative diseases, here the effects of seafood-derived Pls on undifferentiated and differentiated human SH-SY5Y neuroblastoma cells exposed to amyloid-β1–42 was analyzed. Transcriptional profiles indicated th...

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Autores principales: Junli Feng, Gongshuai Song, Qing Shen, Xi Chen, Qingcheng Wang, Shunyuan Guo, Manman Zhang
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/532e638f68444a3c99fc0143f18f40db
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spelling oai:doaj.org-article:532e638f68444a3c99fc0143f18f40db2021-12-01T08:23:34ZProtect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells1663-436510.3389/fnagi.2021.773713https://doaj.org/article/532e638f68444a3c99fc0143f18f40db2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fnagi.2021.773713/fullhttps://doaj.org/toc/1663-4365To investigate the underlying mechanisms of decreased plasmalogens (Pls) levels in neurodegenerative diseases, here the effects of seafood-derived Pls on undifferentiated and differentiated human SH-SY5Y neuroblastoma cells exposed to amyloid-β1–42 was analyzed. Transcriptional profiles indicated that a total of 6,581 differentially expressed genes (DEGs) were significantly identified among different experimental groups, and KEGG analysis indicated that these DEGs were related to AD, endocytosis, synaptic vesicle cycle, autophagy and cellular apoptosis. After Pls treatment, the striking expression changes of ADORA2A, ATP6V1C2, CELF6, and SLC18A2 mRNA strongly suggest that Pls exerts a beneficial role in alleviating AD pathology partly by modulating the neurotransmitter release and synaptic transmission at the transcriptional level. Besides these, GPCRs are also broadly involved in Pls-signaling in neuronal cells. These results provide evidence for supporting the potential use of Pls as an effective therapeutic approach for AD.Junli FengGongshuai SongQing ShenXi ChenQingcheng WangShunyuan GuoManman ZhangFrontiers Media S.A.articleAlzheimer’s diseaseplasmalogensSH-SY5Y cellsgene expressiontranscriptional profilesNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571ENFrontiers in Aging Neuroscience, Vol 13 (2021)
institution DOAJ
collection DOAJ
language EN
topic Alzheimer’s disease
plasmalogens
SH-SY5Y cells
gene expression
transcriptional profiles
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
spellingShingle Alzheimer’s disease
plasmalogens
SH-SY5Y cells
gene expression
transcriptional profiles
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Junli Feng
Gongshuai Song
Qing Shen
Xi Chen
Qingcheng Wang
Shunyuan Guo
Manman Zhang
Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
description To investigate the underlying mechanisms of decreased plasmalogens (Pls) levels in neurodegenerative diseases, here the effects of seafood-derived Pls on undifferentiated and differentiated human SH-SY5Y neuroblastoma cells exposed to amyloid-β1–42 was analyzed. Transcriptional profiles indicated that a total of 6,581 differentially expressed genes (DEGs) were significantly identified among different experimental groups, and KEGG analysis indicated that these DEGs were related to AD, endocytosis, synaptic vesicle cycle, autophagy and cellular apoptosis. After Pls treatment, the striking expression changes of ADORA2A, ATP6V1C2, CELF6, and SLC18A2 mRNA strongly suggest that Pls exerts a beneficial role in alleviating AD pathology partly by modulating the neurotransmitter release and synaptic transmission at the transcriptional level. Besides these, GPCRs are also broadly involved in Pls-signaling in neuronal cells. These results provide evidence for supporting the potential use of Pls as an effective therapeutic approach for AD.
format article
author Junli Feng
Gongshuai Song
Qing Shen
Xi Chen
Qingcheng Wang
Shunyuan Guo
Manman Zhang
author_facet Junli Feng
Gongshuai Song
Qing Shen
Xi Chen
Qingcheng Wang
Shunyuan Guo
Manman Zhang
author_sort Junli Feng
title Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
title_short Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
title_full Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
title_fullStr Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
title_full_unstemmed Protect Effects of Seafood-Derived Plasmalogens Against Amyloid-Beta (1–42) Induced Toxicity via Modulating the Transcripts Related to Endocytosis, Autophagy, Apoptosis, Neurotransmitter Release and Synaptic Transmission in SH-SY5Y Cells
title_sort protect effects of seafood-derived plasmalogens against amyloid-beta (1–42) induced toxicity via modulating the transcripts related to endocytosis, autophagy, apoptosis, neurotransmitter release and synaptic transmission in sh-sy5y cells
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/532e638f68444a3c99fc0143f18f40db
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