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miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells

BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder which mainly affects the elderly population of various societies. The main hallmark of this disease is the loss of dopaminergic (DA) neurons. So far, numerous studies have implied the role of microRNAs in fine‐tuning cellular...

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Autores principales: Shanesazzade, Zahra, Peymani, Maryam, Ghaedi, Kamran, Nasr Esfahani, Mohammad Hossein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305653/
https://www.ncbi.nlm.nih.gov/pubmed/30221494
http://dx.doi.org/10.1002/mgg3.469
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author Shanesazzade, Zahra
Peymani, Maryam
Ghaedi, Kamran
Nasr Esfahani, Mohammad Hossein
author_facet Shanesazzade, Zahra
Peymani, Maryam
Ghaedi, Kamran
Nasr Esfahani, Mohammad Hossein
author_sort Shanesazzade, Zahra
collection PubMed
description BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder which mainly affects the elderly population of various societies. The main hallmark of this disease is the loss of dopaminergic (DA) neurons. So far, numerous studies have implied the role of microRNAs in fine‐tuning cellular processes including apoptosis. Studies have also shown that miR‐34a is mainly involved in age‐related disorders including Alzheimer's disease, and its expression is usually higher in the brain sample patients. Furthermore, the key role of miR‐34a in the expression of BCL‐2, and thus, in vitro and in vivo apoptosis has been revealed. miR‐34a/BCL‐2 axis is therefore of critical importance in inducing or inhibiting apoptosis. METHODS: In this study, human SH‐SY5Y cells were treated with MPP+ and the expression of miR‐34a and BCL2 was assessed. RESULTS: Our results also showed that treating human SH‐SY5Y neuronal cells using MPP(+) to induce oxidative stress and apoptosis led to the upregulation of miR‐34a, as compared to the nontreated control group. Moreover, evaluating the expression level of BCL‐2 in these cells indicated a contradictory pattern, as compared with miR‐34a. It was also revealed that the expression of BCL‐2 was significantly decreased in MPP(+)‐treated cells, thereby confirming previous studies regarding a new concept. In this study, we show that miR‐34a/BCL‐2 axis is directly correlated with oxidative stress and apoptosis in SH‐SY5Y cells as a model of DA neurons. CONCLUSION: miR‐34a and its target gene, BCL‐2, play a possible role in the induction of apoptosis in DA neurons, and therefore, they have a potential role in the pathogenesis of PD. Consequently, the therapeutic potential of miR‐34a could be considered in order to inhibit the progression of PD.
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spelling pubmed-63056532019-01-02 miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells Shanesazzade, Zahra Peymani, Maryam Ghaedi, Kamran Nasr Esfahani, Mohammad Hossein Mol Genet Genomic Med Original Articles BACKGROUND: Parkinson's disease (PD) is a neurodegenerative disorder which mainly affects the elderly population of various societies. The main hallmark of this disease is the loss of dopaminergic (DA) neurons. So far, numerous studies have implied the role of microRNAs in fine‐tuning cellular processes including apoptosis. Studies have also shown that miR‐34a is mainly involved in age‐related disorders including Alzheimer's disease, and its expression is usually higher in the brain sample patients. Furthermore, the key role of miR‐34a in the expression of BCL‐2, and thus, in vitro and in vivo apoptosis has been revealed. miR‐34a/BCL‐2 axis is therefore of critical importance in inducing or inhibiting apoptosis. METHODS: In this study, human SH‐SY5Y cells were treated with MPP+ and the expression of miR‐34a and BCL2 was assessed. RESULTS: Our results also showed that treating human SH‐SY5Y neuronal cells using MPP(+) to induce oxidative stress and apoptosis led to the upregulation of miR‐34a, as compared to the nontreated control group. Moreover, evaluating the expression level of BCL‐2 in these cells indicated a contradictory pattern, as compared with miR‐34a. It was also revealed that the expression of BCL‐2 was significantly decreased in MPP(+)‐treated cells, thereby confirming previous studies regarding a new concept. In this study, we show that miR‐34a/BCL‐2 axis is directly correlated with oxidative stress and apoptosis in SH‐SY5Y cells as a model of DA neurons. CONCLUSION: miR‐34a and its target gene, BCL‐2, play a possible role in the induction of apoptosis in DA neurons, and therefore, they have a potential role in the pathogenesis of PD. Consequently, the therapeutic potential of miR‐34a could be considered in order to inhibit the progression of PD. John Wiley and Sons Inc. 2018-09-16 /pmc/articles/PMC6305653/ /pubmed/30221494 http://dx.doi.org/10.1002/mgg3.469 Text en © 2018 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Shanesazzade, Zahra
Peymani, Maryam
Ghaedi, Kamran
Nasr Esfahani, Mohammad Hossein
miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title_full miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title_fullStr miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title_full_unstemmed miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title_short miR‐34a/BCL‐2 signaling axis contributes to apoptosis in MPP(+)‐induced SH‐SY5Y cells
title_sort mir‐34a/bcl‐2 signaling axis contributes to apoptosis in mpp(+)‐induced sh‐sy5y cells
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305653/
https://www.ncbi.nlm.nih.gov/pubmed/30221494
http://dx.doi.org/10.1002/mgg3.469
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