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The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes
INTRODUCTION: MicroRNAs (miRNAs or miRs) are non-coding RNAs. Studies have shown that miRNAs are expressed aberrantly in stroke. The miR1 enhances ischemic damage, and a previous study has demonstrated that reduction of miR1 level has a neuroprotective effect on the Middle Cerebral Artery Occlusion...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Iranian Neuroscience Society
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019842/ https://www.ncbi.nlm.nih.gov/pubmed/33850618 http://dx.doi.org/10.32598/bcn.11.6.324.3 |
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author | Talebi, Anis Rahnema, Mehdi Bigdeli, Mohammad Reza |
author_facet | Talebi, Anis Rahnema, Mehdi Bigdeli, Mohammad Reza |
author_sort | Talebi, Anis |
collection | PubMed |
description | INTRODUCTION: MicroRNAs (miRNAs or miRs) are non-coding RNAs. Studies have shown that miRNAs are expressed aberrantly in stroke. The miR1 enhances ischemic damage, and a previous study has demonstrated that reduction of miR1 level has a neuroprotective effect on the Middle Cerebral Artery Occlusion (MCAO). Since apoptosis is one of the important processes in neural protection, the possible effect of miR1 on this pathway has been tested in this study. Post-ischemic administration of miR1 antagomir reduces infarct volume via bcl-w and bad expression. METHODS: Rats were divided into four experimental groups: sham, control, positive control, and antagomir treatment group. One hour after MCAO surgery, the rats were received intravenously (Tail vein) 0.1 mL Normal Saline (NS), 0.1 mL rapamycin, and 300 pmol/g miR1 antagomir (soluble in 0.1 mL normal saline) in control, positive control, and treatment group, respectively. Twenty-four hours after reperfusion infarct volume was measured. The expression of miR1, bcl-w, and bad were analyzed using real-time PCR in sham, control, and treated groups. RESULTS: Our results indicate that administration of miR1 antagomir reduces infarct volume significantly, it also decreases miR1 and bad expression while increases bcl-w expression. CONCLUSION: Understanding the precise neuroprotective mechanism of miR1 antagomir can make it a proper treatment and an innovative approach for stroke therapy. |
format | Online Article Text |
id | pubmed-8019842 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Iranian Neuroscience Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-80198422021-04-12 The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes Talebi, Anis Rahnema, Mehdi Bigdeli, Mohammad Reza Basic Clin Neurosci Research Paper INTRODUCTION: MicroRNAs (miRNAs or miRs) are non-coding RNAs. Studies have shown that miRNAs are expressed aberrantly in stroke. The miR1 enhances ischemic damage, and a previous study has demonstrated that reduction of miR1 level has a neuroprotective effect on the Middle Cerebral Artery Occlusion (MCAO). Since apoptosis is one of the important processes in neural protection, the possible effect of miR1 on this pathway has been tested in this study. Post-ischemic administration of miR1 antagomir reduces infarct volume via bcl-w and bad expression. METHODS: Rats were divided into four experimental groups: sham, control, positive control, and antagomir treatment group. One hour after MCAO surgery, the rats were received intravenously (Tail vein) 0.1 mL Normal Saline (NS), 0.1 mL rapamycin, and 300 pmol/g miR1 antagomir (soluble in 0.1 mL normal saline) in control, positive control, and treatment group, respectively. Twenty-four hours after reperfusion infarct volume was measured. The expression of miR1, bcl-w, and bad were analyzed using real-time PCR in sham, control, and treated groups. RESULTS: Our results indicate that administration of miR1 antagomir reduces infarct volume significantly, it also decreases miR1 and bad expression while increases bcl-w expression. CONCLUSION: Understanding the precise neuroprotective mechanism of miR1 antagomir can make it a proper treatment and an innovative approach for stroke therapy. Iranian Neuroscience Society 2020 2020-11-01 /pmc/articles/PMC8019842/ /pubmed/33850618 http://dx.doi.org/10.32598/bcn.11.6.324.3 Text en Copyright© 2020 Iranian Neuroscience Society This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
spellingShingle | Research Paper Talebi, Anis Rahnema, Mehdi Bigdeli, Mohammad Reza The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title | The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title_full | The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title_fullStr | The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title_full_unstemmed | The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title_short | The Positive Effect of MiR1 Antagomir on Ischemic Neurological Disorders Via Changing the Expression of Bcl-w and Bad Genes |
title_sort | positive effect of mir1 antagomir on ischemic neurological disorders via changing the expression of bcl-w and bad genes |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8019842/ https://www.ncbi.nlm.nih.gov/pubmed/33850618 http://dx.doi.org/10.32598/bcn.11.6.324.3 |
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