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MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA

The present study aimed to determine the expression of vascular endothelial growth factor A (VEGFA) and microRNA (miRNA/miR)-27a in hippocampal tissues, and serum from a depression model of rats. In addition, the present study aimed to understand the mechanism of regulation of miR-27a in depression....

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Autores principales: Cui, Jian, Gong, Cunqi, Cao, Baorui, Li, Longfei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5921192/
https://www.ncbi.nlm.nih.gov/pubmed/29731825
http://dx.doi.org/10.3892/etm.2018.5942
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author Cui, Jian
Gong, Cunqi
Cao, Baorui
Li, Longfei
author_facet Cui, Jian
Gong, Cunqi
Cao, Baorui
Li, Longfei
author_sort Cui, Jian
collection PubMed
description The present study aimed to determine the expression of vascular endothelial growth factor A (VEGFA) and microRNA (miRNA/miR)-27a in hippocampal tissues, and serum from a depression model of rats. In addition, the present study aimed to understand the mechanism of regulation of miR-27a in depression. A total of 40 male rats were selected, and divided into the control and depression model groups. The rats in the model group were subjected to 14 types of stimulations to model depression. By determining the body weight, syrup consumption rate and open field test score, the extent of depression in the rats was evaluated. Quantitative-polymerase chain reaction was used to determine the expression of VEGFA mRNA and miR-27a in hippocampal tissues, and serum. ELISA was used to measure the content of VEGFA protein in serum, while western blotting was employed to determine the expression of VEGFA protein in hippocampal tissues. A dual luciferase assay was carried out to identify the interactions between VEGFA mRNA and miR-27a. The rats in the depression model group showed depression symptoms and the depression model was successfully constructed. Rats with depression had lower VEGFA mRNA and protein expression in the hippocampus, and peripheral blood compared with the control group. Rats in the depression model group had reduced levels of miR-27a in the hippocampus and peripheral blood, which may be associated with the levels of VEGFA. miR-27a was able to bind with the 3′-untranslated region of VEGFA mRNA to regulate its expression. The present study demonstrated that miR-27a expression in hippocampal tissues and blood from rats with depression is upregulated, while the expression of VEGFA mRNA and protein is downregulated. miR-27a may participate in the pathological process of depression in rats by regulating VEGFA.
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spelling pubmed-59211922018-05-04 MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA Cui, Jian Gong, Cunqi Cao, Baorui Li, Longfei Exp Ther Med Articles The present study aimed to determine the expression of vascular endothelial growth factor A (VEGFA) and microRNA (miRNA/miR)-27a in hippocampal tissues, and serum from a depression model of rats. In addition, the present study aimed to understand the mechanism of regulation of miR-27a in depression. A total of 40 male rats were selected, and divided into the control and depression model groups. The rats in the model group were subjected to 14 types of stimulations to model depression. By determining the body weight, syrup consumption rate and open field test score, the extent of depression in the rats was evaluated. Quantitative-polymerase chain reaction was used to determine the expression of VEGFA mRNA and miR-27a in hippocampal tissues, and serum. ELISA was used to measure the content of VEGFA protein in serum, while western blotting was employed to determine the expression of VEGFA protein in hippocampal tissues. A dual luciferase assay was carried out to identify the interactions between VEGFA mRNA and miR-27a. The rats in the depression model group showed depression symptoms and the depression model was successfully constructed. Rats with depression had lower VEGFA mRNA and protein expression in the hippocampus, and peripheral blood compared with the control group. Rats in the depression model group had reduced levels of miR-27a in the hippocampus and peripheral blood, which may be associated with the levels of VEGFA. miR-27a was able to bind with the 3′-untranslated region of VEGFA mRNA to regulate its expression. The present study demonstrated that miR-27a expression in hippocampal tissues and blood from rats with depression is upregulated, while the expression of VEGFA mRNA and protein is downregulated. miR-27a may participate in the pathological process of depression in rats by regulating VEGFA. D.A. Spandidos 2018-05 2018-03-09 /pmc/articles/PMC5921192/ /pubmed/29731825 http://dx.doi.org/10.3892/etm.2018.5942 Text en Copyright: © Cui et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Cui, Jian
Gong, Cunqi
Cao, Baorui
Li, Longfei
MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title_full MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title_fullStr MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title_full_unstemmed MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title_short MicroRNA-27a participates in the pathological process of depression in rats by regulating VEGFA
title_sort microrna-27a participates in the pathological process of depression in rats by regulating vegfa
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5921192/
https://www.ncbi.nlm.nih.gov/pubmed/29731825
http://dx.doi.org/10.3892/etm.2018.5942
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