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miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach
OBJECTIVE: The endothelial cells overexpress the adhesion molecules in the leukocyte diapedesis pathway, developing vessel subendothelial molecular events. In this study, miR-194 and miR-27a were predicted and investigated on the expression of adhesion molecules in HUVEC cells. The SELE, SELP, and J...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8830077/ https://www.ncbi.nlm.nih.gov/pubmed/35144666 http://dx.doi.org/10.1186/s13104-022-05920-9 |
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author | Shaikhnia, Farhad Ghasempour, Ghasem Mohammadi, Asghar Shabani, Mohammad Najafi, Mohammad |
author_facet | Shaikhnia, Farhad Ghasempour, Ghasem Mohammadi, Asghar Shabani, Mohammad Najafi, Mohammad |
author_sort | Shaikhnia, Farhad |
collection | PubMed |
description | OBJECTIVE: The endothelial cells overexpress the adhesion molecules in the leukocyte diapedesis pathway, developing vessel subendothelial molecular events. In this study, miR-194 and miR-27a were predicted and investigated on the expression of adhesion molecules in HUVEC cells. The SELE, SELP, and JAM-B adhesion molecules involved in the leukocyte tethering were predicted on the GO-enriched gene network. Following transfection of PEI-miRNA particles into HUVEC cells, the SELE, SELP, and JAM-B gene expression levels were evaluated by real-time qPCR. Furthermore, the monocyte-endothelial adhesion was performed using adhesion assay kit. RESULTS: In agreement with the prediction results, the cellular data showed that miR-27a and miR-194 decrease significantly the SELP and JAM-B expression levels in HUVECs (P < 0.05). Moreover, both the miRNAs suppressed the monocyte adhesion to endothelial cells. Since the miR-27a inhibited significantly the monocyte-endothelial adhesion (P = 0.0001) through the suppression of SELP and JAM-B thus it might relate to the leukocyte diapedesis pathway. |
format | Online Article Text |
id | pubmed-8830077 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-88300772022-02-11 miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach Shaikhnia, Farhad Ghasempour, Ghasem Mohammadi, Asghar Shabani, Mohammad Najafi, Mohammad BMC Res Notes Research Note OBJECTIVE: The endothelial cells overexpress the adhesion molecules in the leukocyte diapedesis pathway, developing vessel subendothelial molecular events. In this study, miR-194 and miR-27a were predicted and investigated on the expression of adhesion molecules in HUVEC cells. The SELE, SELP, and JAM-B adhesion molecules involved in the leukocyte tethering were predicted on the GO-enriched gene network. Following transfection of PEI-miRNA particles into HUVEC cells, the SELE, SELP, and JAM-B gene expression levels were evaluated by real-time qPCR. Furthermore, the monocyte-endothelial adhesion was performed using adhesion assay kit. RESULTS: In agreement with the prediction results, the cellular data showed that miR-27a and miR-194 decrease significantly the SELP and JAM-B expression levels in HUVECs (P < 0.05). Moreover, both the miRNAs suppressed the monocyte adhesion to endothelial cells. Since the miR-27a inhibited significantly the monocyte-endothelial adhesion (P = 0.0001) through the suppression of SELP and JAM-B thus it might relate to the leukocyte diapedesis pathway. BioMed Central 2022-02-10 /pmc/articles/PMC8830077/ /pubmed/35144666 http://dx.doi.org/10.1186/s13104-022-05920-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Note Shaikhnia, Farhad Ghasempour, Ghasem Mohammadi, Asghar Shabani, Mohammad Najafi, Mohammad miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title | miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title_full | miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title_fullStr | miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title_full_unstemmed | miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title_short | miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
title_sort | mir-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach |
topic | Research Note |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8830077/ https://www.ncbi.nlm.nih.gov/pubmed/35144666 http://dx.doi.org/10.1186/s13104-022-05920-9 |
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