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Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis

BACKGROUND: Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. METHODS: The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC ce...

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Autores principales: Rui, Xueqi, Wu, Xinning, Rong, Zheyi, Wang, Zipeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9832782/
https://www.ncbi.nlm.nih.gov/pubmed/36627571
http://dx.doi.org/10.1186/s12872-023-03038-9
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author Rui, Xueqi
Wu, Xinning
Rong, Zheyi
Wang, Zipeng
author_facet Rui, Xueqi
Wu, Xinning
Rong, Zheyi
Wang, Zipeng
author_sort Rui, Xueqi
collection PubMed
description BACKGROUND: Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. METHODS: The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. RESULTS: The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. CONCLUSION: Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis.
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spelling pubmed-98327822023-01-12 Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis Rui, Xueqi Wu, Xinning Rong, Zheyi Wang, Zipeng BMC Cardiovasc Disord Research BACKGROUND: Atherosclerosis (AS) is a common frequently-occurring disease in the clinic and a serious threat to human health. This research aimed to explore the value between GASL1 and AS. METHODS: The expression and values of GASL1 in AS patients were revealed by qRT-PCR and ROC curve. The HUVEC cells were induced by ox-LDL to construct in-vitro models. Cell viability was detected by MTT assay, and apoptosis was detected by flow cytometry. The inflammatory situation was reflected by the ELISA assay. Double luciferase reporter gene assay verified the regulatory relationship between GASL1 and miR-106a, miR-106a and LKB1. RESULTS: The levels of GASL1 was lower in AS group than those in control group. The value of GASL1 in predicting AS patients was also tested by the ROC curve. After HUVEC cells were induced by ox-LDL, the levels of GASL1 and LKB1 decreased significantly, while the level of miR-106a increased significantly. Upregulation of LKB1 reversed the effect of upregulation of GASL1 on viability, apoptosis, and inflammation of HUVEC cells induced by ox-LDL. CONCLUSION: Overexpression of GASL1 might suppress ox-LDL-induced HUVEC cell viability, apoptosis, and inflammation by regulating miR-106a/LKB1 axis. BioMed Central 2023-01-10 /pmc/articles/PMC9832782/ /pubmed/36627571 http://dx.doi.org/10.1186/s12872-023-03038-9 Text en © The Author(s) 2023 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
Rui, Xueqi
Wu, Xinning
Rong, Zheyi
Wang, Zipeng
Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title_full Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title_fullStr Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title_full_unstemmed Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title_short Upgulation of lncRNA GASL1 inhibits atherosclerosis by regulating miR-106a/LKB1 axis
title_sort upgulation of lncrna gasl1 inhibits atherosclerosis by regulating mir-106a/lkb1 axis
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9832782/
https://www.ncbi.nlm.nih.gov/pubmed/36627571
http://dx.doi.org/10.1186/s12872-023-03038-9
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