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miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response
miR-150 was found to target the 3′-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significa...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8186154/ https://www.ncbi.nlm.nih.gov/pubmed/34092081 http://dx.doi.org/10.1177/17534259211018800 |
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author | Yao, Yanfen Wang, Hong Xi, Xueqin Sun, Wei Ge, Junke Li, Pibao |
author_facet | Yao, Yanfen Wang, Hong Xi, Xueqin Sun, Wei Ge, Junke Li, Pibao |
author_sort | Yao, Yanfen |
collection | PubMed |
description | miR-150 was found to target the 3′-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases. |
format | Online Article Text |
id | pubmed-8186154 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-81861542021-06-21 miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response Yao, Yanfen Wang, Hong Xi, Xueqin Sun, Wei Ge, Junke Li, Pibao Innate Immun Original Articles miR-150 was found to target the 3′-untranslated regions of AKT3, and the AKT pathway was affected by SR protein kinase 1 (SRPK1). However, the expression and significance of miR-150, AKT3 and SRPK1 in acute lung injury (ALI) were not clear. Here, we found that the expression of miR-150 was significantly reduced, while the expression of AKT3 and SRPK1 were markedly increased in LPS-treated A549, THP-1 and RAW 264.7 cells. miR-150 significantly decreased levels of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α, reduced the expression of AKT3, but had no impact on SRPK1 expression compared with the control group in LPS-treated A549, THP-1 and RAW 264.7 cells. AKT3 silencing only reduced the production of pro-inflammatory cytokines and showed no effect on miR-150 and SRPK1 expression. Finally, we observed that miR-150 mimics and/or silencing of SRPK1 decreased the expression of AKT3 mRNA. Besides, over-expression of miR-150 or silencing of SRPK1 also reduced the expression of AKT3 protein, which exhibited the lowest level in the miR-150 mimics plus si-SRPK1 group. However, si-SRPK1 had no effect on miR-150 level. In conclusion, miR-150 and SRPK1 separately and cooperatively participate into inflammatory responses in ALI through regulating AKT3 pathway. Increased miR-150 and silenced SRPK1 may be a novel potential factor for preventing and treating more inflammatory lung diseases. SAGE Publications 2021-06-06 2021-05 /pmc/articles/PMC8186154/ /pubmed/34092081 http://dx.doi.org/10.1177/17534259211018800 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Articles Yao, Yanfen Wang, Hong Xi, Xueqin Sun, Wei Ge, Junke Li, Pibao miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title | miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title_full | miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title_fullStr | miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title_full_unstemmed | miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title_short | miR-150 and SRPK1 regulate AKT3 expression to participate in LPS-induced inflammatory response |
title_sort | mir-150 and srpk1 regulate akt3 expression to participate in lps-induced inflammatory response |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8186154/ https://www.ncbi.nlm.nih.gov/pubmed/34092081 http://dx.doi.org/10.1177/17534259211018800 |
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