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miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells
BACKGROUND: We investigated whether microRNA-155-5p is involved in the differentiation of bone marrow mesenchymal stem cells (BMSCs) into alveolar type II epithelial (AT II) cells by regulating the Wnt signaling pathway, thus participating in the development of acute respiratory distress syndrome (A...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6049011/ https://www.ncbi.nlm.nih.gov/pubmed/29936517 http://dx.doi.org/10.12659/MSM.910316 |
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author | Jiang, Jing Song, Zhifang Zhang, Lanyue |
author_facet | Jiang, Jing Song, Zhifang Zhang, Lanyue |
author_sort | Jiang, Jing |
collection | PubMed |
description | BACKGROUND: We investigated whether microRNA-155-5p is involved in the differentiation of bone marrow mesenchymal stem cells (BMSCs) into alveolar type II epithelial (AT II) cells by regulating the Wnt signaling pathway, thus participating in the development of acute respiratory distress syndrome (ARDS). MATERIAL/METHODS: Serum levels of microRNA-155-5p in 50 ARDS patients and 50 normal controls were detected by quantitative real-time PCR (qRT-PCR). Marrow mesenchymal stem cells (MCSs) were isolated from mouse bone marrow and identified by flow cytometry. Subsequently, the effect of microRNA-155-5p on differentiation of BMSCs into AT II cells was evaluated by detecting the expression levels of AT II-specific genes. The expression levels of proteins in the Wnt signaling pathway after overexpression or knockdown of microRNA-155-5p were detected by Western blot. RESULTS: Serum levels of microRNA-155-5p in ARDS patients were significantly higher than that in normal controls. Expression levels of AT II-specific genes were enhanced after downregulating microRNA-155-5p in BMSCs. MicroRNA-155-5p overexpression showed the opposite result. Furthermore, microRNA-155-5p inhibited the expression levels of proteins in the Wnt signaling pathway. CONCLUSIONS: MicroRNA-155-5p can attenuate the differentiation of BMSCs into AT II cells by inhibiting the Wnt signaling pathway, thus promoting the progression of ARDS. |
format | Online Article Text |
id | pubmed-6049011 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60490112018-07-18 miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells Jiang, Jing Song, Zhifang Zhang, Lanyue Med Sci Monit Animal Study BACKGROUND: We investigated whether microRNA-155-5p is involved in the differentiation of bone marrow mesenchymal stem cells (BMSCs) into alveolar type II epithelial (AT II) cells by regulating the Wnt signaling pathway, thus participating in the development of acute respiratory distress syndrome (ARDS). MATERIAL/METHODS: Serum levels of microRNA-155-5p in 50 ARDS patients and 50 normal controls were detected by quantitative real-time PCR (qRT-PCR). Marrow mesenchymal stem cells (MCSs) were isolated from mouse bone marrow and identified by flow cytometry. Subsequently, the effect of microRNA-155-5p on differentiation of BMSCs into AT II cells was evaluated by detecting the expression levels of AT II-specific genes. The expression levels of proteins in the Wnt signaling pathway after overexpression or knockdown of microRNA-155-5p were detected by Western blot. RESULTS: Serum levels of microRNA-155-5p in ARDS patients were significantly higher than that in normal controls. Expression levels of AT II-specific genes were enhanced after downregulating microRNA-155-5p in BMSCs. MicroRNA-155-5p overexpression showed the opposite result. Furthermore, microRNA-155-5p inhibited the expression levels of proteins in the Wnt signaling pathway. CONCLUSIONS: MicroRNA-155-5p can attenuate the differentiation of BMSCs into AT II cells by inhibiting the Wnt signaling pathway, thus promoting the progression of ARDS. International Scientific Literature, Inc. 2018-06-24 /pmc/articles/PMC6049011/ /pubmed/29936517 http://dx.doi.org/10.12659/MSM.910316 Text en © Med Sci Monit, 2018 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Animal Study Jiang, Jing Song, Zhifang Zhang, Lanyue miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title | miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title_full | miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title_fullStr | miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title_full_unstemmed | miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title_short | miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells |
title_sort | mir-155-5p promotes progression of acute respiratory distress syndrome by inhibiting differentiation of bone marrow mesenchymal stem cells to alveolar type ii epithelial cells |
topic | Animal Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6049011/ https://www.ncbi.nlm.nih.gov/pubmed/29936517 http://dx.doi.org/10.12659/MSM.910316 |
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