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MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis
Aim: To explore the effects of miR-141-3p on intestinal epithelial cells in necrotizing enterocolitis and the underlying mechanism. Results: The expression of miR-141-3p was significantly downregulated in serum samples of patients with NEC and LPS-treated Caco-2 cells. The in vitro assays showed tha...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585103/ https://www.ncbi.nlm.nih.gov/pubmed/32702669 http://dx.doi.org/10.18632/aging.103608 |
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author | Li, Xiang Wang, Ying Wang, Yijiang He, Xingbo |
author_facet | Li, Xiang Wang, Ying Wang, Yijiang He, Xingbo |
author_sort | Li, Xiang |
collection | PubMed |
description | Aim: To explore the effects of miR-141-3p on intestinal epithelial cells in necrotizing enterocolitis and the underlying mechanism. Results: The expression of miR-141-3p was significantly downregulated in serum samples of patients with NEC and LPS-treated Caco-2 cells. The in vitro assays showed that miR-141-3p mimics inhibited expression of IL-6 and TNF-α and reduced PI positive rate of the LPS-treated Caco-2 cells. Next, receptor interacting protein kinase 1 (RIPK1) was identified as the downstream molecule of miR-141-3p, and RIPK1 overexpression aggravated LPS-induced Caco-2 cell injury, which was ameliorated by miR-141-3p mimics. Finally, we found miR-141-3p mimics inhibited upregulation of necroptosis-related molecules and interaction of RIPK1 and RIPK3 in LPS-treated Caco-2 cells. Conclusion: Our research indicated that miR-141-3p protected intestinal epithelial cells from LPS damage by suppressing RIPK1-mediated inflammation and necroptosis, providing an alternative perspective to explore the pathogenesis of NEC. Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-141-3p in serum samples of participants and lipopolysaccharide (LPS)-treated Caco-2 cells. Cell Counting Kit-8 (CCK-8) assay, Propidium Iodide (PI) staining and detection of inflammatory cytokines were performed to evaluate the role of miR-141-3p in LPS-treated Caco-2 cells. TargetScanHuman database and luciferase reporter gene assay were utilized to confirm the direct downstream molecule of miR-141-3p. Western blot analysis was used to explore the mechanism. |
format | Online Article Text |
id | pubmed-7585103 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-75851032020-11-03 MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis Li, Xiang Wang, Ying Wang, Yijiang He, Xingbo Aging (Albany NY) Research Paper Aim: To explore the effects of miR-141-3p on intestinal epithelial cells in necrotizing enterocolitis and the underlying mechanism. Results: The expression of miR-141-3p was significantly downregulated in serum samples of patients with NEC and LPS-treated Caco-2 cells. The in vitro assays showed that miR-141-3p mimics inhibited expression of IL-6 and TNF-α and reduced PI positive rate of the LPS-treated Caco-2 cells. Next, receptor interacting protein kinase 1 (RIPK1) was identified as the downstream molecule of miR-141-3p, and RIPK1 overexpression aggravated LPS-induced Caco-2 cell injury, which was ameliorated by miR-141-3p mimics. Finally, we found miR-141-3p mimics inhibited upregulation of necroptosis-related molecules and interaction of RIPK1 and RIPK3 in LPS-treated Caco-2 cells. Conclusion: Our research indicated that miR-141-3p protected intestinal epithelial cells from LPS damage by suppressing RIPK1-mediated inflammation and necroptosis, providing an alternative perspective to explore the pathogenesis of NEC. Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-141-3p in serum samples of participants and lipopolysaccharide (LPS)-treated Caco-2 cells. Cell Counting Kit-8 (CCK-8) assay, Propidium Iodide (PI) staining and detection of inflammatory cytokines were performed to evaluate the role of miR-141-3p in LPS-treated Caco-2 cells. TargetScanHuman database and luciferase reporter gene assay were utilized to confirm the direct downstream molecule of miR-141-3p. Western blot analysis was used to explore the mechanism. Impact Journals 2020-07-23 /pmc/articles/PMC7585103/ /pubmed/32702669 http://dx.doi.org/10.18632/aging.103608 Text en Copyright: © 2020 Li et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Li, Xiang Wang, Ying Wang, Yijiang He, Xingbo MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title | MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title_full | MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title_fullStr | MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title_full_unstemmed | MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title_short | MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
title_sort | mir-141-3p ameliorates ripk1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7585103/ https://www.ncbi.nlm.nih.gov/pubmed/32702669 http://dx.doi.org/10.18632/aging.103608 |
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