Role and mechanism of miR-871-3p/Megf8 in regulating formaldehyde-induced cardiomyocyte inflammation and congenital heart disease
Copyright © 2023 Elsevier B.V. All rights reserved..
OBJECTIVE AND DESIGN: We aimed to investigate the molecular mechanism underlying formaldehyde (FA)-induced congenital heart disease (CHD) using in vitro and in vivo models.
MATERIALS AND SUBJECTS: Neonatal rat heart tissues and H9C2 cells were used for in vitro studies, while FA-exposed new-born rats were used for in vivo studies.
TREATMENT: H9C2 cells were exposed to FA concentrations of 0, 50, 100 and 150 μM/mL for 24 h.
METHODS: Whole transcriptome gene sequencing identified differentially expressed miRNAs in neonatal rat heart tissues, while Real-time quantitative PCR (RT-qPCR) assessed miR-871-3p and Megf8 expression. RNA pull-down and dual-luciferase reporter assays determined miR-871-3p and Megf8 relationships. Inflammatory cytokine expression was assessed by western blotting. A FA-induced CHD model was used to validate miR-871-3p regulatory effects in vivo.
RESULTS: We identified 89 differentially expressed miRNAs, with 28 up-regulated and 61 down-regulated (fold change ≥ 2.0, P < 0.05). Inflammation (interleukin) and signalling pathways were found to control FA-induced cardiac dysplasia. miR-871-3p was upregulated in FA-exposed heart tissues, modulated inflammation, and directly targeted Megf8. In vivo experiments showed miR-871-3p knockdown inhibited FA-induced inflammation and CHD.
CONCLUSION: We demonstrated miR-871-3p's role in FA-induced CHD by targeting Megf8, providing potential targets for CHD intervention and improved diagnosis and treatment strategies.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:126 |
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Enthalten in: |
International immunopharmacology - 126(2024) vom: 05. Jan., Seite 111297 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Yuan, Xiaoli [VerfasserIn] |
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Links: |
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Themen: |
1HG84L3525 |
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Anmerkungen: |
Date Completed 20.02.2024 Date Revised 03.04.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.intimp.2023.111297 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM365307130 |
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500 | |a published: Print-Electronic | ||
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520 | |a Copyright © 2023 Elsevier B.V. All rights reserved. | ||
520 | |a OBJECTIVE AND DESIGN: We aimed to investigate the molecular mechanism underlying formaldehyde (FA)-induced congenital heart disease (CHD) using in vitro and in vivo models | ||
520 | |a MATERIALS AND SUBJECTS: Neonatal rat heart tissues and H9C2 cells were used for in vitro studies, while FA-exposed new-born rats were used for in vivo studies | ||
520 | |a TREATMENT: H9C2 cells were exposed to FA concentrations of 0, 50, 100 and 150 μM/mL for 24 h | ||
520 | |a METHODS: Whole transcriptome gene sequencing identified differentially expressed miRNAs in neonatal rat heart tissues, while Real-time quantitative PCR (RT-qPCR) assessed miR-871-3p and Megf8 expression. RNA pull-down and dual-luciferase reporter assays determined miR-871-3p and Megf8 relationships. Inflammatory cytokine expression was assessed by western blotting. A FA-induced CHD model was used to validate miR-871-3p regulatory effects in vivo | ||
520 | |a RESULTS: We identified 89 differentially expressed miRNAs, with 28 up-regulated and 61 down-regulated (fold change ≥ 2.0, P < 0.05). Inflammation (interleukin) and signalling pathways were found to control FA-induced cardiac dysplasia. miR-871-3p was upregulated in FA-exposed heart tissues, modulated inflammation, and directly targeted Megf8. In vivo experiments showed miR-871-3p knockdown inhibited FA-induced inflammation and CHD | ||
520 | |a CONCLUSION: We demonstrated miR-871-3p's role in FA-induced CHD by targeting Megf8, providing potential targets for CHD intervention and improved diagnosis and treatment strategies | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Cardiomyocyte | |
650 | 4 | |a Congenital heart disease | |
650 | 4 | |a Formaldehyde | |
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700 | 1 | |a Sun, Pin |e verfasserin |4 aut | |
700 | 1 | |a Song, Xiaoxia |e verfasserin |4 aut | |
700 | 1 | |a Ma, Jianmin |e verfasserin |4 aut | |
700 | 1 | |a Sun, Ruicong |e verfasserin |4 aut | |
700 | 1 | |a Yu, Tao |e verfasserin |4 aut | |
700 | 1 | |a Jiang, Zhirong |e verfasserin |4 aut | |
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