Knockdown of miR-27a reduces TGFβ-induced EMT and H2O2-induced oxidative stress through regulating mitochondrial autophagy
AJTR Copyright © 2023..
OBJECTIVES: The present research aimed at clarifying the role played by miR-27a in the context of intrauterine adhesion (IUA) by focusing on its impact on TGFβ1-induced epithelial-mesenchymal transition (EMT), migration, oxidative stress, and mitochondrial autophagy in endometrial stromal cells (ESCs).
METHODS: We employed the Cell Counting Kit CCK-8/WST-8 assay to assess ESC proliferation, flow cytometric analysis and an Annexin-V-FITCV-FITC Apoptosis Detection kit to determine cell apoptosis, and wound healing and transwell assays to evaluate cell migration. Besides, intracellular reactive oxygen species (ROS) levels measured by the Reactive Oxygen Species Assay Kit were analyzed by flow cytometry, and protein expression levels were quantified by Western blotting analysis.
RESULTS: Knockdown of miR-27a inhibited TGFβ1-induced EMT and H2O2-induced oxidative stress in ESCs. H2O2-induced miR-27a suppressed PINK1 expression, leading to inhibition of mitophagy. MiR-27a promoted TGFβ1 or H2O2-induced EMT through PINK1.
CONCLUSIONS: miR-27a plays a crucial role in endometrial fibrosis. It regulates TGFβ1-induced EMT, migration, oxidative stress, and apoptosis in ESCs. Additionally, miR-27a impacts mitophagy through PINK1 suppression upon H2O2 induction. Our findings highlight miR-27a as a potential therapeutic target for IUA treatment, shedding light on its multifaceted involvement in the mechanism of intrauterine adhesion fibrosis.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
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| Enthalten in: |
American journal of translational research - 15(2023), 10 vom: 08., Seite 6071-6082 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Zhao, Fangfang [VerfasserIn] |
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| Themen: |
EMT |
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| Anmerkungen: |
Date Revised 17.11.2023 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM364607610 |
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| 041 | |a eng | ||
| 100 | 1 | |a Zhao, Fangfang |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Knockdown of miR-27a reduces TGFβ-induced EMT and H2O2-induced oxidative stress through regulating mitochondrial autophagy |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
| 338 | |a Band |b nc |2 rdacarrier | ||
| 500 | |a Date Revised 17.11.2023 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a AJTR Copyright © 2023. | ||
| 520 | |a OBJECTIVES: The present research aimed at clarifying the role played by miR-27a in the context of intrauterine adhesion (IUA) by focusing on its impact on TGFβ1-induced epithelial-mesenchymal transition (EMT), migration, oxidative stress, and mitochondrial autophagy in endometrial stromal cells (ESCs) | ||
| 520 | |a METHODS: We employed the Cell Counting Kit CCK-8/WST-8 assay to assess ESC proliferation, flow cytometric analysis and an Annexin-V-FITCV-FITC Apoptosis Detection kit to determine cell apoptosis, and wound healing and transwell assays to evaluate cell migration. Besides, intracellular reactive oxygen species (ROS) levels measured by the Reactive Oxygen Species Assay Kit were analyzed by flow cytometry, and protein expression levels were quantified by Western blotting analysis | ||
| 520 | |a RESULTS: Knockdown of miR-27a inhibited TGFβ1-induced EMT and H2O2-induced oxidative stress in ESCs. H2O2-induced miR-27a suppressed PINK1 expression, leading to inhibition of mitophagy. MiR-27a promoted TGFβ1 or H2O2-induced EMT through PINK1 | ||
| 520 | |a CONCLUSIONS: miR-27a plays a crucial role in endometrial fibrosis. It regulates TGFβ1-induced EMT, migration, oxidative stress, and apoptosis in ESCs. Additionally, miR-27a impacts mitophagy through PINK1 suppression upon H2O2 induction. Our findings highlight miR-27a as a potential therapeutic target for IUA treatment, shedding light on its multifaceted involvement in the mechanism of intrauterine adhesion fibrosis | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a EMT | |
| 650 | 4 | |a MiR-27a | |
| 650 | 4 | |a PINK1 | |
| 650 | 4 | |a intrauterine adhesion | |
| 650 | 4 | |a oxidative stress | |
| 700 | 1 | |a Wei, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Dongping |e verfasserin |4 aut | |
| 700 | 1 | |a Guo, Yi |e verfasserin |4 aut | |
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