Paralemmin-3 augments lipopolysaccharide-induced acute lung injury with M1 macrophage polarization via the notch signaling pathway
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved..
BACKGROUND: Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action.
METHODS: An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization.
RESULTS: PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling.
CONCLUSION: PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:320 |
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| Enthalten in: |
Respiratory physiology & neurobiology - 320(2024) vom: 31. Jan., Seite 104203 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Chen, Xuxin [VerfasserIn] |
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| Links: |
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| Themen: |
Acute respiratory distress syndrome |
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| Anmerkungen: |
Date Completed 15.01.2024 Date Revised 15.01.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.resp.2023.104203 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM365944009 |
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| 245 | 1 | 0 | |a Paralemmin-3 augments lipopolysaccharide-induced acute lung injury with M1 macrophage polarization via the notch signaling pathway |
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| 500 | |a Date Completed 15.01.2024 | ||
| 500 | |a Date Revised 15.01.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved. | ||
| 520 | |a BACKGROUND: Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action | ||
| 520 | |a METHODS: An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization | ||
| 520 | |a RESULTS: PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling | ||
| 520 | |a CONCLUSION: PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Acute respiratory distress syndrome | |
| 650 | 4 | |a Alveolar macrophage | |
| 650 | 4 | |a Notch signaling | |
| 650 | 4 | |a Paralemmin-3 | |
| 650 | 4 | |a Polarization | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a PALM3 protein, rat |2 NLM | |
| 700 | 1 | |a Wang, Fan |e verfasserin |4 aut | |
| 700 | 1 | |a Tang, Jian |e verfasserin |4 aut | |
| 700 | 1 | |a Meng, Jiguang |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Zhihai |e verfasserin |4 aut | |
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