Knockdown of angiopoietin-like 4 suppresses sepsis-induced acute lung injury by blocking the NF-κB pathway activation and hindering macrophage M1 polarization and pyroptosis
Copyright © 2023 Elsevier Ltd. All rights reserved..
OBJECTIVE: Sepsis-induced acute lung injury (ALI) is a life-threatening disease. Macrophage pyroptosis has been reported to exert function in ALI. We aimed to investigate the mechanisms of ANGPTL4-mediated cell pyroptosis in sepsis-induced ALI, thus providing new insights into the pathogenesis and prevention and treatment measures of sepsis-induced ALI.
METHODS: In vivo animal models and in vitro cell models were established by cecal ligation and puncture (CLP) method and lipopolysaccharide-induced macrophages RAW264.7. ANGPTL4 was silenced in CLP mice or macrophages, followed by the determination of ANGPTL4 expression in bronchoalveolar lavage fluid (BALF) or macrophages. Lung histopathology was observed by H&E staining, with pathological injury scores evaluated and lung wet and dry weight ratio recorded. M1/M2 macrophage marker levels (iNOS/CD86/Arg1), inflammatory factor (TNF-α/IL-6/IL-1β/iNOS) expression in BALF, cell death and pyroptosis, NLRP3 inflammasome, cell pyroptosis-related protein (NLRP3/Cleaved-caspase-1/caspase-1/GSDMD-N) levels, NF-κB pathway activation were assessed by RT-qPCR/ELISA/flow cytometry/Western blot, respectively.
RESULTS: ANGPTL4 was highly expressed in mice with sepsis-induced ALI, and ANGPTL4 silencing ameliorated sepsis-induced ALI in mice. In vivo, ANGPTL4 silencing repressed M1 macrophage polarization and macrophage pyroptosis in mice with sepsis-induced ALI. In vitro, ANGPTL4 knockout impeded LPS-induced activation and pyroptosis of M1 macrophages and hindered LPS-induced activation of the NF-κB pathway in macrophages.
CONCLUSION: Knockdown of ANGPTL4 blocks the NF-κB pathway activation, hinders macrophage M1 polarization and pyroptosis, thereby suppressing sepsis-induced ALI.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 2023 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:94 |
|---|---|
| Enthalten in: |
Toxicology in vitro : an international journal published in association with BIBRA - 94(2023) vom: 16. Feb., Seite 105709 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Sun, Baisheng [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 15.12.2023 Date Revised 15.12.2023 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.tiv.2023.105709 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM36313798X |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM36313798X | ||
| 003 | DE-627 | ||
| 005 | 20231227131730.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.tiv.2023.105709 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1226.xml |
| 035 | |a (DE-627)NLM36313798X | ||
| 035 | |a (NLM)37820748 | ||
| 035 | |a (PII)S0887-2333(23)00158-3 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Sun, Baisheng |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Knockdown of angiopoietin-like 4 suppresses sepsis-induced acute lung injury by blocking the NF-κB pathway activation and hindering macrophage M1 polarization and pyroptosis |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 15.12.2023 | ||
| 500 | |a Date Revised 15.12.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 Elsevier Ltd. All rights reserved. | ||
| 520 | |a OBJECTIVE: Sepsis-induced acute lung injury (ALI) is a life-threatening disease. Macrophage pyroptosis has been reported to exert function in ALI. We aimed to investigate the mechanisms of ANGPTL4-mediated cell pyroptosis in sepsis-induced ALI, thus providing new insights into the pathogenesis and prevention and treatment measures of sepsis-induced ALI | ||
| 520 | |a METHODS: In vivo animal models and in vitro cell models were established by cecal ligation and puncture (CLP) method and lipopolysaccharide-induced macrophages RAW264.7. ANGPTL4 was silenced in CLP mice or macrophages, followed by the determination of ANGPTL4 expression in bronchoalveolar lavage fluid (BALF) or macrophages. Lung histopathology was observed by H&E staining, with pathological injury scores evaluated and lung wet and dry weight ratio recorded. M1/M2 macrophage marker levels (iNOS/CD86/Arg1), inflammatory factor (TNF-α/IL-6/IL-1β/iNOS) expression in BALF, cell death and pyroptosis, NLRP3 inflammasome, cell pyroptosis-related protein (NLRP3/Cleaved-caspase-1/caspase-1/GSDMD-N) levels, NF-κB pathway activation were assessed by RT-qPCR/ELISA/flow cytometry/Western blot, respectively | ||
| 520 | |a RESULTS: ANGPTL4 was highly expressed in mice with sepsis-induced ALI, and ANGPTL4 silencing ameliorated sepsis-induced ALI in mice. In vivo, ANGPTL4 silencing repressed M1 macrophage polarization and macrophage pyroptosis in mice with sepsis-induced ALI. In vitro, ANGPTL4 knockout impeded LPS-induced activation and pyroptosis of M1 macrophages and hindered LPS-induced activation of the NF-κB pathway in macrophages | ||
| 520 | |a CONCLUSION: Knockdown of ANGPTL4 blocks the NF-κB pathway activation, hinders macrophage M1 polarization and pyroptosis, thereby suppressing sepsis-induced ALI | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Acute lung injury | |
| 650 | 4 | |a Angiopoietin-like 4 | |
| 650 | 4 | |a M1 polarization | |
| 650 | 4 | |a Macrophage | |
| 650 | 4 | |a Pyroptosis | |
| 650 | 4 | |a Sepsis | |
| 650 | 7 | |a Angiopoietins |2 NLM | |
| 650 | 7 | |a Caspases |2 NLM | |
| 650 | 7 | |a EC 3.4.22.- |2 NLM | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a NLR Family, Pyrin Domain-Containing 3 Protein |2 NLM | |
| 650 | 7 | |a Angptl4 protein, mouse |2 NLM | |
| 700 | 1 | |a Bai, Lina |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Qinglin |e verfasserin |4 aut | |
| 700 | 1 | |a Sun, Yubo |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Mei |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jiazhi |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Xiaoli |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Meng |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Toxicology in vitro : an international journal published in association with BIBRA |d 1987 |g 94(2023) vom: 16. Feb., Seite 105709 |w (DE-627)NLM086842579 |x 1879-3177 |7 nnns |
| 773 | 1 | 8 | |g volume:94 |g year:2023 |g day:16 |g month:02 |g pages:105709 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.tiv.2023.105709 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 94 |j 2023 |b 16 |c 02 |h 105709 | ||