SIRT1 ameliorated septic associated-lung injury and macrophages apoptosis via inhibiting endoplasmic reticulum stress
Copyright © 2022. Published by Elsevier Inc..
BACKGROUND: The inappropriate apoptosis of macrophages plays an important role in the pathogenesis of sepsis-induced acute lung injury, however, the detailed regulatory mechanisms remain largely unknown. As an endogenous apoptosis pathway, endoplasmic reticulum (ER) stress plays an important role in cell damage in patients with sepsis. Clarifying the ER stress response and its effect on macrophages during the development of sepsis is helpful to explore new strategies for the prevention and treatment of ALI in sepsis.
METHODS: The mouse model and the RAW264.7 inflammation model were stimulated with LPS to establish in vivo and in vitro. We explored the effects of different expression levels of silent information regulator factor 2-related enzyme 1 (SIRT1) on the ER stress response and apoptosis of macrophages in the sepsis-related injury model.
RESULTS: Our studies found that the increased expression of SIRT1 can significantly improve sepsis-related lung injury and relieve lung inflammation. SRT1720, a SIRT1 activator, can significantly inhibit the ER stress response of lung tissue and macrophages, inhibit the expression of pro-apoptotic proteins, promote the expression of anti-apoptotic proteins, and reduce macrophages of apoptosis. While the EX527, an inhibitor of SIRT1, had the opposite effect.
CONCLUSION: SIRT1 can significantly improve sepsis-associated lung injury and LPS-induced macrophage apoptosis. This protective effect is closely related to its inhibition of the ER stress response via the PERK/eIF2-α/ATF4/CHOP pathway.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:97 |
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| Enthalten in: |
Cellular signalling - 97(2022) vom: 25. Sept., Seite 110398 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wang, Fuquan [VerfasserIn] |
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| Links: |
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| Themen: |
Acute lung injury |
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| Anmerkungen: |
Date Completed 04.08.2022 Date Revised 24.10.2022 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.cellsig.2022.110398 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM343315343 |
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| 500 | |a Date Completed 04.08.2022 | ||
| 500 | |a Date Revised 24.10.2022 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2022. Published by Elsevier Inc. | ||
| 520 | |a BACKGROUND: The inappropriate apoptosis of macrophages plays an important role in the pathogenesis of sepsis-induced acute lung injury, however, the detailed regulatory mechanisms remain largely unknown. As an endogenous apoptosis pathway, endoplasmic reticulum (ER) stress plays an important role in cell damage in patients with sepsis. Clarifying the ER stress response and its effect on macrophages during the development of sepsis is helpful to explore new strategies for the prevention and treatment of ALI in sepsis | ||
| 520 | |a METHODS: The mouse model and the RAW264.7 inflammation model were stimulated with LPS to establish in vivo and in vitro. We explored the effects of different expression levels of silent information regulator factor 2-related enzyme 1 (SIRT1) on the ER stress response and apoptosis of macrophages in the sepsis-related injury model | ||
| 520 | |a RESULTS: Our studies found that the increased expression of SIRT1 can significantly improve sepsis-related lung injury and relieve lung inflammation. SRT1720, a SIRT1 activator, can significantly inhibit the ER stress response of lung tissue and macrophages, inhibit the expression of pro-apoptotic proteins, promote the expression of anti-apoptotic proteins, and reduce macrophages of apoptosis. While the EX527, an inhibitor of SIRT1, had the opposite effect | ||
| 520 | |a CONCLUSION: SIRT1 can significantly improve sepsis-associated lung injury and LPS-induced macrophage apoptosis. This protective effect is closely related to its inhibition of the ER stress response via the PERK/eIF2-α/ATF4/CHOP pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Acute lung injury | |
| 650 | 4 | |a Endoplasmic reticulum stress | |
| 650 | 4 | |a Macrophages | |
| 650 | 4 | |a SIRT1 | |
| 650 | 4 | |a sepsis | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a Sirt1 protein, mouse |2 NLM | |
| 650 | 7 | |a EC 3.5.1.- |2 NLM | |
| 650 | 7 | |a Sirtuin 1 |2 NLM | |
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| 700 | 1 | |a Ma, Jiamin |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jingxu |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Ming |e verfasserin |4 aut | |
| 700 | 1 | |a Xia, Haifa |e verfasserin |4 aut | |
| 700 | 1 | |a Yao, Shanglong |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Dingyu |e verfasserin |4 aut | |
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