Proteasome inhibition promotes autophagy and protects from endoplasmic reticulum stress in rat alveolar macrophages exposed to hypoxia‐reoxygenation injury

Alveolar macrophages play vital roles in acute lung injury, and macrophage response to hypoxia play relevant roles to disease mechanisms. There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is invol...

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Veröffentlicht in:Journal of cellular physiology 2018-10, Vol.233 (10), p.6748-6758
Hauptverfasser: Fan, Tao, Huang, Zhixin, Wang, Wei, Zhang, Boyou, Xu, Yao, Mao, Zhangfan, Chen, Lei, Hu, Hao, Geng, Qing
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container_end_page 6758
container_issue 10
container_start_page 6748
container_title Journal of cellular physiology
container_volume 233
creator Fan, Tao
Huang, Zhixin
Wang, Wei
Zhang, Boyou
Xu, Yao
Mao, Zhangfan
Chen, Lei
Hu, Hao
Geng, Qing
description Alveolar macrophages play vital roles in acute lung injury, and macrophage response to hypoxia play relevant roles to disease mechanisms. There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is involved in the regulation of these processes. However, the functional role of proteasome in alveolar macrophages exposed to hypoxia‐reoxygenation (H/R) injury is unknown. We aimed to investigate the function of proteasome on alveolar macrophages exposed to H/R and the underlying mechanisms. NR8383 cells were pretreated with proteasome activator sulforaphane (SFN) or inhibitor MG‐132 for 1 hr, and then submitted to 2/6 hr, 4/6 hr, and 6/6 hr H/R treatment. Cell viability was assessed with MTT assay. Autophagy was monitored using electron transmission microscope and flow cytometry and western blotting. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were equally analyzed by western blotting. Cell apoptosis was detected by immunohistochemistry, caspase3/7 activity, and western blotting. The viability of NR8383 cells exposed to H/R was affected by proteasome activity and proteasome inhibition significantly inhibited cell death. Treatment with MG‐132 led to autophagy activation and induced the survival of NR8383 cells exposed to H/R. Pretreatment with SFN significantly decreased cell autophagy and induced cell death. ER stress was activated in H/R‐treated NR8383 cells, and SFN further promoted ER stress whereas proteasome inhibition led to contrary results. Proteasome inhibtion hindered cell apoptosis as demonstrated by decreased caspase‐3/7 activity, immunolabelling, and western blot results. Proteasome inhibition might be a promising approach for treating H/R injury‐related lung diseases. MG‐132 pretreatment strengthened autophagy. MG‐132 pretreatment strengthened ER stress. MG‐132 pretreatment decreased cell apoptosis.
doi_str_mv 10.1002/jcp.26516
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There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is involved in the regulation of these processes. However, the functional role of proteasome in alveolar macrophages exposed to hypoxia‐reoxygenation (H/R) injury is unknown. We aimed to investigate the function of proteasome on alveolar macrophages exposed to H/R and the underlying mechanisms. NR8383 cells were pretreated with proteasome activator sulforaphane (SFN) or inhibitor MG‐132 for 1 hr, and then submitted to 2/6 hr, 4/6 hr, and 6/6 hr H/R treatment. Cell viability was assessed with MTT assay. Autophagy was monitored using electron transmission microscope and flow cytometry and western blotting. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were equally analyzed by western blotting. Cell apoptosis was detected by immunohistochemistry, caspase3/7 activity, and western blotting. 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There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is involved in the regulation of these processes. However, the functional role of proteasome in alveolar macrophages exposed to hypoxia‐reoxygenation (H/R) injury is unknown. We aimed to investigate the function of proteasome on alveolar macrophages exposed to H/R and the underlying mechanisms. NR8383 cells were pretreated with proteasome activator sulforaphane (SFN) or inhibitor MG‐132 for 1 hr, and then submitted to 2/6 hr, 4/6 hr, and 6/6 hr H/R treatment. Cell viability was assessed with MTT assay. Autophagy was monitored using electron transmission microscope and flow cytometry and western blotting. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were equally analyzed by western blotting. Cell apoptosis was detected by immunohistochemistry, caspase3/7 activity, and western blotting. 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Huang, Zhixin ; Wang, Wei ; Zhang, Boyou ; Xu, Yao ; Mao, Zhangfan ; Chen, Lei ; Hu, Hao ; Geng, Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3536-911508d01947038f8030af730c13c39e95c2366b130505c6e69eba6f9243411c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>alveolar macrophages</topic><topic>Alveoli</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Autophagy - genetics</topic><topic>Caspase</topic><topic>Cell death</topic><topic>Cell Hypoxia - drug effects</topic><topic>Cell Hypoxia - genetics</topic><topic>Cell Survival - drug effects</topic><topic>Endoplasmic reticulum</topic><topic>endoplasmic reticulum stress</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Exposure</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>hypoxia‐ reoxygenation injury</topic><topic>Immunohistochemistry</topic><topic>Injuries</topic><topic>Isothiocyanates - pharmacology</topic><topic>Lung diseases</topic><topic>Lung Diseases - drug therapy</topic><topic>Lung Diseases - genetics</topic><topic>Lung Diseases - pathology</topic><topic>Macrophages</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Macrophages, Alveolar - pathology</topic><topic>Mortality</topic><topic>Phagocytosis</topic><topic>Pretreatment</topic><topic>proteasome</topic><topic>Proteasome activator</topic><topic>Proteasome Endopeptidase Complex - drug effects</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>Protein folding</topic><topic>Proteins</topic><topic>Rats</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Stresses</topic><topic>Sulforaphane</topic><topic>Ubiquitin</topic><topic>Unfolded Protein Response</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fan, Tao</creatorcontrib><creatorcontrib>Huang, Zhixin</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Zhang, Boyou</creatorcontrib><creatorcontrib>Xu, Yao</creatorcontrib><creatorcontrib>Mao, Zhangfan</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Hu, Hao</creatorcontrib><creatorcontrib>Geng, Qing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; 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There is growing evidence that cell death pathways play crucial roles in physiological and pathological settings and that the ubiquitin‐proteasome system is involved in the regulation of these processes. However, the functional role of proteasome in alveolar macrophages exposed to hypoxia‐reoxygenation (H/R) injury is unknown. We aimed to investigate the function of proteasome on alveolar macrophages exposed to H/R and the underlying mechanisms. NR8383 cells were pretreated with proteasome activator sulforaphane (SFN) or inhibitor MG‐132 for 1 hr, and then submitted to 2/6 hr, 4/6 hr, and 6/6 hr H/R treatment. Cell viability was assessed with MTT assay. Autophagy was monitored using electron transmission microscope and flow cytometry and western blotting. The endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways were equally analyzed by western blotting. Cell apoptosis was detected by immunohistochemistry, caspase3/7 activity, and western blotting. The viability of NR8383 cells exposed to H/R was affected by proteasome activity and proteasome inhibition significantly inhibited cell death. Treatment with MG‐132 led to autophagy activation and induced the survival of NR8383 cells exposed to H/R. Pretreatment with SFN significantly decreased cell autophagy and induced cell death. ER stress was activated in H/R‐treated NR8383 cells, and SFN further promoted ER stress whereas proteasome inhibition led to contrary results. Proteasome inhibtion hindered cell apoptosis as demonstrated by decreased caspase‐3/7 activity, immunolabelling, and western blot results. Proteasome inhibition might be a promising approach for treating H/R injury‐related lung diseases. MG‐132 pretreatment strengthened autophagy. MG‐132 pretreatment strengthened ER stress. 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subjects alveolar macrophages
Alveoli
Animals
Apoptosis
Apoptosis - drug effects
Autophagy
Autophagy - drug effects
Autophagy - genetics
Caspase
Cell death
Cell Hypoxia - drug effects
Cell Hypoxia - genetics
Cell Survival - drug effects
Endoplasmic reticulum
endoplasmic reticulum stress
Endoplasmic Reticulum Stress - drug effects
Endoplasmic Reticulum Stress - genetics
Exposure
Flow cytometry
Humans
Hypoxia
hypoxia‐ reoxygenation injury
Immunohistochemistry
Injuries
Isothiocyanates - pharmacology
Lung diseases
Lung Diseases - drug therapy
Lung Diseases - genetics
Lung Diseases - pathology
Macrophages
Macrophages, Alveolar - drug effects
Macrophages, Alveolar - metabolism
Macrophages, Alveolar - pathology
Mortality
Phagocytosis
Pretreatment
proteasome
Proteasome activator
Proteasome Endopeptidase Complex - drug effects
Proteasome Endopeptidase Complex - metabolism
Protein folding
Proteins
Rats
Reperfusion Injury - drug therapy
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Stresses
Sulforaphane
Ubiquitin
Unfolded Protein Response
Western blotting
title Proteasome inhibition promotes autophagy and protects from endoplasmic reticulum stress in rat alveolar macrophages exposed to hypoxia‐reoxygenation injury
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