Endoplasmic reticulum chaperone GRP78 mediates cigarette smoke-induced necroptosis and injury in bronchial epithelium

Wang, Yong; Zhou, Jia; Xu, Xu-Chen; Li, Zhou-Yang; Chen, Hai-Pin; Ying, Songmin; Li, Wen; Shen, Huahao; Chen, Zhihua

doi:10.2147/copd.s150633

Cited by 20 publications

(14 citation statements)

References 37 publications

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“…We and others further found that necroptosis in bronchial epithelial cells play an important role in CS-induced airway inflammation. 9,24 The present study indicated that necroptosis also regulated CSE-induced inflammatory responses in BMDMs. There is a dynamic interaction between macrophages and airway epithelium in the lung, and they may cooperatively regulated inflammatory responses in the COPD pathogenesis.…”

Section: Discussionsupporting

confidence: 55%

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<p>Necroptosis Mediates Cigarette Smoke-Induced Inflammatory Responses in Macrophages</p>

Wang¹,

Wang²,

Wu³

et al. 2020

COPD

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Introduction: Cigarette smoke (CS)-induced inflammation in macrophages is involved in the pathological process of chronic obstructive pulmonary disease (COPD). Necroptosis, which is a form of programmed necrosis, has a close relationship with robust inflammation, while its roles in COPD are unclear. Materials and Methods: Necroptosis markers were measured in mouse alveolar macrophages and cultured bone marrow-derived macrophages (BMDMs). Necroptosis inhibitors were used to block necroptosis in BMDMs, and inflammatory cytokines were detected. We further explored the related signaling pathways. Results: In this study, we demonstrated the way in which necroptosis, in addition to its upstream and downstream signals, regulates CS-induced inflammatory responses in macrophages. We observed that CS exposure caused a significant increase in the levels of necroptosis markers (receptor interacting kinases [RIPK] 1 and 3) in mouse alveolar macrophages and BMDMs. Pharmacological inhibition of RIPK1 or 3 caused a significant suppression in CS extract (CSE)-induced inflammatory cytokines, chemokine ligands (CXCL) 1 and 2, and interleukin (IL)-6 in BMDMs. CSE-induced necroptosis was regulated by mitochondrial reactive oxygen species (mitoROS), which also promoted inflammation in BMDMs. Furthermore, necroptosis regulated CSE-induced inflammatory responses in BMDMs, most likely through activation of the nuclear factor-κB pathway. Conclusion: Taken together, our results demonstrate that mitoROS-dependent necroptosis is essential for CS-induced inflammation in BMDMs and suggest that inhibition of necroptosis in macrophages may represent effective therapeutic approaches for COPD patients.

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Section: Discussionsupporting

confidence: 55%

“…7 Mizumura et al showed that necroptosis participates in the process of COPD, 8 and we also found that necroptosis plays an important role in CS-induced airway injury. 9 Airway epithelial necroptosis is closely related to COPD pathogenesis. However, the underlying mechanisms of necroptosis in COPD have yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

<p>Necroptosis Mediates Cigarette Smoke-Induced Inflammatory Responses in Macrophages</p>

Wang¹,

Wang²,

Wu³

et al. 2020

COPD

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“…Exposure to CS increased the levels of DAMPs and numbers of neutrophils in bronchoalveolar lavage fluid in mice, and this effect was statistically reduced on treatment with the necroptosis inhibitor necrostatin-1. 46 More recently, Wang et al 47 , 48 reported a novel regulatory mechanism of necroptosis-mediated inflammation. Endoplasmic reticulum chaper-one GRP78 promoted a CSE-induced inflammatory response and mucus hyperproduction in airway epithelial cells, likely through the upregulation of necroptosis and subsequent activation of the nuclear factor-κB and activator protein-1 pathways.…”

Section: Necroptosis: a Critical Regulator Of Cell Death In Copdmentioning

confidence: 99%

“…Endoplasmic reticulum chaper-one GRP78 promoted a CSE-induced inflammatory response and mucus hyperproduction in airway epithelial cells, likely through the upregulation of necroptosis and subsequent activation of the nuclear factor-κB and activator protein-1 pathways. 48 In contrast, the mTOR suppresses the CS-induced inflammatory cytokines interleukin-6 and interleukin-8 through the nuclear factor-kB pathway, likely through the modulation of autophagy, apoptosis, and necroptosis. 47 These results suggest that necroptosis might be a promising therapeutic target for emphysema and inflammation.…”

Section: Necroptosis: a Critical Regulator Of Cell Death In Copdmentioning

confidence: 99%

Autophagy, selective autophagy, and necroptosis in COPD

Mizumura¹,

Maruoka²,

Shimizu³

et al. 2018

COPD

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COPD is characterized by persistent respiratory symptoms and airflow limitation, caused by a mixture of small airway disease and pulmonary emphysema. Programmed cell death has drawn the attention of COPD researchers because emphysema is thought to result from epithelial cell death caused by smoking. Although apoptosis has long been thought to be the sole form of programmed cell death, recent studies have reported the existence of a genetically programmed and regulated form of necrosis called necroptosis. Autophagy was also previously considered a form of programmed cell death, but this has been reconsidered. However, recent studies have revealed that autophagy can regulate programmed cell death, including apoptosis and necroptosis. It is also becoming clear that autophagy can selectively degrade specific proteins, organelles, and invading bacteria by a process termed “selective autophagy” and that this process is related to the pathogenesis of human diseases. In this review, we outline the most recent studies implicating autophagy, selective autophagy, and necroptosis in COPD. Strategies targeting these pathways may yield novel therapies for COPD.

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“…The role of the ER in necroptosis has been evidenced using necrostatin-1, an inhibitor of necroptosis, which has a protective effect on the endoplasmic reticulum and mitochondria and alleviates ER stress after spinal cord injury [92]. Furthermore, Grp78 promotes an inflammatory response through the upregulation of necroptosis and subsequent activation of NF-κB and AP-1 pathways [93]. The depletion of reticulocalbin 1, an ER-resident Ca 2+ -binding protein, induces Grp78, activates PERK, and phosphorylates eIF2α.…”

Section: The Role Of Er In Necroptosismentioning

confidence: 99%

Endoplasmic Reticulum Stress during Mammalian Follicular Atresia

Torres‐Ramírez¹,

Ortíz²,

Escobar-Sánchez³

et al. 2019

Endoplasmic Reticulum

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Follicles are ovarian structures that contain a single germ cell. During the mammalian reproductive lifetime, ovarian follicles mature through the process of follicular development, with the aim of selecting oocytes for ovulation. As part of this process, several follicles are eliminated by means of follicular atresia, a mechanism that mainly involves apoptosis. Nevertheless, it has been shown that there are other routes of programmed cell death in the ovary including autophagy, paraptosis, and necroptosis. Surprisingly, the endoplasmic reticulum is involved in these different programmed cell death pathways. Moreover, there are several evidences for the pathways triggered by intra-and extracellular signals in endoplasmic reticulum-induced cell death. Thus, it is important to analyze the participation of endoplasmic reticulum in follicular atresia.

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Endoplasmic reticulum chaperone GRP78 mediates cigarette smoke-induced necroptosis and injury in bronchial epithelium

Cited by 20 publications

References 37 publications

<p>Necroptosis Mediates Cigarette Smoke-Induced Inflammatory Responses in Macrophages</p>

<p>Necroptosis Mediates Cigarette Smoke-Induced Inflammatory Responses in Macrophages</p>

Autophagy, selective autophagy, and necroptosis in COPD

Endoplasmic Reticulum Stress during Mammalian Follicular Atresia

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