PMID- 37915073
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231104
IS  - 1476-9255 (Print)
IS  - 1476-9255 (Electronic)
IS  - 1476-9255 (Linking)
VI  - 20
IP  - 1
DP  - 2023 Nov 1
TI  - Soluble epoxide hydrolase deficiency attenuates airway inflammation in COPD via 
      IRE1alpha/JNK/AP-1 signaling pathway.
PG  - 36
LID - 10.1186/s12950-023-00361-y [doi]
LID - 36
AB  - BACKGROUND: Soluble Epoxide Hydrolase (sEH) metabolizes anti-inflammatory 
      epoxyeicosatrienoic acids and critically affects airway inflammation in chronic 
      obstructive pulmonary disease (COPD). Considering the excessive endoplasmic 
      reticulum stress is associated with the earlier onset of COPD. The role of sEH 
      and endoplasmic reticulum stress in the pathogenesis of COPD remains unknown. 
      METHOD: 16 weeks of cigarette-exposed mice were used to detect the relationship 
      between sEH and endoplasmic reticulum stress in COPD. Human epithelial cells were 
      used in vitro to determine the regulation mechanism of sEH in endoplasmic 
      reticulum stress induced by cigarette smoke. RESULTS: sEH deficiency helps reduce 
      emphysema formation after smoke exposure by alleviating endoplasmic reticulum 
      stress response. sEH deficiency effectively reverses the upregulation of 
      phosphorylation IRE1alpha and JNK and the nuclear expression of AP-1, alleviating the 
      secretion of inflammatory factors induced by cigarette smoke extract. 
      Furthermore, the treatment with endoplasmic reticulum stress and IRE1alpha inhibitor 
      downregulated cigarette smoke extract-induced sEH expression and the secretion of 
      inflammatory factors. CONCLUSION: sEH probably alleviates airway inflammatory 
      response and endoplasmic reticulum stress via the IRE1alpha/JNK/AP-1 pathway, which 
      might attenuate lung injury caused by long-term smoking and provide a new 
      pharmacological target for preventing and treating COPD.
CI  - (c) 2023. The Author(s).
FAU - Yu, Yue
AU  - Yu Y
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Yang, Ailin
AU  - Yang A
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - He, Xin
AU  - He X
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Wu, Bo
AU  - Wu B
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Wu, Yanjun
AU  - Wu Y
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Li, Yunxiao
AU  - Li Y
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Nie, Shan
AU  - Nie S
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China.
FAU - Xu, Bo
AU  - Xu B
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China. 
      xubo_ally@126.com.
FAU - Wang, Haoyan
AU  - Wang H
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China. 
      haoyanw@ccmu.edu.cn.
FAU - Yu, Ganggang
AU  - Yu G
AD  - Department of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical 
      University, No, 95 Yong An Road, Xichen District, Beijing, 100050, China. 
      gangyu.603@163.com.
LA  - eng
GR  - 82000042/National Natural Science Foundation of China/
GR  - 82000043/National Natural Science Foundation of China/
GR  - 81870029/National Natural Science Foundation of China/
GR  - 81700038/National Natural Science Foundation of China/
GR  - 2020-2022/Key Clinical Specialty Construction Program of Beijing/
PT  - Journal Article
DEP - 20231101
PL  - England
TA  - J Inflamm (Lond)
JT  - Journal of inflammation (London, England)
JID - 101232234
PMC - PMC10621191
OTO - NOTNLM
OT  - COPD
OT  - Cigarette smoke
OT  - Endoplasmic reticulum stress
OT  - Inflammation
OT  - Soluble epoxide hydrolase
COIS- The authors declare that they have no conflict of interest.
EDAT- 2023/11/02 06:42
MHDA- 2023/11/02 06:43
PMCR- 2023/11/01
CRDT- 2023/11/02 00:49
PHST- 2023/08/22 00:00 [received]
PHST- 2023/10/09 00:00 [accepted]
PHST- 2023/11/02 06:43 [medline]
PHST- 2023/11/02 06:42 [pubmed]
PHST- 2023/11/02 00:49 [entrez]
PHST- 2023/11/01 00:00 [pmc-release]
AID - 10.1186/s12950-023-00361-y [pii]
AID - 361 [pii]
AID - 10.1186/s12950-023-00361-y [doi]
PST - epublish
SO  - J Inflamm (Lond). 2023 Nov 1;20(1):36. doi: 10.1186/s12950-023-00361-y.