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@article{Li:2022:10.21037/jtd-22-315,
author = {Li, C and Zhang, H and Wei, L and Liu, Q and Xie, M and Weng, J and Wang, X and Chung, KF and Adcock, IM and Chen, Y and Li, F},
doi = {10.21037/jtd-22-315},
journal = {Journal of Thoracic Disease},
title = {Role of TRPA1/TRPV1 in acute ozone exposure induced murine model of airway inflammation and bronchial hyperresponsiveness},
url = {http://dx.doi.org/10.21037/jtd-22-315},
volume = {14},
year = {2022}
}

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TY  - JOUR
AB  - Background: Transient receptor potential (TRP) ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) mediatethe development of lung injury and inflammation. This study investigated the role and mechanism of theTRPA1/TRPV1 pathway in airway inflammation and bronchial hyperresponsiveness (BHR) induced byacute ozone exposure.Methods: C57BL/6 mice (8–10 weeks) were intraperitoneally injected with phosphate buffered saline(PBS), A967079 (TRPA1 inhibitor) or AMG9810 (TRPV1 inhibitor) 1 h before or after ozone exposure(2.5 ppm, 3 h). BHR, cell counts in bronchoalveolar lavage (BAL) fluid, oxidative stress biomarkers,inflammatory cytokines, TRPA1 and TPRV1 protein levels, mitochondrial dynamics- and mitophagy-relatedprotein levels, and activities of mitochondrial respiratory chain (MRC) in lung were measured.Results: The preventive treatment effect was similar to the therapeutic treatment effect. Both A967079 andAMG9810 intervention suppressed BHR, inflammatory cytokines, total BAL fluid cells, malondialdehyde(MDA) levels and inflammatory cytokines mRNA including Substance P (SP), Keratinocyte-DerivedChemokine (KC), interleukin18 (IL-18) and chemokine (C-X-C motif) ligand 8 (CXCL8) expression, andenhanced reduced glutathione (GSH)/oxidized glutathione (GSSG) levels compared with ozone-exposedmice. A967079 and AMG9810 intervention inhibited dynamin-related protein (DRP1), mitochondrial fissionfactor (MFF), Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) and Sequestosome 1 (SQSTM1)/p62expression, increased Optic atrophy 1 (OPA1), mitofusin 2 (MFN2) and PTEN-induced putative kinase 1(PINK1) expression, and up-regulated the activities of MRC complex III and V in lung tissue.Conclusions: The results show that both TRPA1 and TRPV1 pathways are involved in acute ozoneexposure-induced airway inflammation and BHR and influence oxidative stress, mitochondrial qualitycontrol and MRC activity, which could be a potential target for clinical therapy of respiritory disease
AU  - Li,C
AU  - Zhang,H
AU  - Wei,L
AU  - Liu,Q
AU  - Xie,M
AU  - Weng,J
AU  - Wang,X
AU  - Chung,KF
AU  - Adcock,IM
AU  - Chen,Y
AU  - Li,F
DO  - 10.21037/jtd-22-315
PY  - 2022///
SN  - 2072-1439
TI  - Role of TRPA1/TRPV1 in acute ozone exposure induced murine model of airway inflammation and bronchial hyperresponsiveness
T2  - Journal of Thoracic Disease
UR  - http://dx.doi.org/10.21037/jtd-22-315
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000821238600001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://jtd.amegroups.com/article/view/65958/html
UR  - http://hdl.handle.net/10044/1/98308
VL  - 14
ER  -

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