Calcitriol/vitamin D receptor system alleviates PM2.5-induced human bronchial epithelial damage through upregulating mitochondrial bioenergetics in association with regulation of HIF-1α/PGC-1α signaling
Issued Date
2024-10-01
Resource Type
ISSN
13826689
eISSN
18727077
Scopus ID
2-s2.0-85204580457
Journal Title
Environmental Toxicology and Pharmacology
Volume
111
Rights Holder(s)
SCOPUS
Bibliographic Citation
Environmental Toxicology and Pharmacology Vol.111 (2024)
Suggested Citation
Chatsirisupachai A., Muanjumpon P., Jeayeng S., Onkoksong T., Pluempreecha M., Soingam T., Panich U. Calcitriol/vitamin D receptor system alleviates PM2.5-induced human bronchial epithelial damage through upregulating mitochondrial bioenergetics in association with regulation of HIF-1α/PGC-1α signaling. Environmental Toxicology and Pharmacology Vol.111 (2024). doi:10.1016/j.etap.2024.104568 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/101419
Title
Calcitriol/vitamin D receptor system alleviates PM2.5-induced human bronchial epithelial damage through upregulating mitochondrial bioenergetics in association with regulation of HIF-1α/PGC-1α signaling
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Corresponding Author(s)
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Abstract
PM2.5 exposure causes lung injury by triggering oxidative stress, mitochondrial dysfunction, and modulating HIF-1α signaling. Calcitriol activates VDR, which regulates cellular homeostasis. This study evaluated the protective role of the calcitriol/VDR system in PM2.5-induced damage to BEAS-2B bronchial epithelial cells by reducing oxidative stress, upregulating mitochondrial bioenergetics, and downregulating HIF-1α. We found that the calcitriol/VDR system decreased ROS formation and restored mitochondrial bioenergetics in PM2.5-treated cells. This improvement correlated with reduced HIF-1α nuclear translocation and increased PGC-1α protein and mitochondrial gene expressions. This study is the first to suggest that targeting the calcitriol/VDR system could be a promising pharmacological strategy for mitigating PM2.5-induced lung epithelial damage by promoting mitochondrial bioenergetics and regulating PGC-1α and HIF-1α signaling.