Author/Authors :
Zou, Weifeng The State Key Laboratory of Respiratory Disease - Guangzhou Chest Hospital, Guangzhou, Guangdong, China , He, Fang The Research Center of Experiment Medicine - Guangzhou Medical University, Guangzhou, Guangdong, China , Liu, Sha The State Key Laboratory of Respiratory Disease - Guangzhou Institute of Respiratory Diseases - Guangzhou Medical University, Guangzhou, Guangdong, China , Pu, Jinding The State Key Laboratory of Respiratory Disease - Guangzhou Institute of Respiratory Diseases - Guangzhou Medical University, Guangzhou, Guangdong, China , Hu, Jinxing The State Key Laboratory of Respiratory Disease - Guangzhou Chest Hospital, Guangzhou, Guangdong, China , Sheng, Qing The State Key Laboratory of Respiratory Disease - Guangzhou Chest Hospital, Guangzhou, Guangdong, China , Zhu, Tao The State Key Laboratory of Respiratory Disease - Guangzhou Chest Hospital, Guangzhou, Guangdong, China , Zhu, Tianhua Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China , Li, Bing The Research Center of Experiment Medicine - Guangzhou Medical University, Guangzhou, Guangdong, China , Ran, Pixin The State Key Laboratory of Respiratory Disease - Guangzhou Institute of Respiratory Diseases - Guangzhou Medical University, Guangzhou, Guangdong, China
Abstract :
Background. ,e aim of the present study was to test whether fine particulate matter (PM2.5) induces the expression of plateletderived growth factor-AB (PDGF-AB), PDGF-BB, and transforming growth factor-β1 (TGF-β1) in human bronchial epithelial
cells (HBECs) in vitro via high-mobility group box 1 (HMGB1) receptor for advanced glycation end products (RAGE) signaling.
Methods. Sprague-Dawley rats were exposed to motor vehicle exhaust (MVE) or clean air. HBECs were either transfected with
a small interfering RNA (siRNA) targeting HMGB1 or incubated with anti-RAGE antibodies and subsequently stimulated with
PM2.5. Results. ,e expression of HMGB1 and RAGE was elevated in MVE-treated rats compared with untreated rats, and PM2.5
increased the secretion of HMGB1 and upregulated RAGE expression and the translocation of nuclear factor κB (NF-κB) into the
nucleus of HBECs. ,is activation was accompanied by an increase in the expression of PDGF-AB, PDGF-BB, and TGF-β1. ,e
HMGB1 siRNA prevented these effects. Anti-RAGE antibodies attenuated the activation of NF-κB and decreased the secretion of
TGF-β1, PDGF-AB, and PDGF-BB from HBECs. Conclusion. PM2.5 induces the expression of TGF-β1, PDGF-AB, and PDGF-BB
in vitro via HMGB1-RAGE signaling, suggesting that this pathway may contribute to the airway remodeling observed in patients
with COPD.
