+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

PM2.5 Induced the Expression of Fibrogenic Mediators via HMGB1-RAGE Signaling in Human Airway Epithelial Cells



PM2.5 Induced the Expression of Fibrogenic Mediators via HMGB1-RAGE Signaling in Human Airway Epithelial Cells



Canadian Respiratory Journal 2018: 1817398



The aim of the present study was to test whether fine particulate matter (PM2.5) induces the expression of platelet-derived 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. 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. The 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. This activation was accompanied by an increase in the expression of PDGF-AB, PDGF-BB, and TGF-β1. The 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. 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.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 065412505

Download citation: RISBibTeXText

PMID: 29670673

DOI: 10.1155/2018/1817398


Related references

HMGB1 Enhances the AGE-Induced Expression of CTGF and TGF-β via RAGE-Dependent Signaling in Renal Tubular Epithelial Cells. American Journal of Nephrology 41(3): 257-266, 2016

HMGB1 attenuates TGF-β-induced epithelial-mesenchymal transition of FaDu hypopharyngeal carcinoma cells through regulation of RAGE expression. Molecular and Cellular Biochemistry 431(1-2): 1-10, 2017

Upregulation of miR-107 expression following hyperbaric oxygen treatment suppresses HMGB1/RAGE signaling in degenerated human nucleus pulposus cells. Arthritis Research and Therapy 21(1): 42, 2019

Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling. Respiratory Research 20(1): 27, 2019

Conditionally induced RAGE expression by proximal airway epithelial cells in transgenic mice causes lung inflammation. Respiratory Research 15: 133, 2015

Diesel particulate matter induces receptor for advanced glycation end-products (RAGE) expression in pulmonary epithelial cells, and RAGE signaling influences NF-κB-mediated inflammation. Environmental Health Perspectives 119(3): 332-336, 2011

Systematic analysis of multiwalled carbon nanotube-induced cellular signaling and gene expression in human small airway epithelial cells. Toxicological Sciences 133(1): 79-89, 2013

Plantamajoside Inhibits Lipopolysaccharide-Induced MUC5AC Expression and Inflammation through Suppressing the PI3K/Akt and NF-κB Signaling Pathways in Human Airway Epithelial Cells. Inflammation 41(3): 795-802, 2018

Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells. Frontiers in Immunology 7: 341, 2016

The activation of HMGB1 as a progression factor on inflammation response in normal human bronchial epithelial cells through RAGE/JNK/NF-κB pathway. Molecular and Cellular Biochemistry 380(1-2): 249-257, 2014

HMGB1 activates nuclear factor-κB signaling by RAGE and increases the production of TNF-α in human umbilical vein endothelial cells. Immunobiology 215(12): 956-962, 2011

Nicotine-induced epithelial-mesenchymal transition via Wnt/β-catenin signaling in human airway epithelial cells. American Journal of Physiology. Lung Cellular and Molecular Physiology 304(4): L199-L209, 2013

Nicotine-induced epithelial-mesenchymal transition via Wnt/beta-catenin signaling in human airway epithelial cells. 2013

Nicotine Induced Epithelial-Mesenchymal Transition via Wnt/beta-catenin Signaling in Human Airway Epithelial Cells. 2013

Mineral dusts directly induce epithelial and interstitial fibrogenic mediators and matrix components in the airway wall. American Journal of Respiratory and Critical Care Medicine 158(6): 1907-1913, 1998