PT  - JOURNAL ARTICLE
AU  - Junling Li
AU  - Lei Fang
AU  - Daiana Stolz
AU  - Michael Tamm
AU  - Michael Roth
TI  - Exogenous HSP60 stimulates airway smooth muscle cell remodeling via MAPK p38 pathway
AID  - 10.1183/13993003.congress-2020.3310
DP  - 2020 Sep 07
TA  - European Respiratory Journal
PG  - 3310
VI  - 56
IP  - suppl 64
4099  - http://erj.ersjournals.com/content/56/suppl_64/3310.short
4100  - http://erj.ersjournals.com/content/56/suppl_64/3310.full
SO  - Eur Respir J2020 Sep 07; 56
AB  - Background: Asthma is characterized by airway inflammation and remodeling. We reported earlier that heat shock protein-60 (HSP60) was secreted by bronchial epithelial cells of asthma patients. HSP60 activated mitogen-activated protein kinases p38, thereby controlling tissue remodeling and the action of CCAAT/enhancer-binding proteins (C/EBP) α/β.Objective: The effect of exogenous human recombinant HSP60 (eHSP60) on the activation of p38 and C/EBPs, as well as on remodeling of airway smooth muscle cells (ASMC).Methods: ASMC were obtained from healthy controls and asthma patients. ASMC were treated with eHSP60 (10 µM) and/or p38 inhibitors (SB2053580, 10 µM). The cellular proteins were collected and the expression of total p38, phosphorylated p38, C/EBP-α/β, fibronectin, α-smooth muscle actin (SMA) and collagen-I were measured by Western-blotting.Results: Treatment with eHSP60 significantly increased the phosphorylation of p38 and the expression of C/EBP-α/β, fibronectin, SMA and collagen-I. Inhibition of p38 decreased eHSP60-induced phosphorylation of p38, and expression of C/EBP-α/β, fibronectin, SMA and collagen-I. In healthy control ASMC, eHSP60 did neither increase phosphorylation of p38, nor expression of C/EBP-α/β, fibronectin, SMA and collagen-I.Conclusion: This is the first report that ASMC of asthma patients respond in a disease specific manner to HSP60 by activation of p38. This suggests HSP60 to be a novel target for therapy and diagnosis.FootnotesCite this article as: European Respiratory Journal 2020; 56: Suppl. 64, 3310.This abstract was presented at the 2020 ERS International Congress, in session “Respiratory viruses in the "pre COVID-19" era”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).