Klotho improves Der p1-induced bronchial epithelial cell damage by inhibiting endoplasmic reticulum stress to regulate mitochondrial function

Asthma is a prevalent chronic pediatric lung disease which is commonly perceived as a syndrome of airway inflammation characterized by cough and wheeze in clinic. Klotho is implicated in diverse cellular activities, including inflammation, oxidative stress and apoptosis. This paper aims to explore the role of klotho in asthma and investigate the relevant molecular reaction mechanisms. To this end, we used Der p1 to induce an in vitro asthma model in BEAS-2B cells. Klotho expression was manipulated in Der p1-induced BEAS-2B cells with overexpression and its effects on Der p1-induced pathologies including apoptosis and inflammatory cytokine levels and the expressions of oxidative stress-related markers and major mediators in endoplasmic reticulum stress (ER stress) were investigated. Mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (mPTP) opening were also detected. Our data demonstrated that Der p1 stimulation decreased klotho expression and klotho overexpression inhibited the Der p1-induced inflammation, oxidative stress and apoptosis. Overexpressing klotho inhibited ER stress to modulate mitochondrial function. The inhibitory effects of klotho overexpression were reversed by ER stress agonist tunicamycin. This paper validated the role of klotho in asthma pathogenies and developed prospective therapeutic targets for asthma treatment. •Klotho elevation inhibits Der p1-inducedER stress in BEAS-2B cells to regulate mitochondrial function.•Klotho elevation inhibits Der p1-induced inflammation and oxidative stress in BEAS-2B cells via inhibiting ER stress.•Klotho elevation inhibits Der p1-induced apoptosis in BEAS-2B cells via inhibiting ER stress.