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<p>Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness and remodeling, where epithelial dysfunction plays a crucial role. In this study, the role of adrenoceptor alpha 2&#xa0;A (ADRA2A) in asthma was investigated using bioinformatics, in vitro, and in vivo models. Differential gene expression analysis identified ADRA2A was significantly upregulated in asthmatic tissues. BEAS-2B cells treated with lipopolysaccharide (LPS) exhibited increased expression of ADRA2A, along with elevated levels of pro-inflammatory cytokines and apoptosis. Knockdown of ADRA2A in these cells reduced inflammation and apoptosis, while overexpression exacerbated these effects. In an ovalbumin (OVA)-induced asthma mouse model, ADRA2A knockdown led to a significant reduction in airway hyperresponsiveness, pulmonary edema, inflammatory cell infiltration, and goblet cell hyperplasia. The phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), a key signaling pathway involved in inflammation and apoptosis, was also reduced following ADRA2A knockdown, both in vitro and in vivo. In conclusions, these findings suggest that ADRA2A contributes to the pathogenesis of asthma by modulating the ERK signaling pathway, making it a potential therapeutic target for managing airway inflammation and remodeling in asthmatic patients.</p>

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ADRA2A contributes to airway inflammation and apoptosis in asthma through the ERK signaling in vitro and in vivo

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月26日

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  • Fang Zhou,
  • Jia Cai,
  • Lin Chen,
  • Xiaowu Tan,
  • Chaoqian Li

摘要

Asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness and remodeling, where epithelial dysfunction plays a crucial role. In this study, the role of adrenoceptor alpha 2 A (ADRA2A) in asthma was investigated using bioinformatics, in vitro, and in vivo models. Differential gene expression analysis identified ADRA2A was significantly upregulated in asthmatic tissues. BEAS-2B cells treated with lipopolysaccharide (LPS) exhibited increased expression of ADRA2A, along with elevated levels of pro-inflammatory cytokines and apoptosis. Knockdown of ADRA2A in these cells reduced inflammation and apoptosis, while overexpression exacerbated these effects. In an ovalbumin (OVA)-induced asthma mouse model, ADRA2A knockdown led to a significant reduction in airway hyperresponsiveness, pulmonary edema, inflammatory cell infiltration, and goblet cell hyperplasia. The phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), a key signaling pathway involved in inflammation and apoptosis, was also reduced following ADRA2A knockdown, both in vitro and in vivo. In conclusions, these findings suggest that ADRA2A contributes to the pathogenesis of asthma by modulating the ERK signaling pathway, making it a potential therapeutic target for managing airway inflammation and remodeling in asthmatic patients.