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Background <p>Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease among preterm infants, largely attributed to hyperoxia-induced injury to alveolar epithelial cells. Excessive endoplasmic reticulum (ER) stress plays a vital role in BPD progression. SRPRA, a subunit of the ER-localized SRP receptor, is upregulated in BPD, while its function and link with ER stress remain largely unclear. This study aimed to explore the role of SRPRA in hyperoxia-induced BPD and its underlying mechanism.</p> Methods <p>A hyperoxia-exposed alveolar type II epithelial cell (AECII) model was established to mimic BPD in vitro. Cell viability, cell proliferation and apoptosis were detected by CCK-8, EdU assay and flow cytometry, respectively. The secretion of inflammatory factors was evaluated via ELISA assay. ROS levels were detected by DCFH-DA fluorescence staining. Commercial kits were used to detect MDA and SOD levels. The SRPRA mRNA level and protein expression was measured using qRT-PCR and Western blot. Expression levels of apoptosis-related proteins (Bax, Bcl2), inflammation-related proteins (iNOS, Cox2) and CHOP pathway-related proteins were assessed by western blotting.</p> Results <p>SRPRA was markedly upregulated in hyperoxia-induced alveolar epithelial cells. Hyperoxia stimulation decreased viability and proliferation, and enhanced apoptosis in AECIIs, accompanied by elevated inflammatory responses and oxidative stress. SRPRA knockdown alleviated hyperoxia-induced cell damage, inflammation and oxidative stress, and downregulated the expression of CHOP (a key mediator of ER stress). The protective effects mediated by SRPRA silencing were largely reversed by thapsigargin.</p> Conclusion <p>SRPRA knockdown alleviates hyperoxia-induced AECII injury by attenuating CHOP-mediated ER stress. Our findings reveal the pathogenic role of SRPRA in BPD, and suggest SRPRA as a potential therapeutic target for this disease.</p>

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SRPRA affects hyperoxia-induced bronchopulmonary dysplasia by modulating endoplasmic reticulum stress through the CHOP pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月19日

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  • Yanlin Tan,
  • Shisi Xiong,
  • Wenchang Ni,
  • Liyan Wang,
  • Junmei Bian

摘要

Background

Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease among preterm infants, largely attributed to hyperoxia-induced injury to alveolar epithelial cells. Excessive endoplasmic reticulum (ER) stress plays a vital role in BPD progression. SRPRA, a subunit of the ER-localized SRP receptor, is upregulated in BPD, while its function and link with ER stress remain largely unclear. This study aimed to explore the role of SRPRA in hyperoxia-induced BPD and its underlying mechanism.

Methods

A hyperoxia-exposed alveolar type II epithelial cell (AECII) model was established to mimic BPD in vitro. Cell viability, cell proliferation and apoptosis were detected by CCK-8, EdU assay and flow cytometry, respectively. The secretion of inflammatory factors was evaluated via ELISA assay. ROS levels were detected by DCFH-DA fluorescence staining. Commercial kits were used to detect MDA and SOD levels. The SRPRA mRNA level and protein expression was measured using qRT-PCR and Western blot. Expression levels of apoptosis-related proteins (Bax, Bcl2), inflammation-related proteins (iNOS, Cox2) and CHOP pathway-related proteins were assessed by western blotting.

Results

SRPRA was markedly upregulated in hyperoxia-induced alveolar epithelial cells. Hyperoxia stimulation decreased viability and proliferation, and enhanced apoptosis in AECIIs, accompanied by elevated inflammatory responses and oxidative stress. SRPRA knockdown alleviated hyperoxia-induced cell damage, inflammation and oxidative stress, and downregulated the expression of CHOP (a key mediator of ER stress). The protective effects mediated by SRPRA silencing were largely reversed by thapsigargin.

Conclusion

SRPRA knockdown alleviates hyperoxia-induced AECII injury by attenuating CHOP-mediated ER stress. Our findings reveal the pathogenic role of SRPRA in BPD, and suggest SRPRA as a potential therapeutic target for this disease.