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

Yanlin Tan1, Shisi Xiong1, Wenchang Ni1

  • 1Department of Pediatrics, Wuhan Third Hospital, No. 216 Guanshan Avenue, Hongshan District, 430000, Wuhan, China.

Journal of Cardiothoracic Surgery
|July 18, 2026
PubMed

Insights

Reducing SRPRA levels protects against lung injury in premature infants by decreasing endoplasmic reticulum (ER) stress. This finding highlights SRPRA as a potential therapeutic target for bronchopulmonary dysplasia (BPD).

Area of Science:

  • Cell Biology
  • Pulmonology
  • Molecular Biology

Background:

  • Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants, often caused by hyperoxia-induced alveolar epithelial cell injury.
  • Excessive endoplasmic reticulum (ER) stress is a key factor in BPD progression.
  • The role of SRPRA, upregulated in BPD, in ER stress and disease mechanisms is unclear.

Purpose of the Study:

  • To investigate the role of SRPRA in hyperoxia-induced BPD.
  • To elucidate the underlying mechanisms connecting SRPRA, ER stress, and BPD pathogenesis.

Main Methods:

  • Established a hyperoxia-exposed alveolar type II epithelial cell (AECII) model in vitro.
  • Assessed cell viability, proliferation, apoptosis, inflammation, and oxidative stress.
  • Quantified SRPRA, apoptosis, inflammation, and ER stress (CHOP pathway) markers using qRT-PCR and Western blotting.

Main Results:

  • SRPRA was upregulated in hyperoxia-induced AECIIs.
  • Hyperoxia impaired AECII viability and increased apoptosis, inflammation, and oxidative stress.
  • SRPRA knockdown mitigated hyperoxia-induced damage and inflammation by downregulating CHOP-mediated ER stress.

Conclusions:

  • SRPRA knockdown protects against hyperoxia-induced AECII injury by reducing CHOP-mediated ER stress.
  • SRPRA plays a pathogenic role in BPD and represents a potential therapeutic target.
Abstract

Keywords:
Bronchopulmonary dysplasiaCHOPInflammationOxidative stressSRPRA

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