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Autophagy regulates hyperoxia-induced intracellular accumulation of surfactant protein C in alveolar type II cells

Liang Zhang1, Shuang Zhao2, Li-Jie Yuan3

  • 1Department of Neonatology, The First Affiliated Hospital of China Medical University, 155 Nan Jing Northern Street, Shenyang, 110001, Liaoning, China.

Molecular and Cellular Biochemistry
|July 1, 2015
PubMed

Insights

Hyperoxia causes surfactant protein C (SP-C) accumulation in lung cells by triggering autophagy via JNK signaling. Inhibiting this pathway may offer a new therapy for hyperoxic lung injury.

Area of Science:

  • Pulmonary Medicine
  • Cell Biology
  • Neonatal Research

Background:

  • Surfactant protein C (SP-C) deficiency is linked to bronchopulmonary dysplasia in infants.
  • The precise mechanism of SP-C involvement in hyperoxia-induced lung injury remains unclear.

Purpose of the Study:

  • To investigate the role of SP-C in hyperoxia-induced lung injury.
  • To elucidate the cellular mechanisms, including autophagy and signaling pathways, involved in SP-C regulation during hyperoxia.

Main Methods:

  • Utilized a neonatal rat model of bronchopulmonary dysplasia (BPD) and MLE-12 mouse alveolar epithelial cells.
  • Employed immunohistochemistry, immunofluorescence, ELISA, and electron microscopy to assess SP-C levels and cellular structures.
  • Investigated the effects of autophagy inhibition (3-Methyladenine, Atg7 knockdown) and JNK signaling inhibition (SP600125).

Main Results:

  • Hyperoxia led to SP-C accumulation within alveolar epithelial type II cells.
  • Accumulated lamellar bodies co-localized with autophagosomes, indicating impaired autophagy.
  • Inhibition of autophagy or JNK signaling effectively reduced SP-C accumulation.
  • Hyperoxia-induced Atg7 expression and SP-C accumulation were mediated by JNK signaling.

Conclusions:

  • Hyperoxia induces SP-C accumulation in alveolar epithelial cells through JNK-mediated autophagy.
  • Targeted inhibition of the autophagic pathway presents a potential therapeutic strategy for hyperoxic lung injury.

Keywords:
Alveolar type II cellsAutophagyHyperoxiaSurfactant protein C

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