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PAR2 Overexpression is Involved in the Occurrence of Hyperoxygen-Induced Bronchopulmonary Dysplasia in Rats
1Department of Pediatrics, Chengdu Medical College, Chengdu, China.
Insights
Protease-activated receptor 2 (PAR2) drives lung injury in bronchopulmonary dysplasia by increasing IL-18 via the P38 MAPK/NF-κB pathway. This highlights PAR2 as a therapeutic target for this chronic infant lung disease.
Area of Science:
- Pulmonary Medicine
- Neonatology
- Inflammation Research
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants, marked by impaired alveolar development and lung fibrosis.
- Protease-activated receptor 2 (PAR2) is identified as a key inflammatory mediator in lung injury.
- PAR2's pro-inflammatory role is primarily linked to the P38 MAPK/NF-κB signaling pathway.
Purpose of the Study:
- To investigate the role of PAR2 in hyperoxia-induced lung injury, a model relevant to BPD.
- To elucidate the signaling pathway through which PAR2 contributes to lung damage.
Main Methods:
- Newborn rats were exposed to hyperoxia (>60% oxygen) or normal air.
- Lung tissues were collected at postnatal days 1, 4, 7, and 10.
- Pathological changes and expression levels of PAR2, P38 MAPK, NF-κB, and IL-18 were assessed.
Main Results:
- Hyperoxia exposure led to delayed alveolar development, septal thickening, and structural abnormalities in rat lungs.
- Expression of PAR2, P38 MAPK, NF-κB, and IL-18 was significantly elevated in hyperoxic lungs compared to controls.
- These molecular changes were observed at key postnatal time points (P4, P7, P10).
Conclusions:
- PAR2 activation is implicated in the pathogenesis of lung injury caused by persistent hyperoxia.
- Activated PAR2 promotes IL-18 overexpression via the P38 MAPK/NF-κB pathway.
- This PAR2-driven pathway represents a potential mechanism underlying PAR2-mediated lung injury in bronchopulmonary dysplasia.
Background:
Bronchopulmonary dysplasia is a chronic lung disease commonly seen in preterm infants. It is characterized by delayed development of the alveoli and lung fibrosis. Protease-activated receptor 2 (PAR2) is an inflammatory driver that plays a proinflammatory role mainly through the P38 MAPK/NF-κB signaling pathway.
Methods:
Newborn rat pups were kept under air or oxygen at >60% concentration. Lung tissues were collected at postnatal days (P) 1, 4, 7, and 10 to observe pathological changes and take measurements.
Results:
In the hyperoxic group, P4 and P7 rats showed delayed alveolar development, septal thickening, and disturbances in alveolar structure.PAR2, P38 MAPK, NF-κB, and IL-18 expression at P4, P7, and P10 was significantly higher than in the air group.
Conclusion:
PAR2 is involved in lung injury induced by persistent hyperoxia. Activated PAR2 promotes IL-18 overexpression through the P38 MAPK/NF-κB signaling pathway, which may be an important mechanism of PAR2-mediated lung injury in bronchopulmonary dysplasia.
