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Published on: May 4, 2020
Cell Division Cycle 2 Protects Neonatal Rats Against Hyperoxia-Induced Bronchopulmonary Dysplasia
Zhongying Li1, Yanhong Chen2, Wenrong Li3
1Department of Pediatric, Binzhou People's Hospital, Binzhou, China.
Insights
Cell division cycle 2 (CDC2) protects against hyperoxia-induced lung injury in neonatal rats. Upregulating CDC2 improves cell viability and reduces apoptosis and inflammation, alleviating lung damage in bronchopulmonary dysplasia (BPD).
Area of Science:
- Cell Biology
- Pulmonary Medicine
- Neonatology
Background:
- Bronchopulmonary dysplasia (BPD) is a critical lung disease affecting preterm infants, often exacerbated by hyperoxia.
- Understanding the molecular mechanisms underlying BPD pathogenesis is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the role of cell division cycle 2 (CDC2) in the histopathological changes associated with hyperoxia-induced BPD.
- To assess the impact of CDC2 on lung cell viability, apoptosis, and inflammation in a rat model of BPD.
Main Methods:
- Neonatal rats and A549 lung cells were exposed to hyperoxia to induce BPD.
- CDC2 mRNA and protein expression were quantified using qRT-PCR and Western blot.
- Lung tissue fibrosis was evaluated using hematoxylin-eosin staining.
- Cell viability and apoptosis were assessed via CCK-8 assay and flow cytometry.
- Inflammatory markers (TNF-α, IL-6, IL-1β) were measured using ELISA.
- In vivo studies involved injecting pcDNA3.1-CDC2 into rats to evaluate CDC2's protective effects.
Main Results:
- CDC2 expression was significantly decreased in hyperoxia-induced BPD lung tissues and A549 cells.
- Fibrosis and histopathological damage were increased in the lungs of BPD rats.
- Overexpression of CDC2 enhanced cell viability and Bcl-2 expression while reducing apoptosis, Bax, caspase-3 expression, and inflammation in hyperoxia-exposed A549 cells.
- Upregulation of CDC2 ameliorated lung tissue damage in the BPD rat model.
Conclusions:
- CDC2 plays a protective role in hyperoxia-induced lung injury.
- Overexpressing CDC2 promotes cell viability and inhibits apoptosis and inflammation, thereby alleviating lung histopathological changes in neonatal BPD.
- CDC2 represents a potential therapeutic target for managing BPD.
Purpose:
Hyperoxia-induced bronchopulmonary dysplasia (BPD) is a lung disease in preterm infants. We aimed to explore the role of cell division cycle 2 (CDC2) on histopathologic changes of lung tissues, as well as the viability, apoptosis, and inflammation of lung cells in rats with hyperoxia-induced BPD.
Materials And Methods:
Hyperoxia-induced BPD in neonatal rats and hyperoxia-induced A549 cells were constructed. The mRNA expression of CDC2 was detected by qRT-PCR. The fibrosis score of lung tissues was evaluated by hematoxylin-eosin staining. The viability and apoptosis of A549 cells were detected by cell counting kit-8 assay and flow cytometry. The protein expressions of bcl-2, bax, and caspase-3 were measured by western blot. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β in A549 cells were detected by enzyme-linked immunosorbent assay. The pcDNA3.1-CDC2 was injected into rats to determine the role of CDC2 in hyperoxia-induced BPD in vivo.
Results:
The expression of CDC2 was decreased in lung tissues of neonatal rats with hyperoxia-induced BPD and hyperoxia-induced A549 cells. The fibrosis score was increased in the lung tissues of neonatal rats with hyperoxia-induced BPD. Overexpression of CDC2 increased the viability and protein expression of bcl-2; and inhibited the apoptosis, inflammation, and protein expression of bax and caspase-3 in hyperoxia-induced A549 cells. Up-regulation of CDC2 alleviated the histopathologic changes in lung tissues of neonatal rats with hyperoxia-induced BPD.
Conclusion:
Overexpression of CDC2 promoted the viability and inhibited the apoptosis and inflammation of hyperoxia-induced cells, and alleviated the histopathologic changes of lung tissues in neonatal rats with hyperoxia-induced BPD.
