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[Dynamic expression and role of SUMO-modified C/EBPα in preterm rats with bronchopulmonary dysplasisa induced by
Yue Zhu1, Hong-Yan Lu, Xiao-Bo Hao
1Department of Pediatrics, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, China. lhy5154@163.com.
Insights
Hyperoxia exposure in preterm rats increased SUMO-modified C/EBPα, potentially causing lung cell over-proliferation and differentiation issues in bronchopulmonary dysplasia (BPD). This study highlights a novel mechanism in BPD development.
Area of Science:
- Neonatal Physiology
- Cellular Biology
- Pulmonary Medicine
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting preterm infants.
- Hyperoxia exposure is a primary cause of BPD, leading to lung injury and impaired development.
- The role of SUMO-modified CCAAT enhancer binding protein alpha (C/EBPα) in hyperoxia-induced lung injury is not well understood.
Purpose of the Study:
- To investigate the expression of SUMO-modified C/EBPα in a preterm rat model of BPD induced by hyperoxia.
- To explore the potential role of SUMO-modified C/EBPα in the pathogenesis of BPD.
Main Methods:
- Preterm rats were exposed to hyperoxia to induce BPD.
- Lung tissues were analyzed for glycogen content (PAS staining) and cell proliferation (Ki67 immunohistochemistry).
- Protein levels of SUMO1, C/EBPα, and SUMO-modified C/EBPα were quantified using Western blot and co-immunoprecipitation.
Main Results:
- Hyperoxia exposure led to altered glycogen content and increased Ki67 expression in lung tissues.
- Expression of C/EBPα decreased over time in hyperoxia-exposed rats, while SUMO1 and SUMO-modified C/EBPα were significantly upregulated.
- SUMO-modified C/EBPα positively correlated with glycogen content and Ki67 expression.
Conclusions:
- Increased expression of SUMO-modified C/EBPα may contribute to alveolar epithelial cell over-proliferation and differentiation disorders in BPD.
- This suggests a potential therapeutic target for managing BPD.
- SUMOylation of C/EBPα plays a critical role in hyperoxia-induced lung injury.
Objective:
To study the expression of SUMO-modified CCAAT enhancer binding protein α (C/EBPα) in preterm rat model of bronchopulmonary dysplasisa (BPD) induced by hyperoxia exposure and its role.
Methods:
Eighteen preterm rats were randomly divided into an air group and a hyperoxia group (n=9 each). The model of BPD was prepared in preterm rats exposed to hyperoxia. The rats from the two groups were sacrificed on postnatal days 4, 7 and 14 respectively (3 rats at each time) and lung tissues were harvested. Periodic acid-Schiff (PAS) staining was used to observe the differentiation of rat lung tissues. Ki67 expression was detected by immunohistochemistry. Western blot was used to measure the protein expression of small ubiquitin-related modifier-1(SUMO1) and C/EBPα. A co-immunoprecipitation assay was performed to measure the protein expression of SUMO-modified C/EBPα.
Results:
Compared with the air group, the hyperoxia group showed a decreased glycogen content in the lung tissue on postnatal day 4, and an increased content on postnatal days 7 and 14. Over the time of hyperoxia exposure, the hyperoxia group showed an increased expression of Ki67 in the lung tissue compared with the air group at all time points. Compared with the air group, the protein expression of C/EBPα increased on postnatal day 4 and decreased on postnatal days 7 and 14 in the hyperoxia group (P<0.05). The hyperoxia group had significantly upregulated expression of SUMO1 and SUMO-modified C/EBPα compared with the air group at all time points (P<0.05). In the hyperoxia group, the protein expression of SUMO-modified C/EBPα was positively correlated with the glycogen content (r=0.529, P<0.05) and the expression of Ki67 (r=0.671, P<0.05).
Conclusions:
Hyperoxia may induce over-proliferation and differentiation disorders of alveolar epithelial cells in preterm rat model of BPD, possibly through an increased expression of SUMO-modified C/EBP&alpha.
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