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Published on: October 19, 2013
[Increased expression of fatty acid binding protein 4 in lungs of preterm rats after hyperoxic lung injury]
Wei Wang1, Zhi-Rui Cui, Li-Xia Cai
1Department of Pediatrics, Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China. xpluo@tjh.tjmu.edu.cn.
Insights
Fatty acid binding protein 4 (FABP4) levels rise in preterm rat lungs following hyperoxic lung injury. This increase in FABP4 may play a role in the development of bronchopulmonary dysplasia (BPD).
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Biochemistry
Context:
- Bronchopulmonary dysplasia (BPD) is a significant complication in preterm infants.
- Hyperoxia is a known risk factor contributing to BPD pathogenesis.
- Fatty acid binding protein 4 (FABP4) is implicated in inflammatory processes.
Purpose:
- To investigate the expression of FABP4 in the lungs and bronchoalveolar lavage fluid (BALF) of preterm rats exposed to hyperoxia (60% O2).
- To determine the relationship between altered FABP4 expression and the development of BPD.
- To quantify FABP4 protein and mRNA levels in lung tissue and FABP4 in BALF.
Summary:
- Hyperoxic lung injury was induced in Sprague-Dawley rats within 6 hours of birth.
- FABP4 protein and mRNA levels in lung tissue, as well as FABP4 levels in BALF, were significantly elevated in the hyperoxic group compared to controls at postnatal days 3, 7, and 14.
- FABP4 immunoreactivity was observed in alveolar macrophages, bronchial epithelial cells, and endothelial cells.
Impact:
- The findings suggest that elevated FABP4 levels in preterm rat lungs following hyperoxic exposure may contribute to the pathogenesis of BPD.
- This study highlights FABP4 as a potential biomarker and therapeutic target for BPD.
- Understanding FABP4's role could lead to novel strategies for preventing or treating BPD.
Objective:
To study the expression of fatty acid binding protein 4 (FABP4) in lungs and bronchoalveolar lavage fluid (BALF) of preterm rats exposed to 60% O2 and to elucidate the relationship between the changes of FABP4 expression and the pathogenesis of bronchopulmonary dysplasia (BPD).
Methods:
Hyperoxic lung injury was induced by exposing to 60% O2 in Spraque-Dawley rats within 6 hours after birth. Rats exposed to air were used as the control group. The lungs from groups aged postnatal days 3, 7 and 14 were removed and dissected from the main bronchi for analysis. Eight rats of each group were used to assess expression of FABP4 in lungs by immunohistochemistry and ELISA. Lung FABP4 mRNA levels were measured by semi-quantitative reverse transcription polymerase chain reaction. The levels of FABP4 in BALF were measured using ELISA.
Results:
FABP4 immunoreactivity was detected in the majority of alveolar macrophages, bronchial epithelial cells and endothelial cells. FABP4 protein levels in lung tissues in the hyperoxic exposure group increased significantly compared with the control group on days 3, 7 and 14 after birth (P<0.05), and FABP4 mRNA levels in lung tissues also increased significantly in the hyperoxic exposure group compared with the control group on days 7 and 14 after birth (P<0.05). The hyperoxic exposure group demonstrated increased FABP4 levels in BALF compared with the control group on days 7 and 14 after birth (P<0.05).
Conclusions:
FABP4 levels increase in preterm rat lungs after hyperoxic lung injury, which may contribute to the pathogenesis of BPD.
