Temporal expression of Notch in preterm rat lungs exposed to hyperoxia.
- Author:
Hong, WANG
;
Liwen, CHANG
;
Wenbin, LI
- Publication Type:Journal Article
- MeSH:
Aerobiosis;
Animals, Newborn;
Lung/*pathology;
Lung Diseases/etiology;
Lung Diseases/*metabolism;
Lung Diseases/pathology;
RNA, Messenger/biosynthesis;
RNA, Messenger/genetics;
Random Allocation;
Rats, Sprague-Dawley;
Receptors, Notch/*biosynthesis;
Receptors, Notch/genetics
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2005;25(2):159-61, 165
- CountryChina
- Language:English
-
Abstract:
To explore the mechanism of Notch in hyperoxia-induced preterm rat lung injury, 2-days-old preterm SD rats were randomized into control and hyperoxia group (FiO2 > or = 0.85). On day 1, 7, 14 and 21, 8 rat pups of each time point were used to assess histopathological changes of lung with HE staining and to evaluate the expression of Notch1 and Notch3 with immunohistochemistry. Notch1, Notch3, Aquaprin5 (AQP5) and surfactant protein C (SP-C) mRNA were measured by reverse transcription polymerase chain reaction (RT-PCR). The results showed that the lung injury in the hyperoxia group was characterized by retarded lung alveolization and differentiation of alveolar epithelial type II cells (AEC II). Positive staining of Notch1 in hyperoxia group was weaker than controls at every time point (except for day 7), while positive staining of Notch3 was much stronger (P < 0.05, P < 0.01). Notch1, Notch3 mRNA level showed similar change as protein level. AQP5, SP-C mRNA decreased significantly as compared with that of the controls (P < 0.01). We are led to conclude that hyperoxia results in abnormal expression of Notch, which is likely to contribute to the pathogenesis of lung injury through regulating proliferation and transdifferentiation of alveolar epithelial cells.
