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Expression and significance of transcriptional co-activator with PDZ-binding motif in neonatal rat with chronic lung disease induced by hyperoxia / 中国小儿急救医学
Chinese Pediatric Emergency Medicine ; (12): 521-526, 2020.
Article in Chinese | WPRIM | ID: wpr-864951
ABSTRACT

Objective:

To investigate expression level of transcriptional co-activator with PDZ-binding motif(TAZ) in neonatal rats with chronic lung diseases induced by hyperoxia and explore its potential role in the disease.

Methods:

The model of high-oxygen-induced lung injury in neonatal rats was established by continuous inhalation of high-concentration oxygen.The rats in experimental group inhaled 85% oxygen, while the rats in control group inhaled air.The lung tissues were collected at the 1st, 3rd, 7th, 14th and 21st day, and the lung tissue sections were stained with hematoxylin and eosin staining to observe the pathological changes of the lung.In addition, the dynamic expressions of TAZ, surfactant protein C(SPC) and aquaporin-5(AQP5) in lung tissue were detected by real-time PCR, western blot and immunohistochemistry staining.

Results:

In the experimental group, with the prolongation of oxygen inhalation time, we found that the alveolar cavity increased, the number decreased, the alveolar septum thickened, and the alveolar structure was simplified.Compared with the control group, there was no difference in TAZ, SPC and AQP5 expression at 1st and 3rd days in the lung tissue in the experimental group( P>0.05). However, at 7, 14 and 21 days, the expression of TAZ in mRNA and protein level in lung tissue in experimental group decreased significantly, and the expression of SPC in mRNA and protein level increased significantly, while the expression of AQP5 in mRNA and protein level decreased, the differences were all statistically significant( P<0.05).

Conclusion:

Hyperoxia can cause alveolar structure disorder and pulmonary arrested development in neonatal rat.The expression levels of SPC and AQP5 show that the injury of type Ⅰ alveolar epithelial cells (AEC Ⅰ) is severe.Although the number of type Ⅱ alveolar epithelial cells (AEC Ⅱ) increased, but its differentiation capacity decreased obviously.The decrease of TAZ expression may cause AEC Ⅱ lose the function of differentiation into AEC Ⅰ.
Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Pediatric Emergency Medicine Year: 2020 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Pediatric Emergency Medicine Year: 2020 Type: Article