Changes in pulmonary tissue structure and KL-6/MUC1 expression in a newborn rat model of hyperoxia-induced bronchopulmonary dysplasia.

Following preterm birth, levels of Krebs von den Lungen-6/mucin 1 (KL-6/MUC1) in serum correlate closely with the development of advanced bronchopulmonary dysplasia (BPD), but the role of KL-6/MUC1 in the development of BPD is unclear. To explore whether a relationship exists between KL-6/MUC1 and pathological changes in BPD and verify such a clinical finding, we established a newborn rat model of 95% oxygen-induced BPD. The development of pulmonary alveoli was evaluated by determining the radial alveolar count (RAC) and examining the location, distribution, and expression of KL-6/MUC1 in pulmonary tissues using a fluorescent immunoassay, Western blot, and reverse transcription polymerase chain reaction. The synchronic expression levels of KL-6/MUC1 in serum, bronchoalveolar lavage fluid (BALF) and pulmonary tissues were examined using an enzyme-linked immunosorbent assay. The mean RAC in the hyperoxia group was significantly lower than in normoxia controls, whereas the expression levels of KL-6/MUC1 were higher. On days 1, 3, 7, and 14, the mean RACs in hyperoxic rats were 15.00, 12.67, 12.00, and 11.33, respectively. The expression levels of KL-6/MUC1 peaked in the experimental group on day 1, and began to decrease slightly after day 3. The expression levels of KL-6/MUC1 in serum and BALF were associated with KL-6/MUC1 expression in pulmonary tissues. We suggest that increased lung KL-6/MUC1 expression appears to be closely associated with impairment of alveolarization in a newborn rat model of hyperoxia-induced BPD. Changes in lung KL-6/MUC1 expression can be evaluated effectively and less invasively by monitoring KL-6/MUC1 in serum and BALF.

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