Objective：To investigate the expression level of long non-coding RNA（lncRNA）GM15886 in lung tissues of bronchopulmonary dysplasia（BPD）induced by hyperoxia in neonatal mice and its mechanism in BPD. Methods：High expressed GM15886 was selected by previous lncRNA microarray. IntaRNA，Multi Experiment Matrix and Ensemble database were applied to predict GM15886 target genes. Sixty-four newly born C57BL/6J mice were randomly divided into the hyperoxic group and the air group，with 32 mice in each group. Newborn mice in the hyperoxia group were exposed to 95% oxygen，while those in the air group were exposed to air. Mice were sacrificed on day 0，day 3，day 5 and day 7，respectively，and the pathological changes of pulmonary tissues were analyzed via HE staining，the expression levels of GM15886 and homeodomain-interacting protein kinase 1（HIPK1）mRNA was detected by using QPCR，the expression of HIPK1 at different time points was detected by immunohistochemistry. Results：IntaRNA predicted the end of GM15886 sequence overlaps with the gene HIPK1. The expression of GM15886 in neonatal mice in the hyperoxia group increased gradually on day 3，day 5 and day 7，（1.91±0.28，2.12±0.38，and 2.35±0.43，respectively），and the differences were statistically significant compared with day 0（all P < 0.05）. The relative expressions of HIPK1 on day 3，day 5 and day 7 were 1.16±0.33，0.92±0.31，and 3.12±0.46，respectively. The expression level on day 7 was higher than that on day 0，day 3，day 5（all P < 0.05）. The expression of HIPK1 protein changed in the same way as mRNA. Conclusion：With the extension of hyperoxic exposure time，the expression of GM15886 in lung tissues increased gradually. GM15886 might participate in the pathogenesis of BPD by relugating HIPK1 expression.