Hyperoxia-induced chronic lung disease in newborn rats is associated with increased activation of phosphorylated ERK1/2 in lung fibroblasts.
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Objective To investigate dynamic changes of extracellular signal regulated protein kinase (ERK) 1/2 in lung fibroblast of newborn rats with chronic lung disease (CLD) caused by hyperoxia.Methods Full-term newborn rats were randomly divided into two groups:air-exposed group and hyperoxia - exposed with 90% oxygen group.Rats were sacrificed separately 3 d,7 d and 14 days after exposure to air or 90% oxygen. Then lung fibroblasts of rats were isolated and primarily cultured. By using Immunocystochemistry,Western-blot and RT-PCR methods,the levels of ERK1/2 protein and expressions of ERK1/2 mRNA were measured. Results The levels of p-ERK1/2 protein in lung fibroblast in the hyperoxia group were significant higher on the 7th day and 14th day after exposure to 90% oxygen compared with those in the air-exposed group (P <0.01 ).And the levels of total ERK1/2 protein and expressions of ERK1/2 mRNA did not change noticeably and were not significantly different between two groups (P >0.05 ).Conclusions The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.
Hyperoxia-associated p-ERK1/2 upregulation in rat lung fibroblasts is hypothesis-generating; leaves open therapeutic relevance in neonatal lung disease.
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Hu et al. (2012) studied this question.
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