2011PubMedRequires access

[Expression of ERK1/2 protein in lung tissues of newborn rats with hyperoxia-induced chronic lung disease].

Yu Hu, Xueyan Liu, Jianhua Fu, Xindong Xue

Open publisher page 0 citations

Abstract

OBJECTIVE: To study the expression of extracellular signal regulated protein kinase (ERK) 1/2 in lung tissues of newborn rats with chronic lung disease (CLD) caused by hyperoxia. METHODS: Forty-eight full-term newborn rats were randomly divided into two groups: hyperoxia and control. The two groups were exposed to a hyperoxic gas mixture (0.90 O(2)) for an induction of CLD and room air within 12 hrs after birth, respectively. The levels of ERK1/2 protein and mRNA in lung tissues were measured using immunohistochemistry, Western blot and real-time PCR methods on postnatal days 3, 7 and 14. The severity of pulmonary fibrosis was evaluated. RESULTS: The expression of p-ERK protein in lung tissues in the hyperoxia group was significantly higher than that in the control group on postnatal days 7 and 14 (P<0.01). There were no significant differences in the levels of total ERK1/2 protein and ERK1/2 mRNA. CONCLUSIONS: The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.

About this research paper

What this paper is about

OBJECTIVE: To study the expression of extracellular signal regulated protein kinase (ERK) 1/2 in lung tissues of newborn rats with chronic lung disease (CLD) caused by hyperoxia. METHODS: Forty-eight full-term newborn rats were randomly divided into two groups: hyperoxia and control. The two groups were exposed to a hyperoxic gas mixture (0.90 O(2)) for an induction of CLD and room air within 12 hrs after birth, respectively. The levels of ERK1/2 protein and mRNA in lung tissues were measured using immunohistochemistry, Western blot and real-time PCR methods on postnatal days 3, 7 and 14. The severity of pulmonary fibrosis was evaluated. RESULTS: The expression of p-ERK protein in lung tissues in the hyperoxia group was significantly higher than that in the control group on postnatal days 7 and 14 (P<0.01). There were no significant differences in the levels of total ERK1/2 protein and ERK1/2 mRNA. CONCLUSIONS: The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVE: To study the expression of extracellular signal regulated protein kinase (ERK) 1/2 in lung tissues of newborn rats with chronic lung disease (CLD) caused by hyperoxia. METHODS: Forty-eight full-term newborn rats were randomly divided into two groups: hyperoxia and control. The two groups were exposed to a hyperoxic gas mixture (0.90 O(2)) for an induction of CLD and room air within 12 hrs after birth, respectively. The levels of ERK1/2 protein and mRNA in lung tissues were measured using immunohistochemistry, Western blot and real-time PCR methods on postnatal days 3, 7 and 14. The severity of pulmonary fibrosis was evaluated. RESULTS: The expression of p-ERK protein in lung tissues in the hyperoxia group was significantly higher than that in the control group on postnatal days 7 and 14 (P<0.01). There were no significant differences in the levels of total ERK1/2 protein and ERK1/2 mRNA. CONCLUSIONS: The activation of phosphorated ERK1/2 may lead to lung fibrosis caused by hyperoxia in newborn rats.

Key concepts: Hyperoxia, Lung, Western blot, Immunohistochemistry, Medicine, Messenger RNA, Bronchopulmonary dysplasia, Pulmonary fibrosis

Related papers

Back to paper searchBrowse research topicsOriginal source
[Expression of ERK1/2 protein in lung tissues of newborn rats with hyperoxia-induced chronic lung disease]. — Research Paper | ScholarLens