Neonatal Hyperoxia Induces Pulmonary Hypertension and Rho-kinase Expression in Rats

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Abstract

Background: Chronic oxygen exposure induces pulmonary hypertension in newborn rats. Rho-kinase is upregulated in animal models of hypoxia-induced pulmonary hypertension and Rho-kinase inhibitors decrease the pulmonary arterial pressure. Less is known about the response of Rho-kinase in hyperoxia-induced lung injury in neonates. A rat model of hyperoxia-induced pulmonary injury was established and the expression of Rho-kinase was also assessed in the lungs of newborn rats exposed to prolonged hyperoxia. Methods: Experimental rat pups were exposed to 1 wk of > 95% O2 and a further 2 wk of 60% O2. Control pups were exposed to room air over the same periods. Lung tissues were obtained for biochemical and histochemical assays on postnatal Day 21. Results: Hyperoxia significantly increased type I collagen mRNA expression and total collagen content on postnatal Day 21. Rho-kinase activity was measured as the ratio of phosphorylated ERM to ERM (ezrin, radixin, and moesin) and the ratio was significantly increased on postnatal Day 21 following hyperoxic exposure. Hyperoxic exposure for 3 wk also induced structural features of pulmonary hypertension, as indicated by increased right ventricular hypertrophy and arterial medial wall thickening. Conclusions: The results suggested that Rho-kinase might be involved in the pathogenesis of hyperoxia-induced pulmonary hypertension.
Original languageEnglish
Pages (from-to)59-64
Number of pages6
Journal中華民國兒童胸腔醫學會雜誌
Volume9
Issue number3
Publication statusPublished - 2013

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rho-Associated Kinases
Hyperoxia
Pulmonary Hypertension
Lung Injury
Lung
Right Ventricular Hypertrophy
Collagen Type I
Arterial Pressure
Collagen
Animal Models
Air
Oxygen
Messenger RNA

Keywords

  • Collagen
  • hyperoxia
  • pulmonary hypertension
  • Rho-kinase

Cite this

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title = "Neonatal Hyperoxia Induces Pulmonary Hypertension and Rho-kinase Expression in Rats",
abstract = "Background: Chronic oxygen exposure induces pulmonary hypertension in newborn rats. Rho-kinase is upregulated in animal models of hypoxia-induced pulmonary hypertension and Rho-kinase inhibitors decrease the pulmonary arterial pressure. Less is known about the response of Rho-kinase in hyperoxia-induced lung injury in neonates. A rat model of hyperoxia-induced pulmonary injury was established and the expression of Rho-kinase was also assessed in the lungs of newborn rats exposed to prolonged hyperoxia. Methods: Experimental rat pups were exposed to 1 wk of > 95{\%} O2 and a further 2 wk of 60{\%} O2. Control pups were exposed to room air over the same periods. Lung tissues were obtained for biochemical and histochemical assays on postnatal Day 21. Results: Hyperoxia significantly increased type I collagen mRNA expression and total collagen content on postnatal Day 21. Rho-kinase activity was measured as the ratio of phosphorylated ERM to ERM (ezrin, radixin, and moesin) and the ratio was significantly increased on postnatal Day 21 following hyperoxic exposure. Hyperoxic exposure for 3 wk also induced structural features of pulmonary hypertension, as indicated by increased right ventricular hypertrophy and arterial medial wall thickening. Conclusions: The results suggested that Rho-kinase might be involved in the pathogenesis of hyperoxia-induced pulmonary hypertension.",
keywords = "Collagen, hyperoxia, pulmonary hypertension, Rho-kinase",
author = "Liang-Ti Huang and Hsiu-Chu Chou and Yeh, {Tsu Fu} and Chung-Ming Chen",
year = "2013",
language = "English",
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pages = "59--64",
journal = "中華民國兒童胸腔醫學會雜誌",
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TY - JOUR

T1 - Neonatal Hyperoxia Induces Pulmonary Hypertension and Rho-kinase Expression in Rats

AU - Huang, Liang-Ti

AU - Chou, Hsiu-Chu

AU - Yeh, Tsu Fu

AU - Chen, Chung-Ming

PY - 2013

Y1 - 2013

N2 - Background: Chronic oxygen exposure induces pulmonary hypertension in newborn rats. Rho-kinase is upregulated in animal models of hypoxia-induced pulmonary hypertension and Rho-kinase inhibitors decrease the pulmonary arterial pressure. Less is known about the response of Rho-kinase in hyperoxia-induced lung injury in neonates. A rat model of hyperoxia-induced pulmonary injury was established and the expression of Rho-kinase was also assessed in the lungs of newborn rats exposed to prolonged hyperoxia. Methods: Experimental rat pups were exposed to 1 wk of > 95% O2 and a further 2 wk of 60% O2. Control pups were exposed to room air over the same periods. Lung tissues were obtained for biochemical and histochemical assays on postnatal Day 21. Results: Hyperoxia significantly increased type I collagen mRNA expression and total collagen content on postnatal Day 21. Rho-kinase activity was measured as the ratio of phosphorylated ERM to ERM (ezrin, radixin, and moesin) and the ratio was significantly increased on postnatal Day 21 following hyperoxic exposure. Hyperoxic exposure for 3 wk also induced structural features of pulmonary hypertension, as indicated by increased right ventricular hypertrophy and arterial medial wall thickening. Conclusions: The results suggested that Rho-kinase might be involved in the pathogenesis of hyperoxia-induced pulmonary hypertension.

AB - Background: Chronic oxygen exposure induces pulmonary hypertension in newborn rats. Rho-kinase is upregulated in animal models of hypoxia-induced pulmonary hypertension and Rho-kinase inhibitors decrease the pulmonary arterial pressure. Less is known about the response of Rho-kinase in hyperoxia-induced lung injury in neonates. A rat model of hyperoxia-induced pulmonary injury was established and the expression of Rho-kinase was also assessed in the lungs of newborn rats exposed to prolonged hyperoxia. Methods: Experimental rat pups were exposed to 1 wk of > 95% O2 and a further 2 wk of 60% O2. Control pups were exposed to room air over the same periods. Lung tissues were obtained for biochemical and histochemical assays on postnatal Day 21. Results: Hyperoxia significantly increased type I collagen mRNA expression and total collagen content on postnatal Day 21. Rho-kinase activity was measured as the ratio of phosphorylated ERM to ERM (ezrin, radixin, and moesin) and the ratio was significantly increased on postnatal Day 21 following hyperoxic exposure. Hyperoxic exposure for 3 wk also induced structural features of pulmonary hypertension, as indicated by increased right ventricular hypertrophy and arterial medial wall thickening. Conclusions: The results suggested that Rho-kinase might be involved in the pathogenesis of hyperoxia-induced pulmonary hypertension.

KW - Collagen

KW - hyperoxia

KW - pulmonary hypertension

KW - Rho-kinase

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