Oxygen upregulates nitric oxide synthase gene expression in ovine fetal pulmonary artery endothelial cells

Amy J. North, Kim S. Lau, Timothy S. Brannon, Leeju C. Wu, Lieselotte B. Wells, Zohre German, Philip W. Shaul

Research output: Contribution to journalArticle

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Abstract

Nitric oxide (NO) is critically involved in oxygen-mediated pulmonary vasodilatation in the fetus and newborn. We determined the effects of prolonged alterations in oxygenation on endothelial NO synthase (eNOS) gene expression in early passage ovine fetal intrapulmonary artery endothelial cells (PAEC). PAEC were exposed to PO2 = 50 or 150 mmHg for 48 h, and eNOS protein expression was evaluated by immunoblot analysis. eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation. In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension. The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity. In parallel, there was a 2.8-fold rise in eNOS mRNA abundance. Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability. This process may play an important role in oxygen modulation of pulmonary vasomotor tone in the fetus and newborn.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume270
Issue number4 14-4
StatePublished - Apr 1996

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Nitric Oxide Synthase
Pulmonary Artery
Sheep
Up-Regulation
Endothelial Cells
Oxygen
Gene Expression
Lung
Fetus
Fetal Proteins
Nitric Oxide Synthase Type III
RNA Stability
Nitric Oxide Synthase Type II
Cell Lineage
Vasodilation
Endothelium
Nitric Oxide
Proteins
Arteries
Epithelial Cells

Keywords

  • bronchiolar epithelium
  • Clara cells
  • persistent pulmonary hypertension of the newborn

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Oxygen upregulates nitric oxide synthase gene expression in ovine fetal pulmonary artery endothelial cells. / North, Amy J.; Lau, Kim S.; Brannon, Timothy S.; Wu, Leeju C.; Wells, Lieselotte B.; German, Zohre; Shaul, Philip W.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 270, No. 4 14-4, 04.1996.

Research output: Contribution to journalArticle

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abstract = "Nitric oxide (NO) is critically involved in oxygen-mediated pulmonary vasodilatation in the fetus and newborn. We determined the effects of prolonged alterations in oxygenation on endothelial NO synthase (eNOS) gene expression in early passage ovine fetal intrapulmonary artery endothelial cells (PAEC). PAEC were exposed to PO2 = 50 or 150 mmHg for 48 h, and eNOS protein expression was evaluated by immunoblot analysis. eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation. In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension. The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity. In parallel, there was a 2.8-fold rise in eNOS mRNA abundance. Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability. This process may play an important role in oxygen modulation of pulmonary vasomotor tone in the fetus and newborn.",
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AU - Lau, Kim S.

AU - Brannon, Timothy S.

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AU - German, Zohre

AU - Shaul, Philip W.

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