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Developmental changes in arginase expression and activity in the lung.

Jaques Belik1, Darakhshanda Shehnaz, Jingyi Pan

  • 1Department of Pediatrics, Physiology and Experimental Medicine, The Hospital for Sick Children Research Institute, and University of Toronto, 555 University Ave., Toronto, Ontario, M5G 1X8 Canada. jaques.belik@sickkids.ca

American Journal of Physiology. Lung Cellular and Molecular Physiology
|January 15, 2008
PubMed
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Arginase II activity and expression are highest in fetal rat lungs, decreasing with age. This suggests arginase plays a key role in regulating pulmonary vascular resistance and nitric oxide production during development.

Area of Science:

  • Pulmonary Medicine
  • Developmental Biology
  • Biochemistry

Background:

  • Arginases and nitric oxide (NO) synthases compete for L-arginine.
  • Increased arginase activity in pulmonary diseases correlates with reduced NO production and smooth muscle relaxation.

Purpose of the Study:

  • To investigate the developmental patterns of arginase activity and isoform expression in the rat lung.
  • To determine if lung arginase activity is highest in the fetus.

Main Methods:

  • Measured arginase isoforms expression and total activity in fetal, newborn, and adult rat lung, pulmonary artery, and bronchial tissue.
  • Assessed pulmonary arterial muscle force generation with and without the arginase inhibitor nor-NOHA.

Main Results:

Related Experiment Videos

  • Arginase II content and total arginase activity were highest in fetal lung, bronchi, and pulmonary artery, decreasing with age.
  • Pulmonary arterial force generation was significantly reduced in fetuses and newborns with arginase inhibition.
  • Bronchial tissue showed no significant change in force generation after arginase inhibition.

Conclusions:

  • Arginase II expression and activity are developmentally regulated, peaking in fetal life.
  • Elevated arginase expression/activity may contribute to high pulmonary vascular resistance and low lung NO production prenatally.