Effect of hypercarbia on surface proteins of cultured bovine endothelial cells

Sharon Rounds, Damani Piggott, Doloretta D. Dawicki, Harrison W. Farber

Research output: Contribution to journalArticle

Abstract

Hypercarbia is a common complication of respiratory failure, and the technique of 'permissive hypercapnia' is used to ventilate individuals with increased peak airway pressures on mechanical ventilators, resulting in elevated arterial PCO2. We studied the effects of hypercarbia on cultured bovine aortic and main pulmonary artery endothelial cell surface proteins, assessing cell surface iodination using lactoperoxidase bound to latex microspheres. We found that 4 h of exposure to 10% CO2 increased the display of substances of apparent molecular masses of 27, 47, and 52 kDa. This effect was not mimicked by acidotic media. Western blots of detergent extracts of main pulmonary artery endothelial cell monolayers did not show increased expression of carbonic anhydrase IV (molecular mass = 52 kDa) after incubation under hypercarbic conditions. Hypercarbia did not change the pattern of [35S]methionine incorporation into endothelial cell proteins. We conclude that hypercarbia of 4-h duration changes iodinated endothelial cell surface proteins. We speculate that this effect may be related to changes in secretion or display of apical cell membrane-associated proteins.

Original languageEnglish (US)
Pages (from-to)L1141-L1146
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume273
Issue number6 17-6
DOIs
StatePublished - Jan 1 1997

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Keywords

  • Anoxia
  • Aortic and pulmonary artery endothelial cells
  • Carbon dioxide
  • Hypercapnia
  • Hypoxia
  • Iodination
  • Lactoperoxidase

ASJC Scopus subject areas

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

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