Research
Print page Print page
Switch language
The Capital Region of Denmark - a part of Copenhagen University Hospital
Published

Downregulation of aquaporin-1 in alveolar microvessels in lungs adapted to chronic heart failure

Research output: Contribution to journalJournal articleResearchpeer-review

  1. The Effect of Different Comorbidities on Survival of Non-small Cells Lung Cancer Patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Risk of chronic bronchitis in twin pairs discordant for smoking

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Genetic Influences on Pulmonary Function: A Large Sample Twin Study

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Genome-wide association study identifies locus at chromosome 2q32.1 associated with syncope and collapse

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Diverse repertoire of human adipocyte subtypes develops from transcriptionally distinct mesenchymal progenitor cells

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Reappraisal of variants previously linked with sudden infant death syndrome: results from three population-based cohorts

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Clinical implications of electrocardiographic bundle branch block in primary care

    Research output: Contribution to journalJournal articleResearchpeer-review

View graph of relations
The threshold pressure for lung edema formation is increased in severe chronic heart failure (CHF) due to reduced microvascular permeability. The water channel aquaporin-1 (AQP1) is present in the pulmonary microvascular endothelium, and a number of studies suggest the importance of AQP1 as a molecular determinant of pulmonary microvascular water transport. The present study examined the abundance and localization of AQP1 in lungs from rats with CHF. We used two different models of CHF: ligation of the left anterior descending coronary artery (LAD ligation) and aorta-banding (AB). Sham-operated rats served as controls. Echocardiographic verification of left ventricular dysfunction, enhanced left ventricular end-diastolic pressure, and right ventricular hypertrophy confirmed the presence of CHF. Western blotting of whole-lung homogenates revealed significant downregulation of AQP1 in LAD-ligated rats (24 h: 58 ± 5% of sham; 3 weeks: 8 ± 3% of sham; 9 weeks: 16 ± 6% of sham) and after AB (30 weeks: 37 ± 5% of sham), whereas the protein levels of the specific endothelial cell marker PECAM-1 was increased 3 weeks after LAD ligation (229 ± 20% of sham), but unchanged after 9 weeks and in the AB rats compared to controls. Immunohistochemical examination 3 weeks after LAD ligation showed intact labeling of PECAM-1 but an almost complete absence of AQP1 in the pulmonary alveolar microvessels in the CHF rats. These results suggest that downregulation of AQP1 in the alveolar microvessels may act as a compensatory mechanism to protect against formation of excessive pulmonary edema in CHF.
Original languageEnglish
JournalLung
Volume189
Issue number2
Pages (from-to)157-66
Number of pages10
ISSN0341-2040
DOIs
Publication statusPublished - 2011

    Research areas

  • Animals, Antigens, CD31, Aorta, Aquaporin 1, Chronic Disease, Coronary Vessels, Disease Models, Animal, Down-Regulation, Endothelium, Vascular, Heart Failure, Ligation, Male, Microvessels, Pulmonary Alveoli, Pulmonary Edema, Rats, Rats, Wistar

ID: 33267722