Related Experiment Video
Updated: Jun 22, 2026

Quantifying Pulmonary Microvascular Density in Mice Across Lobules
Published on: January 3, 2025
Caveolin-1 Expression and Hemodynamics in COPD Patients
Lars C Huber1, Alex Soltermann, Manuel Fischler
1Working Group for Pulmonary Hypertension, Department for Internal Medicine, University Hospital Zurich, Zurich, Switzerland.
Abstract:
Caveolin-1 is a regulator of both intracellular calcium homeostasis and endothelial nitric oxide synthase and may play a pathogenetic role in pulmonary hypertension. In the present study, we aimed to investigate the correlations between pulmonary hemodynamics and vessel morphology including the expression of Caveolin-1 in pulmonary arterioles from patients with chronic obstructive pulmonary disease (COPD) who underwent lung-volume reduction surgery. Staining and subsequent analysis was performed on paraffin-embedded lung tissue from COPD patients (n = 12). Pulmonary arteries with an external diameter of 100-500microm were analysed. Immunhistochemistry with antibodies against caveolin-1 was performed and intensity was assessed. Morphometric data were obtained by using computer-assisted imaging software. The findings were quantified and correlated to hemodynamic data obtained by right-heart catheterization. In COPD patients with pulmonary hypertension (n = 5), the expression of caveolin-1 within the medial smooth muscle cell layer was found to be increased, whereas the intimal caveolin-1 was more prominently expressed in COPD patients with normal pulmonary pressures (n = 7). The ratio between these expression patterns was positively correlated to the mean pulmonary artery pressure. Similar findings were observed for the ratio between intimal and medial thickness as well as for the expression of smooth muscle actin (SMA).Taken together, the expression of caveolin-1 within medial smooth muscle cells of pulmonary arteries in patients with COPD is associated with pulmonary hypertension. Our results thus emphasize a potential novel player in the pathogenesis of COPD-associated pulmonary hypertension.
Related Concept Videos
COPD: Pathogenesis and Clinical Features
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
Chronic Obstructive Pulmonary Disease IV: Clinical Manifestations
Chronic Obstructive Pulmonary Disease II: Emphysema
Chronic Obstructive Pulmonary Disease-IV: Assessement and Diagnostic Studies
Medical History
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

