Abstract
Objectives: Pulmonary arterial hypertension (PAH) is a syndrome resulting from a restricted flow through the pulmonary arterial circulation, giving rise to increased pulmonary vascular resistance (PVR) and ultimately right heart failure. Previous reports have suggested that Galectin-3 (Gal-3) induced endothelial cell morphogenesis and regulated myofibroblast activation. The aim of this study was to determine the diagnostic utility of circulating Gal-3 as a potential biomarker of disease severity in PAH. Methods: Gal-3 was measured in plasma from 31 patients with PAH, diagnosed from the right heart catheterization as well as 18 healthy controls by ELISA. Chronic hypoxia-induced pulmonary hypertension models were established in Sprague-Dawley rats. Lung tissues were collected for histological analysis including Gal-3 lung qualitative localization by immunohistochemistry. Total mRNA was extracted from pulmonary arteries in rats and quantitative polymerase chain reaction was performed with total cellular mRNA to measure Gal-3 expression. Results: Plasma level of Gal-3 was significantly decreased in PAH patients compared with healthy controls (P
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