RESEARCH ARTICLE
Year : 2016  |  Volume : 1  |  Issue : 2  |  Page : 14-20

Galectin-3: A potential biomarker in pulmonary arterial hypertension


1 Department of Cardiology, Xiangya Hospital, Central South University, Changsha, China
2 Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha, China

Correspondence Address:
Prof. Zaixin Yu
Department of Cardiology, Xiangya Hospital, Central South University, 87 Xiangya Road, 410008 Changsha
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2470-7511.248361

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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 < 0.001). Within the subgroups, only by idiopathic PAH (IPAH) patients expressed the lower level of Gal-3 (n = 16, P < 0.001). Gal-3 levels were inversely correlated with mean pulmonary arterial pressure (mPAP) (r = − 0.570, P = 0.021) and PVR (r = − 0.550, P = 0.027), and correlated with cardiac output (r = 0.530, P = 0.035) in IPAH patients. A Gal-3 cutoff value <1.765 ng/ml yielded 93% sensitivity and 88% specificity for IPAH patients. Immunohistochemistry identified Gal-3 distribution throughout the adventitia of the pulmonary arterioles. The expression of Gal-3 mRNA was significantly downregulated in the pulmonary arteries from lung tissue samples in pulmonary hypertension rats. Conclusions: Gal-3 might be involved in the pathogenesis of PAH and plasma Gal-3 could serve as a promising new biomarker of diagnosis and disease severity in IPAH.


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