Patients with primary aldosteronism are associated with increased myocardial fibrosis. Galectin-3 is one of the most important mediators between macrophage activation and myocardial fibrosis. The objective of the study was to investigate whether aldosterone induces galectin-3 secretion in vitro and in vivo. We investigated the possible molecular mechanism of aldosterone-induced galectin-3 secretion in macrophage cell lines (THP-1 and RAW 264.7 cells). Aldosterone induced galectin-3 secretion through mineralocorticoid receptors via the PI3K/Akt and NF-κB transcription signaling pathways. In addition, aldosterone-induced galectin-3 expression enhanced fibrosis-related factor expression in fibroblasts. We observed that galectin-3 mRNA from peripheral blood mononuclear cells and serum galectin-3 levels were both significantly increased in mice implanted with aldosterone pellets on days 7 and 14. We then conducted a prospective preliminary clinical study to investigate the association between aldosterone and galectin-3. Patients with aldosterone-producing adenoma had a significantly higher plasma galectin-3 level than patients with essential hypertension. One year after adrenalectomy, the plasma galectin-3 level had decreased significantly in the patients with aldosterone-producing adenoma. This study demonstrated that aldosterone could induce galectin-3 secretion in vitro and in vivo.
Authors: Yen-Hung Lin, Chia-Hung Chou, Xue-Ming Wu, Yi-Yao Chang, Chi-Sheng Hung, Ying-Hsien Chen, Yu-Lin Tzeng, Vin-Cent Wu, Yi-Lwun Ho, Fon-Jou Hsieh, Kwan-Dun Wu
Keywords: galectin-3, myocardial fibrosis
DOI Number: 10.1371/journal.pone.0095254 Publication Year: 2014
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