Journal
PLOS ONE
Volume 9, Issue 9, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0095254
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Funding
- National Taiwan University Hospital (NTUH) [101-001974]
- National Taiwan University (National Taiwan University Cutting-Edge Steering Research) [10R71608-1]
- NTU-NTUH MediaTek Innovative Medical Electronics Research Center [PC851]
- Taiwan National Science Council [NSC 100-2314-B-002-139, NSC 102-2314-B-002-078-MY3, NSC 101-2911-I-008-001]
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Context: 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. Objective: To investigate whether aldosterone induces galectin-3 secretion in vitro and in vivo. Methods and Results: 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-kappa B 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. Conclusion: This study demonstrated that aldosterone could induce galectin-3 secretion in vitro and in vivo.
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