Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secretory, clear cell, and rhabdoid meningiomas are rare variants of meningiomas characterized by unique histologies and behaviors. Extracellular matrix proteins provide a morphologic structure and influence the biologic behavior of tumors. However, the effects of extracellular matrix proteins on morphologies and biologic behaviors of secretory meningioma, clear cell meningioma, and rhabdoid meningioma have not been established. We evaluated the expression of matrix metalloproteinase 2, matrix metalloproteinase 9, galectin-3, fibronectin, and collagen IV in a series of those rare variants of meningioma and verified their clinicopathologic significance. A total 51 cases included 12 secretory meningiomas, 9 clear cell meningiomas, and 30 rhabdoid meningiomas. Extracellular matrix proteins showed different expression patterns according to the histologic subtypes, and messenger RNA levels were well correlated with immunoexpressions. Secretory meningiomas showed high expressions of fibronectin and galectin-3. Clear cell meningiomas showed high expression of matrix metalloproteinase 2, matrix metalloproteinase 9, and collagen IV. Rhabdoid meningiomas showed high expressions of matrix metalloproteinase 9, galectin-3, and fibronectin. Clinically, high expression of matrix metalloproteinase 9 was associated with tumor recurrence (P < .001) and local invasion at the time of diagnosis (P = .018) among the extracellular matrix-related proteins, and was also associated with shorter recurrence-free survival (P = .025) in the patients with rhabdoid meningioma. In conclusion, the differential expressions of extracellular matrix-related genes according to the histologic subtypes appear to be involved in biologic behavior and clinical outcome, and high matrix metalloproteinase 9 expression is associated with recurrences in rhabdoid meningiomas.
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PMID:Differential expression of extracellular matrix-related genes in rare variants of meningioma. 2299 27

Activation of the mineralocorticoid receptor has been shown to be deleterious in cardiovascular diseases (CVDs). We have recently shown that lipocalin 2 (Lcn2), or neutrophil gelatinase-associated lipocalin (NGAL), is a primary target of aldosterone/mineralocorticoid receptor in the cardiovascular system. Lcn2 is a circulating protein, which binds matrix metalloproteinase 9 and modulates its stability. We hypothesized that Lcn2 could be a mediator of aldosterone/mineralocorticoid receptor profibrotic effects in the cardiovascular system. Correlations between aldosterone and profibrotic markers, such as procollagen type I N-terminal peptide, were investigated in healthy subjects and subjects with abdominal obesity. The implication of Lcn2 in the mineralocorticoid pathway was studied using Lcn2 knockout mice subjected to a nephrectomy/aldosterone/salt (NAS) challenge for 4 weeks. In human subjects, NGAL/matrix metalloproteinase 9 was positively correlated with plasma aldosterone and fibrosis biomarkers. In mice, loss of Lcn2 prevented the NAS-induced increase of plasma procollagen type I N-terminal peptide, as well as the increase of collagen fibers deposition and collagen I expression in the coronary vessels and the aorta. The lack of Lcn2 also blunted the NAS-induced increase in systolic blood pressure. Ex vivo, treatment of human fibroblasts with recombinant Lcn2 induced the expression of collagen I and the profibrotic galectin-3 and cardiotrophin-1 molecules. Our results showed that Lcn2 plays a key role in aldosterone/mineralocorticoid receptor-mediated vascular fibrosis. The clinical data indicate that this may translate in human patients. Lcn2 is, therefore, a new biotarget in cardiovascular fibrosis induced by mineralocorticoid activation.
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PMID:Neutrophil Gelatinase-Associated Lipocalin, a Novel Mineralocorticoid Biotarget, Mediates Vascular Profibrotic Effects of Mineralocorticoids. 2598 63