Galectin-3-binding protein: a serological and histological assessment in accordance with hepatitis C-related liver fibrosis

Abstract

Objectives. Invasive liver biopsy is the current method for the assessment of liver fibrosis. In search of non-invasive alternatives, galectin-3-binding protein was introduced as a candidate-marker of hepatitis C-related fibrosis based on serum proteomics.We investigated the role of galectin-3-binding protein as a single-marker of significant fibrosis and cirrhosis by means of serology and histology and studied the role of glycosylation on the expression in hepatitis C-and alcohol-related cirrhosis. Methods. Sera and available biopsies of hepatitis C patients with various fibrosis-gradesand patients with alcohol-related cirrhosis were used for galectin-3-binding protein measurements by enzyme-linked immunosorbent assay and immunohistochemistry, respectively. Glycosylation-effect was analyzed by Western blot. Data was analyzed in accordance to fibrosis.Results. Galectin-3-binding protein was increased during cirrhosis (22.7 ± 10.1 µg/mL) in contrast to mild (11.3 ± 6.4 µg/mL) and moderate fibrosis (13.4 ± 8.3 µg/mL) (p < 0.001; p = 0.004, respectively). Receiver operator characteristics curves showed areas under the curve of 0.68 and 0.81 for the detection of respectively significant fibrosis and cirrhosis. Similar findings in hepatic expression were obtained, in which cirrhosis was associated with diffuse, parenchymal expression (p = 0.002). The observed difference between hepatitis C-and alcohol-related cirrhosis (13.5 ± 9.0 µg/mL) (p = 0.009) could not be explained by glycosylation. (mean ± standard deviation) Conclusions. Our recent findings confirm our initial proteome results on serological and histological level as well as the role of galectin-3-binding protein as a marker of 4 4 hepatitis C-related fibrosis, especially cirrhosis. Implication of this protein in future multi-marker study should be considered.

Involvement of galectin-3 in cadmium-induced cardiac toxicity

“…Increased inflammation and fibrosis are main determinants of ventricular remodeling. Resent findings support the involvement of galectin-3 in cardiac remodeling and in the fibrotic process and, as suggested by two recent experimental studies of liver and kidney fibrosis (20,21). There is evidence that inflammation contributes to end organ damage.…”

Plasma proteome profiling discovers novel proteins associated with non‐alcoholic fatty liver disease

“…It is strongly associated with components of the metabolic syndrome (Dieplinger & Dieplinger, ), NAFLD, and alcoholic liver disease (ALD) (Bell et al , ; Liu et al , ; Neuman et al , ). LGALS3BP, which was up‐regulated in NAFLD and T2D, is a candidate biomarker for hepatitis C‐related fibrosis and cirrhosis (Cheung et al , ). Interestingly, galectin‐3, the ligand of LGALS3BP, is likewise associated with fibrosis in diverse tissues, for instance, kidney, lung, liver, and heart (Li et al , ).…”

“…AFM has been closely linked to metabolic syndrome, insulin resistance, NAFLD, and alcoholic liver disease (Bell et al , ; Liu et al , ; Neuman et al , ; Kollerits et al , ). LGALS3BP has already been used to build multi‐component classifiers for the prediction of NAFLD (Wood et al , ) and fibrosis in patients with hepatitis C infection (Cheung et al , ). The elevated levels of LGALS3BP and vitronectin (VTN), another extracellular matrix (ECM) protein, are likely a reflection of remodeling of the ECM in liver disease.…”

ABCG2pos lung mesenchymal stem cells are a novel pericyte subpopulation that contributes to fibrotic remodeling

“…This activation of TGF-␤ results in myofibroblast transition of fibroblasts as well as EC, increased collagen deposition (col1a1, col3a1), increased matrix stiffening, and adverse remodeling (41,46). S100A9, galectin 3 (Lgals3bp), and placental growth factor (pgf) have all been identified as biomarkers that indicate the severity of fibrosis in various tissues including IPF (18,39,76,95). Interestingly, galectin 3 interacts with NG2 and promotes migration and invasion of cells (97).…”