TY - JOUR
T1 - Hepatocyte growth factor and its receptor Met are induced in crescentic glomerulonephritis
AU - Rampino, Teresa
AU - Gregorini, Marilena
AU - Camussi, Giovanni
AU - Conaldi, Pier Giulio
AU - Soccio, Grazia
AU - Maggio, Milena
AU - Bottelli, Antonella
AU - Dal Canton, Antonio
PY - 2005/6
Y1 - 2005/6
N2 - Background. In experimental extracapillary glomerulonephritis (EG) podocytes migrate, proliferate and change phenotype, and play a pivotal role in crescent formation. Hepatocyte Growth Factor (HGF) is an injury-induced effector of tissue repair that causes cell migration, growth and transdifferentiation via its receptor Met. Methods. In 11 patients with EG we measured serum levels of HGF and investigated whether serum induces the release of HGF by Peripheral Blood Mononuclear Cells (PBMC). In renal biopsies we studied the expression of Met. In cultured podocytes we studied Met expression, migration, growth and morphological changes induced by recombinant (r) HGF. Results. In patients with EG average serum levels of HGF (0.73 ng/ml) were higher than in normal volunteers (N, 0.10 ng/ml, p <0.01) and in patients with non-crescentic glomerular disease (GD, 0.18 ng/ml, p <0.01). Serum of EG induced a significant HGF release by PBMC (mean 0.58 ng/ml) in comparison with serum of N and GD (0.07 and 0.06 ng/ml, respectively, both p <0.001). Met was strongly expressed in crescents. Cultured podocytes expressed Met, and rHGF induced in podocytes a time- and dose-dependent migration, growth and epithelial to mesenchymal transdifferentiation. Conclusions. These results suggest that HGF/Met system participates in the process of crescent formation by inducing podocyte migration, growth and mesenchymal transformation.
AB - Background. In experimental extracapillary glomerulonephritis (EG) podocytes migrate, proliferate and change phenotype, and play a pivotal role in crescent formation. Hepatocyte Growth Factor (HGF) is an injury-induced effector of tissue repair that causes cell migration, growth and transdifferentiation via its receptor Met. Methods. In 11 patients with EG we measured serum levels of HGF and investigated whether serum induces the release of HGF by Peripheral Blood Mononuclear Cells (PBMC). In renal biopsies we studied the expression of Met. In cultured podocytes we studied Met expression, migration, growth and morphological changes induced by recombinant (r) HGF. Results. In patients with EG average serum levels of HGF (0.73 ng/ml) were higher than in normal volunteers (N, 0.10 ng/ml, p <0.01) and in patients with non-crescentic glomerular disease (GD, 0.18 ng/ml, p <0.01). Serum of EG induced a significant HGF release by PBMC (mean 0.58 ng/ml) in comparison with serum of N and GD (0.07 and 0.06 ng/ml, respectively, both p <0.001). Met was strongly expressed in crescents. Cultured podocytes expressed Met, and rHGF induced in podocytes a time- and dose-dependent migration, growth and epithelial to mesenchymal transdifferentiation. Conclusions. These results suggest that HGF/Met system participates in the process of crescent formation by inducing podocyte migration, growth and mesenchymal transformation.
KW - Crescentic glomerulonephritis
KW - Hepatocyte growth factor
KW - Podocytes
KW - Scatter factor
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U2 - 10.1093/ndt/gfh740
DO - 10.1093/ndt/gfh740
M3 - Article
C2 - 15784643
AN - SCOPUS:20844454104
VL - 20
SP - 1066
EP - 1074
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
SN - 0931-0509
ER -