Hepatocyte growth factor activates quiescent skeletal muscle satellite cells in vitro

Abstract

The effect of hepatocyte growth factor (HGF) on the activation of quiescent rat skeletal muscle satellite cells was evaluated in vitro. Satellite cells from 9-month-old adult rats are quiescent in vivo and when cultured, display a protracted lag phase prior to division that is not present in satellite cells from neonatal or regenerating muscle. Under normal growth conditions, satellite cells divide for the first time between 42 and 60 hr. Hepatocyte growth factor increased proliferation in a dose-dependent fashion prior to 48 hr with half-maximal stimulation at approximately 3 ng/ml; in addition, heparin enhanced this activity. The time course of cyclin-D1 and proliferating cell nuclear antigen (PCNA) expression was accelerated in HGF-treated satellite cells, indicating that cells entered the cell cycle earlier. No significant effects on muscle-derived fibroblast proliferation was observed. The signalling receptor for HGF is the product of the c-met protooncogene, and rtPCR analysis of satellite cells 0-72 hr in culture demonstrated the presence of this message throughout this time period. The presence of c-met in quiescent satellite cells, the ability of HGF to stimulate precocious entry into the cell cycle, and the previously described localization of HGF message in regenerating muscle (Jennische et al., 1993) indicate that HGF could act as an activator of quiescent satellite cells in vivo.

Hepatocyte growth factor/scatter factor activates proliferation in melanoma cells through p38 MAPK, ATF-2 and cyclin D1

“…Both melanoma cell lines were found to have appreciable levels of c-Met, and both showed c-Met phosphorylation, 4.8-and 2.8-fold respectively, 5 min after treatment with HGF/SF (40 ng/ml) in serum free medium ( Figure 1a). HGF/SF can regulate cyclin D1 expression in hepatocytes, muscle satellite cells and melanocytes (Musgrove et al, 1993;Filmus et al, 1994;Albanese et al, 1995;Allen et al, 1995;Alberch et al, 1995;Shambaugh et al, 1996;Bennett and Tonks et , 2000;Halaban, 2000). We found that cyclin D1 protein was up-regulated by 1.9-and 1.7-fold in 37-3N and 37-32 melanoma cell lines, respectively, 24 h after treatment with HGF/SF ( Figure 1b).…”

“…Cyclin D1 has been found to collaborate with oncogenes in cellular transformation (Wang et al, 1994) and the protein levels are frequently elevated in uveal-melanomas (Coupland et al, 2000) and primary melanomas that express the tumor suppressor p16 INK4a (Bales et al, 1999). Cyclin D1 promoter activity and mRNA levels are induced by various growth factors, including epidermal growth factor (EGF), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), integrin-linked kinase (ILK) and HGF/SF (Musgrove et al, 1993;Filmus et al, 1994;Albanese et al, 1995;Allen et al, 1995;Alberch et al, 1995;Shambaugh et al, 1996;Bennett and Tonks, 1997;D'Amico et al, 2000). However, the mechanisms by which HGF/SF up-regulates cyclin D1 in melanoma cells have not been fully elucidated.…”

Release of Hepatocyte Growth Factor from Mechanically Stretched Skeletal Muscle Satellite Cells and Role of pH and Nitric Oxide

“…The one growth factor that has been demonstrated to have the ability to activate quiescent satellite cells in vitro and in vivo is HGF (Allen et al, 1995;Tatsumi et al, 1998). The results of experiments using the stretch of isolated quiescent skeletal muscle satellite cells in the FlexerCell system demonstrated that satellite cell activation occurred earlier in stretched cells than in unstretched control cells and that HGF mediated this process.…”

“…There are two factors that have been demonstrated to activate quiescent satellite cells. The first is hepatocyte growth factor (HGF); HGF can activate quiescent rat muscle satellite cells in vitro and in vivo (Allen et al, 1995;Tatsumi et al, 1998). HGF is a heparin-binding growth factor that has been localized in the extracellular domain of uninjured skeletal muscle fibers, and after injury HGF quickly associates with satellite cells (Tatsumi et al, 1998;Anderson, 2000).…”

Heparinized collagen scaffolds with and without growth factors for the repair of diaphragmatic hernia

“…Growth factors reported to stimulate muscle cells and/or blood vessels viz. hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF), both heparin binding proteins, [11][12][13][14] were attached to the scaffold before implantation. Scaffolds were biochemically and morphologically characterized and implanted into a surgically created diaphragmatic hernia in rats to study degradation, cellular infiltration and tissue regeneration.…”