Expression of hepatocyte growth factor and c-met receptor in gastric mucosa during gastric ulcer healing.
BACKGROUND
Recent studies have shown that hepatocyte growth factor (HGF) has a mitogenic and motogenic activity for gastric mucosal cells. The aim of this study is to ascertain the clinical significance of the expression of HGF and its receptor (c-met) during the course of gastric ulcer healing.


METHODS
Ten patients who underwent endoscopic mucosal resection (EMR) and developed acute gastric ulcer and 20 patients with peptic ulcer of the stomach were enrolled in this study. Tissue samples were serially obtained from both the edge of the ulcer and its neighboring mucosa 0, 2, and 8 weeks after EMR or diagnosis. Gene expression of HGF, c-met, c-myc, and proliferating cell nuclear antigen (PCNA) was semiquantitatively examined by reverse transcription polymerase chain reaction (RT-PCR) using beta-actin as an internal control. In addition, expression of HGF and c-met mRNA with regard to the presence or absence of Helicobacter pylori infection was studied.


RESULTS
In patients after EMR HGF, c-met, c-myc, and PCNA mRNA in the ulcer lesion at 0 week was at the peak of its expression and then decreased with time (P < 0.01, P < 0.05, P < 0.05, and P < 0.05, respectively). In patients who underwent EMR the intensity of HGF mRNA was correlated with that of c-met, c-myc, and PCNA mRNA (P < 0.0001, P = 0.0095, and P = 0.0009, respectively) and that of c-met mRNA was correlated with that of c-myc and PCNA mRNA (P = 0.012 and P < 0.0001, respectively). In patients with peptic ulcer, expression of HGF mRNA decreased with time (0 week versus 8 weeks, P < 0.05; 0 week versus 8 weeks, P < 0.01). c-Met expression was lower at 8 weeks than at 0 week (P < 0.05). The intensity of c-met mRNA was correlated with that of PCNA mRNA (P < 0.0001). H. pyiori-infected mucosa had a higher level of HGF mRNA than non-infected mucosa.


CONCLUSIONS
The present study suggests that HGF is one of the growth factors acting together during healing of gastric ulcer.
Hori
K
K
Second Dept. of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Shiota
G
G
Kawasaki
H
H
D000199:Actins / Q000032:analysis; D000368:Aged; D000369:Aged, 80 and over; D015139:Blotting, Southern; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry*; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori; D017228:Hepatocyte Growth Factor / Q000032:analysis*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D019859:Proto-Oncogene Proteins c-met / Q000032:analysis*; D016271:Proto-Oncogene Proteins c-myc / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013276:Stomach Ulcer / Q000150:complications / Q000378:metabolism* / Q000628:therapy
D000199:Actins; D018809:Proliferating Cell Nuclear Antigen; D016271:Proto-Oncogene Proteins c-myc; D017228:Hepatocyte Growth Factor; D019859:Proto-Oncogene Proteins c-met