mRNA expression of EGF receptor ligands in atrophic gastritis before and after Helicobacter pylori eradication.
BACKGROUND
Epidermal growth factor (EGF) receptor ligands (EGFRL) including transforming growth factor alpha (TGF-alpha), amphiregulin, and heparin binding-EGF (HB-EGF) are involved in gastric mucosal repair in chronic gastritis. Their mRNA expression has been shown to be upregulated after Helicobacter pylori (H.p.)-eradication but little is known about this gene expression in atrophic gastritis. The purpose of our study was to investigate EGFRL mRNA expression in gastric mucosa of patients with atrophic gastritis before and after H.p.-eradication.


METHODS
Antral mucosal biopsies were obtained during endoscopy in 10 H.p. positive patients with atrophic gastritis and in 10 H.p. negative controls with intact mucosa. Total RNA of antral biopsies was extracted and RT-PCR was performed, the PCR-products being measured densitometrically. Values were compared with mRNA expressions in H.p. negative antral mucosa (n=10).


RESULTS
Gastric biopsies revealed mRNA expression for TGF-alpha, amphiregulin and HB-EGF, both in H.p. positive atrophic antritis and in H.p. negative healthy mucosa. The mRNA expression of TGF-alpha in atrophic gastritis was significantly upregulated after H.p.-eradication, whereas that of amphiregulin did not change after this eradication. Expression of HB-EGF mRNA was higher in H.p.-infection than after H.p.-eradication or in H.p. negative healthy subjects.


CONCLUSIONS
H.p. positive atrophic gastritis is associated with differential mRNA expression of EGF receptor ligands. H.p.-eradication in this entity leads to unequal changes of these growth factor expressions compared to chronic active gastritis without atrophy.
Schiemann
Uwe
U
Medical Policlinic, University of Munich 1, Germany.
Konturek
Jan
J
Assert
Ronald
R
Rembiasz
Kazimierz
K
Domschke
Wolfram
W
Konturek
Stanisław
S
Pfeiffer
Aadreas
A
D066258:Amphiregulin; D001483:Base Sequence; D017931:DNA Primers; D066255:EGF Family of Proteins; D004815:Epidermal Growth Factor / Q000235:genetics* / Q000378:metabolism; D066246:ErbB Receptors / Q000378:metabolism*; D005757:Gastritis, Atrophic / Q000150:complications / Q000378:metabolism* / Q000382:microbiology; D006023:Glycoproteins / Q000235:genetics* / Q000378:metabolism; D006133:Growth Substances / Q000235:genetics* / Q000378:metabolism; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy* / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification*; D066257:Heparin-binding EGF-like Growth Factor; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D008024:Ligands; D012333:RNA, Messenger / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016211:Transforming Growth Factor alpha / Q000235:genetics* / Q000378:metabolism
C587848:AREG protein, human; D066258:Amphiregulin; D017931:DNA Primers; D066255:EGF Family of Proteins; D006023:Glycoproteins; D006133:Growth Substances; C587883:HBEGF protein, human; D066257:Heparin-binding EGF-like Growth Factor; D036341:Intercellular Signaling Peptides and Proteins; D008024:Ligands; D012333:RNA, Messenger; D016211:Transforming Growth Factor alpha; D004815:Epidermal Growth Factor; D066246:ErbB Receptors