Growth factors expression in patients with erosive esophagitis

Although the pathogenesis and treatment of erosive esophagitis (EE) is well recognized, little is known about the cellular and molecular mechanisms of mucosal healing in EE patients. In this pilot study, we enrolled typical EE patients to evaluate what kinds of growth factors and their receptors were activated in their injured esophageal mucosa. Forty endoscopically proved EE patients were consecutively enrolled. Messenger RNA expressions, which includes keratinocyte growth factor (KGF) and its receptor (KGFR), epidermal growth factor (EGF) and its receptor (EGFR), hepatocyte growth factor (HGF) and its receptor (HGFR), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and cyclooxygenase (COX)-1 and COX-2, were measured using real-time polymerase chain reaction (PCR). Data were compared between the injured EE mucosa and their normal esophageal mucosa above EE. The mRNA expressions of HGF, HGFR, EGF, VEGF, and COX-2, but not EGFR, KGF, KGFR, bFGF, and COX-1, were significantly increased in the injured mucosa of EE patients compared with those of normal mucosa (P < 0.05). The study found that HGF, HGFR, EGF, VEGF, and, COX-2 are activated in the injured mucosa of EE patients; their activation might be involved in mucosal repair and ulcer healing of EE.

Abbreviations: bFGF, basic fibroblast growth factor, COX, cyclooxygenase, EE, erosive esophagitis, EGF, epidermal growth factor, EGFR, EGF receptor, ERK, extracellular signal regulated kinase, GERD, gastroesophageal reflux disease, HGF, hepatocyte growth factor, HGFR, HGF receptor, KGF, keratinocyte growth factor, KGFR, KGF receptor, NSAIDs, nonsteroidal anti-inflammatory drugs, PCR, polymerase chain reaction, PPI, proton pump inhibitor, SEM, standard error of the mean, VEGF, vascular endothelial growth factor