Original article
Growth factors expression in patients with erosive esophagitis

https://doi.org/10.1016/j.trsl.2008.05.010Get rights and content

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.

Section snippets

Patients and procedures

Patients who had the typical GERD symptoms, such as heartburn and acid regurgitation, who were scheduled to receive upper gastrointestinal panendoscopy acted as candidates for this study. The demographic data of patients in term of age, gender, habit of alcohol drinking, smoking, and current medication were recorded. After an overnight fast, each subject first underwent pharyngeal anesthesia with 10% xylocaine (AstraZeneca AB, Sodertalje, Sweden) and then underwent video upper gastrointestinal

Results

Between October 2007 and February 2008, 40 eligible GERD patients with endoscopically proved EE according to LA grade C or D were consequently enrolled. The mean age was 59.5 ± 1.5 years old (range, 38–75 years). Thirty-two (80%) patients were male, and 8 patients (20%) were female.

Discussion

Our study seems to be the first human study to evaluate what kinds of growth factors or their receptors are activated in the injured mucosa of EE. We found that mRNA expressions of HGF, HGFR (c-Met), EGF, VEGF, and COX-2 but not EGFR, KGF, KGFR, bFGF, and COX-1 were significantly increased in the squamous epithelium of EE when compared with those of normal esophageal mucosa.

Although KGF, KGFR, HGF, HGFR, VEGF, COX-2, and ERK signal-transduction pathways are activated and involved in the

Conclusions

Our study showed that HGF, HGFR, EGF, VEGF, and, COX-2 but not KGF, KGFR, EGFR, bFGF, and COX-1 were activated in the injured mucosa of EE patients. We suggested that understanding their activations may provide another therapeutic role in esophageal mucosal repair of EE patients in the future.

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Supported by Grant V97C1-011 from Taipei Veteran General Hospital, Taipei, Taiwan.

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