WTSA: Heat Shock Protein-27 is Induced by Gastroduodenal Reflux in Esophageal Epithelium

WTSA: Western Thoracic Surgical Association

Search


Home

Annual Meeting

Members
	Member Directory
	Join WTSA
	Members Only

Council

Committees

Journal

Newsletters

Awards

Links

Heat Shock Protein-27 is Induced by Gastroduodenal Reflux in Esophageal Epithelium

David C Mauchley, Xianzhong Meng, Lihua Ao, *David A Fullerton, *Michael J Weyant
University of Colorado, Aurora, CO

BACKGROUND: Exposure of esophageal epithelium to gastric and duodenal contents results in inflammation demonstrated by hyperproliferation and mucosal thickening. Inflammation caused by reflux plays a role in a wide range of esophageal disorders including esophagitis and malignancy. To date there has been little investigation into the molecular mechanisms which underlie esophageal inflammation. Recently in vitro studies have demonstrated upregulation of heat shock protein-27 (Hsp27) in isolated esophageal cells when exposed to acidic stress. Expression of Hsp27 has been shown to promote cell survival and proliferation in several tissue types in response to inflammation. We sought to determine the influence of gastroduodenal reflux (GDR) in vivo on Hsp27 expression in a murine model of gastroduodenal reflux.
METHODS: BALB/c mice (n=8) underwent side-to-side surgical anastamosis of the first portion of the duodenum and GE junction that resulted in continuous exposure of esophageal mucosa to mixed gastric and duodenal contents. Control mice (n=8) consisted of BALB/c mice which were surgically unaltered. Mice were euthanized at 12 weeks using CO₂ inhalation and esophageal tissue was either frozen in embedding medium or homogenized in cell lysis buffer. Immunoblotting using standard techniques was used to detect levels of Hsp27. Levels of Hsp27 were quantified using ImageJ software. Immunofluorescent staining was used to characterize Hsp27 location with positive staining shown in red. ANOVA statistical analysis was used to compare mean band density between groups.
RESULTS: All mice survived the reflux procedure and there was no significant difference in weight gain throughout the study period. Levels of Hsp27 were increased by approximately 75% (p<0.01) in tissue exposed to 12 weeks of mixed reflux compared to that of controls (Fig 1). Expression of Hsp27 mainly localized to the esophageal epithelium (Fig 2).
CONCLUSIONS: We show for the first time that expression of Hsp27 is induced in response to gastroduodenal reflux in vivo. Furthermore, its expression is primarily localized to the epithelial layer which is significantly affected by GDR. This finding suggests that Hsp27 plays an integral role in the esophageal mucosal response to inflammation caused by GDR.

Back to 2009 Annual Meeting
Back to Main Program

Home | About WTSA | Contact Us

www.westernthoracic.org