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1 Division of Gastroenterology and Hepatology, Department of Surgery, Medical College of Wisconsin Dysphagia Institute, Digestive Disease Center, Milwaukee, WI, USA
2 Division of Gastroenterology and Hepatology, Department of Medicine, Medical College of Wisconsin Dysphagia Institute, Digestive Disease Center, Milwaukee, WI, USA
3 Froedtert Memorial Lutheran Hospital, Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee Veteran's Affairs Medical Center, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: dbinion{at}mcw.edu.
Gastroesophageal reflux disease is the most common malady of the esophagus, affecting 7% of the U.S. population. Histological assessment demonstrates classic inflammatory mechanisms including selective leukocyte recruitment and hemorrhage, suggesting a prominent role for the microvasculature. We isolated and characterized human esophageal microvascular endothelial cells (HEMEC) and examined inflammatory activation in response to cytokines, LPS, and acidic pH exposure and identified signaling pathways which underlie activation. HEMEC displayed characteristic morphologic and phenotypic features including acetylated-LDL uptake. TNF-
/LPS activation of HEMEC resulted in upregulation of the cell adhesion molecules ICAM-1, VCAM-1, E-selectin and MAdCAM-1, increased IL-8 production and enhanced leukocyte binding. Both acid and TNF-/LPS activation lead to activation of SAPK/JNK in HEMEC which was linked to VCAM-1 expression and U-937 leukocyte adhesion. Expression of constitutive inducible nitric oxide synthase in HEMEC was in marked contrast to intestinal microvascular endothelial cells. In this study we demonstrate that human esophageal microvascular endothelial cells are phenotypically and functionally distinct from lower gut derived endothelial cells, and will facilitate understanding of inflammatory mechanisms in esophageal inflammation.
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