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    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; human ; DIAGNOSIS ; screening ; DISEASE ; PROTEIN ; DIFFERENTIATION ; MONOCLONAL-ANTIBODY ; TISSUE ; MECHANISM ; TISSUES ; mechanisms ; antibodies ; antibody ; IDENTIFICATION ; DECREASE ; PATHOGENESIS ; MONOCLONAL-ANTIBODIES ; EPITHELIAL-CELLS ; PHENOTYPE ; PROTEIN LEVELS ; CROHNS-DISEASE ; MUCOSA ; INFLAMMATORY-BOWEL-DISEASE ; COLITIS ; ACS5,fatty acid metabolism,human,small intestine ; FATTY-ACID PATTERN ; GASTRIC METAPLASIA ; PYLORIC METAPLASIA ; TRIACSIN-C
    Abstract: Several disorders of the small intestine are associated with disturbances in villus architecture. Thus, an understanding of the molecular mechanisms associated with the differentiation of villi represents an important step in the improvement of the understanding of small intestinal pathology. Screening of antibodies from a hybridoma library led to the identification of an acyl-CoA synthetase 5-specific monoclonal antibody. Protein synthesis, mRNA expression, and the enzyme activity of acyl-CoA synthetase 5 were studied by several methods in human small intestinal tissues with Crohn's disease or coeliac disease, respectively. Acyl-CoA synthetase 5 mRNA and protein levels were substantially reduced in injured small intestinal mucosa. Moreover, impaired synthesis of the acyl-CoA synthetase 5 protein was reflected by a decrease in intramucosal enzyme activity. Subtle changes of the acyl-CoA synthetase 5 pattern correlate with conversion of intestinal epithelial cells to a gastric phenotype. These results suggest that deranged acyl-CoA synthetase 5 expression, synthesis, and activity are closely related to the state of villus architecture and epithelial homeostasis in human small intestine. Copyright (C) 2004 John Wiley Sons, Ltd
    Type of Publication: Journal article published
    PubMed ID: 14743501
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