Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonylphenol, an estrogenic xenobiotic widely used in the manufacture of plastics and detergents, has been found in drinking water and may therefore enter the body through the oral route. Thus, intestinal cells lining the alimentary tract serve as the body's first line of defense against this compound. In this study, the effects of nonylphenol on the human intestinal cell line Caco-2 were determined using transepithelial electrical resistance (TEER) measurement and proteomics. Results show that 10 microM nonylphenol can disrupt the tight-junction permeability of Caco-2 cells in approximately 15 min. Incubating the cells with 1 or 10 microM nonylphenol for 6 days resulted in the enhanced expressions of galectin-3 (approximately 4-fold vs. control with 1 microM; 2-fold with 10 microM), glutathione S-transferase A2 (approximately 8-fold with 1 microM; 5-fold with 10 microM) and peroxiredoxin-1 (approximately 6-fold with 1 microM; 4-fold with 10 microM). These expressions may represent a possible consortium of mechanisms by which the cells protect themselves against nonylphenol-induced stresses. To the best of our knowledge, this is the first study on the effects of nonylphenol on Caco-2 cells.
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PMID:Expressions of galectin-3, glutathione S-transferase A2 and peroxiredoxin-1 by nonylphenol-incubated Caco-2 cells and reduction in transepithelial electrical resistance by nonylphenol. 1605 31

Gene expression profiling in animal models exposed to cigarette mainstream smoke (CS) shapes up as a promising tool for investigating the molecular mechanisms involved in the onset and development of CS-related disease and may aid in the identification of disease candidate genes. Here we report on differential gene expression in lungs of rats exposed for 2, 7, and 13 weeks to 300 and 600 microg total particulate matter/l CS with sacrifice 2, 6, or 20 h after the last exposure. Regarding antioxidant and xenobiotic-metabolizing (phase I/II) enzymes, a stereotypic, mostly transient, expression pattern of differentially expressed genes was observed after each exposure period. The expression patterns were generally dose dependent for antioxidant and phase II genes and not dose dependent for phase I genes at the CS concentrations tested. However, with increasing length of exposure, there was a distinct, mostly sustained and dose-sensitive, expression of genes implicated in innate and adaptive immune responses, clearly pointing to an emerging inflammatory response. Notably, this inflammatory response included the expression of lung disease-related genes not yet linked to CS exposure, such as galectin-3, arginase 1, and chitinase, as well as genes encoding proteolytic enzymes. Finally, our experiments also revealed a CS exposure-dependent shift in the cyclical expression of genes involved in controlling the circadian rhythm. Altogether, these results provide further insight into the molecular mechanisms of CS-dependent disease onset and development and thus may also be useful for defining CS-specific molecular biomarkers of disease.
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PMID:The kinetics of transcriptomic changes induced by cigarette smoke in rat lungs reveals a specific program of defense, inflammation, and circadian clock gene expression. 1687 Jun 87