Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04141 (granulocyte-macrophage colony-stimulating factor)
 6,790 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte-macrophage colony-stimulating factor (GM-CSF), one of major hematopoietic growth factors, activates mature leukocytes. GM-CSF is produced by endothelial cells stimulated with lipopolysaccharide (LPS), and the LPS-induced GM-CSF production may play an important role in the activation of neutrophils on the endothelial surface. 15-Deoxy-delta 12,14-prostaglandin J2 (15d-PGJ2) is a ligand for peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and modulates inflammatory reactions by regulating the expression of various genes. We studied the effect of 15d-PGJ2 on the LPS-induced GM-CSF expression in endothelial cells. Human umbilical vein endothelial cells (HUVEC) were cultured and the expressions of GM-CSF mRNA and protein were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. 15d-PGJ2 inhibited the LPS-induced GM-CSF expression in a concentration-dependent manner; but ciglitazone, another agonist for PPAR-gamma, had no effect. This suggests that 15d-PGJ2 inhibits GM-CSF expression through a mechanism unrelated to PPAR-gamma. 15d-PGJ2 induced, by itself, the expression of interleukin-8, a potent proinflammatory chemokine, in HUVEC. 15d-PGJ2 may regulate inflammatory reactions by controlling the balance of various cytokines.
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PMID:15-Deoxy-delta 12,14-prostaglandin J2 inhibits the expression of granulocyte-macrophage colony-stimulating factor in endothelial cells stimulated with lipopolysaccharide. 1451 69

15-Deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2) is an agonist for peroxisome proliferator-activated receptor-gamma (PPAR-gamma), which plays an important role in various biological processes including inflammatory responses. We have addressed the effect of 15d-PGJ2 on the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in a cell line derived from human bronchial epithelial cells (BEAS-2B). Besides being a hematopoietic growth factor, GM-CSF activates mature leukocytes and is involved in regulation of inflammatory responses. Cultures of BEAS-2B were stimulated with interleukin-1beta (IL-1beta), and the expressions of GM-CSF mRNA and protein were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. IL-1beta stimulated the expression of GM-CSF in BEAS-2B cells in concentration- and time-dependent manners. When the cells were pretreated with 15d-PGJ2 for 1 hour, the IL-1beta-induced GM-CSF expression was inhibited in a concentration-dependent manner (2-50 microM). Ciglitazone, another agonist of PPAR-gamma, did not affect the IL-1beta-induced GM-CSF expression in BEAS-2B cells. A PPAR-gamma antagonist, bisphenol A diglycide ether (BADGE), did not reverse the inhibitory effects of 15d-PGJ2 on GM-CSF expression. 15d-PGJ2 regulates GM-CSF expression in the bronchial epithelium, which may be mediated through a mechanism unrelated to PPAR-gamma.
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PMID:15-Deoxy-delta(12,14)-prostaglandin J2 inhibits the IL-1beta-induced expression of granulocyte-macrophage colony-stimulating factor in BEAS-2B bronchial epithelial cells. 1499