期刊
FASEB JOURNAL
卷 16, 期 14, 页码 253-+出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.02-0239fje
关键词
neutrophil activation; cell adhesion molecules; phagocytosis; cytokines; edema
The 37-kDa protein annexin 1 (Anx-1; lipocortin 1) has been implicated in the regulation of phagocytosis, cell signaling, and proliferation and is postulated to be a mediator of glucocorticoid action in inflammation and in the control of anterior pituitary hormone release. Here, we report that mice lacking the Anx-1 gene exhibit a complex phenotype that includes an altered expression of other annexins as well as of COX-2 and cPLA(2). In carrageenin- or zymosan-induced inflammation, Anx-1(-/-) mice exhibit an exaggerated response to the stimuli characterized by an increase in leukocyte emigration and IL-1beta generation and a partial or complete resistance to the antiinflammatory effects of glucocorticoids. Anx-1(-/-) polymorphonuclear leucocytes exhibited increased spontaneous migratory behavior in vivo whereas in vitro, leukocytes from Anx-1(-/-) mice had reduced cell surface CD 11b (MAC-1) but enhanced CD62L (L-selectin) expression and Anx-1(-/-) macrophages exhibited anomalies in phagocytosis. There are also gender differences in activated leukocyte behavior in the Anx-1(-/-) mice that are not seen in the wild-type animals, suggesting an interaction between sex hormones and inflammation in Anx-1(-/-) animals.
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