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Acta Physiologica Sinica ; (6): 525-529, 2003.
Artículo en Inglés | WPRIM | ID: wpr-290933

RESUMEN

SIP24/24p3 is a secreted murine acute phase protein which has been speculated to play an anti-inflammatory role in vivo. Recently SIP24/24p3 has been found to be able to specifically induce apoptosis in leukocytes. By using (35)S metabolic labeling method, we studied the regulation of SIP24/24p3 by glucocorticoid and pro-inflammatory cytokines IL-6 and TNF-alpha in cultured Balb/c 3T3 and BNL cells. The following results were observed: (1) dexamethasone induced the expression of SIP24/24p3 in both Balb/c 3T3 and BNL cells, the induction was more significant in BNL cells; (2) dexamethasone and IL-6 synergistically induced the expression of SIP24/24p3 in both Balb/c 3T3 and BNL cells; (3) in Balb/c 3T3 cells dexamethasone and TNF-alpha acted synergistically to induce the expression of SIP24/24p3, whereas in BNL cells dexamethasone and TNF-alpha induced the expression of SIP24/24p3 in an additive manner; (4) dexamethasone and IL-6/TNF-alpha acted synergistically in Balb/c 3T3 cells and additively in BNL cells to induce the expression of SIP24/24p3. The inducibility of SIP24/24p3 by multiple factors will help to explain its highly specific expression in vivo. The difference in the expression patterns of SIP24/24p3 in different cell types is also suggestive to its expression and regulation in hepatic and extrahepatic tissues. Finally, the fact that SIP24/24p3 protein can be induced by both pro-inflammatory as well as anti-inflammatory factors is indicative of the important role of SIP24/24p3 in the entire acute phase response process.


Asunto(s)
Animales , Ratones , Proteínas de Fase Aguda , Genética , Células 3T3 BALB , Proteínas Portadoras , Genética , Citocinas , Farmacología , Dexametasona , Farmacología , Sinergismo Farmacológico , Regulación de la Expresión Génica , Interleucina-6 , Farmacología , Lipocalina 2 , Lipocalinas , Ratones Endogámicos BALB C , Proteínas Oncogénicas , Genética , ARN Mensajero , Genética , Factor de Necrosis Tumoral alfa , Farmacología
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