摘要
SIP24/24p3为一小鼠分泌的应急时相反应蛋白,SIP24/24p3在体内的表达是高度组织特异的,其功能包括抗炎症及特异性诱导白细胞凋亡。为研究SIP24/24p3的调控因子及机制,我们在细胞培养中通过35S代谢标记方法定量检测了炎症因子IL-6和TNF-α对SIP24/24p3蛋白的诱导作用。结果显示:IL-6在BALB/c 3T3细胞中诱导SIP24/24p3.在BNL细胞中无诱导作用,而TNF-α在BMLB/c 3T3和BNL细胞中对SIP24/24p3都有诱导作用;IL-6对SIP24/24p3表达的剂量效应在BALB/c 3T3细胞中呈正相关,在BNL细胞中无相关性;TNF-α对SIP24/24p3表达的剂量效应在BALB/c 3T3和BNL细胞中都呈正相关,但在BNL细胞中高浓度的TNF-α导致SIP24/24p3表达量有所降低;在BALB/c 3T3细胞中IL-6和TNF-α对SIP24/24p3的表达有同等诱导作用;而在BNL细胞中FNF-α对SIP24/24p3的表达起主导作用,IL-6是一种起扩增作用的第二诱导信号。这有助于解释SIP24/24p3在体内的高度特异表达,也为阐明应急时相反应蛋白在不同组织中的调控机制提供了依据。
SIP24 ( also called 24p3 ) is a secreted murine acute phase protein which has been speculated to have an anti-inflammatory role in vivo. The expression of SIP24/24p3 in vivo is highly specific. Recently SIP24/24p3 has been reported to be able to specifically induce apoptosis in leukocytes. By using 35S metabolic labeling method, we had showed that: (1 )The pro-inflammatory cytokines IL-6 and TNF-αinduced SIP24/24p3 in cultured BALB/c 3T3 and BNL cells; (2 )The induction patterns of SIP24/24p3 in the two cell lines were different; (3 ) IL-6 and TNF-a played differential roles in the regulation of SIP24/24p3. The regulation of SIP24/24p3 by the pro-inflammatory cytokines may be related to its physiological regulation and function in vivo.
出处
《上海免疫学杂志》
CSCD
北大核心
2003年第5期298-301,共4页
Shanghai Journal of Immunology
基金
国家重点基础研究发展计划资助项目(2001CB510006)
