窖蛋白-1 的过表达通过上调 cPLA2/p38MAPK 加重 LPS 诱导的 AT-1 细胞炎症反应。
Over-expression of caveolin-1 aggravate LPS-induced inflammatory response in AT-1 cells via up-regulation of cPLA2/p38 MAPK.
机构信息
Institute of Respiratory Disease, The Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
出版信息
Inflamm Res. 2010 Jul;59(7):531-41. doi: 10.1007/s00011-010-0157-9. Epub 2010 Jan 23.
OBJECTIVE AND DESIGN
The aim of this study was to study the effect of caveolin-1 on the cytosolic phospholipase A2 (cPLA2), p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappaB (NF-kappaB) in mouse lung alveolar type-1 cells' (AT-1 cells) inflammatory response induced by LPS.
MATERIALS AND METHODS
Gene clone technique was used to over-express caveolin-1 in AT-1 cells by lentivirus vector. The level of tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), cPLA2, p38 MAPK and NF-kappaB was measured by ELISA, western blotting and EMSA.
TREATMENT
AT-1 cells were treated with LPS.
RESULTS
Over-expression of caveolin-1 not only increased the production of pro-inflammatory cytokine TNF-alpha and IL-6, but also enhanced the expression of the cPLA2, p38 MAPK, and NF-kappaB.
CONCLUSIONS
Our data demonstrated that over-expression of caveolin-1 aggravates the AT-1 injury induced by LPS, involving in modulation of the cPLA2 mediated by the cPLA2/p38 MAPK pathway.
目的和设计
本研究旨在研究细胞质磷脂酶 A2（cPLA2）、p38 丝裂原激活蛋白激酶（p38 MAPK）和核因子 kappaB（NF-kappaB）在脂多糖诱导的小鼠肺肺泡型-1 细胞（AT-1 细胞）炎症反应中，窖蛋白-1 的作用。
材料和方法
利用慢病毒载体的基因克隆技术过表达 AT-1 细胞中的窖蛋白-1。通过 ELISA、western blot 和 EMSA 测定肿瘤坏死因子-α（TNF-α）、白细胞介素 6（IL-6）、cPLA2、p38 MAPK 和 NF-kappaB 的水平。
处理
用 LPS 处理 AT-1 细胞。
结果
窖蛋白-1 的过表达不仅增加了促炎细胞因子 TNF-α和 IL-6 的产生，还增强了 cPLA2、p38 MAPK 和 NF-kappaB 的表达。
结论
我们的数据表明，窖蛋白-1 的过表达加重了 LPS 诱导的 AT-1 损伤，涉及 cPLA2/p38 MAPK 通路调节的 cPLA2。
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