Interleukin-1beta induces the expression of aquaporin-4 through a nuclear factor-kappaB pathway in rat astrocytes.
Interleukin-1beta induces the expression of aquaporin-4 through a nuclear factor-kappaB pathway in rat astrocytes.
复制标题
DOI：
--
复制
发表时间：
2006
影响因子：
4.7
通讯作者：
Hiroaki Ito;N. Yamamoto;H. Arima;H. Hirate;T. Morishima;F. Umenishi;T. Tada;K. Asai;H. Katsuya-H.-Kats
中科院分区：
文献类型：
--
作者：
Hiroaki Ito;N. Yamamoto;H. Arima;H. Hirate;T. Morishima;F. Umenishi;T. Tada;K. Asai;H. Katsuya-H.-Kats
已知白细胞介素 (IL)-1β 在各种类型损伤后脑水肿的形成中发挥作用。据报道，水通道蛋白 (AQP)4 也参与脑水肿的进展。我们测试了 AQP4 是响应 IL-1beta 诱导的假设。我们发现在培养的大鼠星形胶质细胞中，IL-1β显着上调AQP4 mRNA和蛋白的表达，并且脑室内给予IL-1β可增加大鼠脑中AQP4蛋白的表达。 IL-1β 对 AQP4 诱导的影响具有浓度和时间依赖性。 IL-1β 对 AQP4 的影响是通过 IL-1β 受体介导的，因为它们通过与 IL-1 受体拮抗剂共孵育而被消除。 IL-1β 似乎增加了 AQP4 mRNA 的水平，但不参与蛋白质从头合成，因为蛋白质合成抑制剂放线菌酮不会抑制 IL-1β 的作用。核因子-kappaB (NF-kappaB) 通路的抑制以浓度依赖性方式阻断 IL-1β 对 AQP4 的诱导。这些发现表明，IL-1β 通过 NF-kappaB 途径诱导 AQP4 表达，而不参与大鼠星形胶质细胞中的从头蛋白质合成。
Interleukin (IL)-1beta is known to play a role in the formation of brain edema after various types of injury. Aquaporin (AQP)4 is also reported to be involved in the progression of brain edema. We tested the hypothesis that AQP4 is induced in response to IL-1beta. We found that expression of AQP4 mRNA and protein was significantly up-regulated by IL-1beta in cultured rat astrocytes, and that intracerebroventricular administration of IL-1beta increased the expression of AQP4 protein in rat brain. The effects of IL-1beta on induction of AQP4 were concentration and time dependent. The effects of IL-1beta on AQP4 were mediated through IL-1beta receptors because they were abolished by co-incubation with IL-1 receptor antagonist. It appeared that IL-1beta increased the level of AQP4 mRNA without involvement of de novo protein synthesis because cycloheximide, a protein synthesis inhibitor, did not inhibit the effects of IL-1beta. Inhibition of the nuclear factor-kappaB (NF-kappaB) pathway blocked the induction of AQP4 by IL-1beta in a concentration-dependent manner. These findings show that IL-1beta induces expression of AQP4 through a NF-kappaB pathway without involvement of de novo protein synthesis in rat astrocytes.