Traumatic brain injury increases TGFβRII expression on endothelial cells
Traumatic brain injury increases TGFβRII expression on endothelial cells
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DOI：
10.1016/j.brainres.2004.03.028
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发表时间：
2004-06-25
期刊：
影响因子：
2.9
通讯作者：
Fabry, Z
中科院分区：
文献类型：
--
作者：
Fee, DB;Sewell, DL;Fabry, Z
转化生长因子β (tgfβ)调节创伤性损伤后的多种生长相关功能。细胞对TGFbeta的反应主要通过细胞表面的TGFbeta受体I （TGFbetaRI）和受体II （TGFbetaRI）以及细胞内的SMAD蛋白介导。我们利用免疫组织化学方法研究了tgfβ受体在创伤性脑损伤（TCI）急性期和慢性期的表达，并用细胞荧光法研究了小鼠脑微血管内皮（EN）细胞的培养。在这里，我们报道TGFbetaRII在脑内皮细胞上的表达在TCI的慢性期显著增加。SMAD3和SMAD4蛋白表达也上调，提示tgfβ受体胞内信号通路激活。当TGFbetaRI和TGFbetaRII在体外培养的小鼠脑微血管EN细胞中表达时，TGFbetaRII在含有BrdU的增殖细胞中表达增加。这些数据表明，TGFbetaRI和TGFbetaRI在脑微血管EN细胞急性期和慢性期的差异表达可能与损伤后EN增殖有关。(C) 2004 Elsevier B.V.版权所有
Transforming growth factor beta (TGFbeta) modulates a variety of growth related functions following traumatic injury. The cellular response to TGFbeta is predominantly mediated through TGFbeta receptor I (TGFbetaRI) and receptor II (TGFbetaRII) on the cell surface and SMAD proteins intracellularly. We investigated the expression of TGFbeta receptors in the acute and chronic phases of a traumatic cerebral injury (TCI) by immunohistochemistry and in cultures of murine brain microvascular endothelial (EN) cells using cytofluorimetry. Here, we report that TGFbetaRII expression significantly increases on brain endothelial cells in the chronic phase of TCI. SMAD3 and SMAD4 protein expression were also upregulated suggesting the activation of TGFbeta receptor intracellular signaling. When TGFbetaRI and TGFbetaRII expression was studied in in vitro cultures of murine brain microvessel EN cells, TGFbetaRII showed increased expression on proliferating cells that are incorporating BrdU. These data show a differential expression of TGFbetaRI and TGFbetaRII on brain microvessel EN cells in the acute and chronic phases of TO that might be associated with EN proliferation following injury. (C) 2004 Elsevier B.V. All rights reserved.