MAPK 诱导损伤后星形胶质细胞中 AQP1 的表达。
MAPK induces AQP1 expression in astrocytes following injury.
机构信息
Department of Neurobiology and Center for Glial Biology in Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
出版信息
Glia. 2010 Jan 15;58(2):209-17. doi: 10.1002/glia.20916.
Abstract
Aquaporin-4 (AQP4) is the principle water channel and the primary route for water transport across astrocytic membranes. AQP4 co-localizes with Kir4.1 channels at astrocytic endfeet, and it has been suggested that these channels cooperate in K(+) and water homeostasis. In response to injury, two additional aquaporins, AQP1 and AQP9, can be detected in astrocytes, yet neither is found in cultured astrocytes, and therefore their contribution to astrocyte water uptake and biology is poorly investigated. In this study, we used a cortical stab wound assay to demonstrate an upregulation of AQP1 following injury in reactive glia. We were able to mimic such injury in astrocytic cultures and show that AQP1 expression is induced within 16 h following injury in vitro. This induction could be blocked by inhibition of MEK1/2 using U0126, and suggests that AQP1 is specifically induced in reactive astrocytes via the mitogen-activated protein kinases signaling pathway.
摘要
水通道蛋白 4（AQP4）是主要的水通道蛋白，也是水跨星形胶质细胞膜转运的主要途径。AQP4 与星形胶质细胞终足的 Kir4.1 通道共定位，有人认为这些通道在 K（+）和水动态平衡中合作。在损伤后，还可以在星形胶质细胞中检测到另外两种水通道蛋白，AQP1 和 AQP9，但在培养的星形胶质细胞中均未发现，因此它们对星形胶质细胞水摄取和生物学的贡献研究甚少。在这项研究中，我们使用皮质刺伤测定法证明了反应性神经胶质细胞损伤后 AQP1 的上调。我们能够在星形胶质细胞培养物中模拟这种损伤，并表明 AQP1 的表达在体外损伤后 16 小时内被诱导。这种诱导可以通过使用 U0126 抑制 MEK1/2 来阻断，这表明 AQP1 是通过有丝分裂原激活的蛋白激酶信号通路特异性诱导反应性星形胶质细胞的。
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