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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >Astrocyte ERK phosphorylation precedes K(+)-induced swelling but follows hypotonicity-induced swelling.
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Astrocyte ERK phosphorylation precedes K(+)-induced swelling but follows hypotonicity-induced swelling.

机译：星形胶质细胞ERK磷酸化先于K（+）引起的肿胀，但随后出现低渗性引起的肿胀。

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摘要

Hypotonicity following water intoxication and/or salt loss leads to mainly astrocytic brain swelling. Astrocytic swelling also occurs following brain trauma or ischemia, together with an increase in extracellular K(+) ([K(+)](o)), stimulating a bumetanide/furosemide/ethacrynic acid-inhibitable cotransporter, NKCC1, that accumulates Na(+) and K(+) together with 2 Cl(-) and osmotically obliged water. Either type of swelling may become fatal and is associated with phosphorylation of extracellular regulated kinases 1 and 2 (ERK(1/2)). Only the swelling associated with elevated [K(+)](o), leads to an increase in astrocytic proliferation and in expression of the astrocytic marker, glial fibrillary acidic protein. These differences prompted us to investigate key aspects of the molecular pathways between hypotonicity-induced and high-K(+)-mediated swelling in primary cultures of mouse astrocytes. In the latter Ca(2+)-mediated, AG1478-inhibitable transactivation of the epidermal growth factor (EGF) receptor leads, via bumetanide-inhibitable activation of the mitogen activated protein (MAP) kinase pathway to ERK phosphorylation and to NKCC1-mediated swelling. In the former, inhibition of the MAP kinase pathway, but not of EGF receptor activation, abolishes ERK phosphorylation, but has no effect on swelling, indicating that activation of ERK is a result, not a cause, of the swelling.
机译：水中毒和/或盐分流失后的低渗性主要导致星形胶质细胞肿胀。脑外伤或局部缺血后也会发生星形胶质细胞肿胀，并伴随细胞外K（+）（[K（+）]（o））的增加，刺激布美他尼/呋塞米/乙炔酸抑制性共转运蛋白NKCC1积聚Na（ +）和K（+）以及2 Cl（-）和渗透性水。两种类型的肿胀都可能致命，并与细胞外调节激酶1和2（ERK（1/2））的磷酸化有关。仅与升高的[K（+）]（o）相关的肿胀导致星形细胞增殖和星形细胞标记神经胶质纤维酸性蛋白表达的增加。这些差异促使我们研究小鼠星形胶质细胞原代培养中低渗诱导的和高K（+）介导的肿胀之间的分子途径的关键方面。在后者的Ca（2+）介导的表皮生长因子（EGF）受体的AG1478抑制反式激活中，通过布美他尼抑制了有丝分裂原活化蛋白（MAP）激酶途径向ERK磷酸化和NKCC1介导的肿胀的抑制。在前者中，抑制MAP激酶途径而不是抑制EGF受体的活化消除了ERK磷酸化，但对肿胀没有影响，表明ERK的活化是肿胀的结果，而不是原因。

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