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Activation of MAP kinase after reversible ATP depletion in LLC-PK1 cells

机译：在LLC-PK1细胞中可逆ATP消耗后MAP激酶的激活

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We examined the effect of recovery following reversible ATP depletion on MAP kinase activity in cultured renal cells of proximal tubular origin (LLC-PK1). We induced ATP depletion by 0.1 mu mol/l antimycin A in combination with substrate deprivation, and obtained recovery by restoration of substrate supply. MAP kinase activity increased from 374 +/- 45 pmol/mg protein/min during ATP depletion to 768 +/- 77 pmol/mg protein/min after 15 min of recovery. We used ATP to activate a representative G-protein coupled receptor, or epidermal growth factor (EGF) to activate receptors with intrinsic tyrosine kinase activity, and measured the effect of these manipulations on MAP kinase activity during ATP depletion or following recovery. ATP and EGF stimulated MAP kinase activity under control conditions, but not during ATP depletion or after recovery. This shows that two distinct signal transduction pathways represented by ATP and EGF are blocked during ATP depletion and recovery. The lack of energy during ATP depletion and the already maximally stimulated MAP kinase during recovery is likely to be the reason for these results. In summary, these findings suggest that MAP kinase may be involved in the physiological response of cells injured by hypoxia. Copyright (C) 2000 S. Karger AG, Basel. [References: 46]
机译：我们检查了可逆ATP消耗后恢复对近端肾小管起源的肾细胞（LLC-PK1）中MAP激酶活性的影响。我们通过0.1μmol / l抗霉素A结合底物剥夺诱导了ATP耗竭，并通过恢复底物供应获得了回收。 MAP激酶活性从ATP消耗期间的374 +/- 45 pmol / mg蛋白质/分钟增加到恢复15分钟后的768 +/- 77 pmol / mg蛋白质/分钟。我们使用ATP激活具有代表性的G蛋白偶联受体，或使用表皮生长因子（EGF）激活具有固有酪氨酸激酶活性的受体，并测量了这些操作对ATP耗竭期间或恢复后对MAP激酶活性的影响。在控制条件下，ATP和EGF刺激MAP激酶的活性，但在ATP耗尽期间或恢复后却没有。这表明在ATP消耗和恢复期间，由ATP和EGF代表的两个不同的信号转导途径被阻断。导致ATP耗竭期间能量不足以及恢复过程中已被最大程度刺激的MAP激酶很可能是这些结果的原因。总之，这些发现表明，MAP激酶可能参与了缺氧损伤细胞的生理反应。版权所有（C）2000 S.Karger AG，巴塞尔。 [参考：46]

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