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首页> 外文期刊>Life sciences >Hydrogen peroxide enhanced Ca 2+-activated BK currents and promoted cell injury in human dermal fibroblasts
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Hydrogen peroxide enhanced Ca 2+-activated BK currents and promoted cell injury in human dermal fibroblasts

机译：过氧化氢增强人皮肤成纤维细胞中Ca 2+激活的BK电流并促进细胞损伤

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Aims: Recent studies have shown that dermal fibroblasts possess multiple types of voltage-dependent K + channels, and the activation of these channels induces apoptosis. In the present study, we aimed to investigate whether hydrogen peroxide (H 2O 2), an oxidative stress inducer, could modulate these channels or induce human dermal fibroblasts injury. Main methods: The effects of H 2O 2 on K + currents were studied using a whole-cell recording. Intracellular PKC levels were measured with a direct human PKC enzyme immunoassay kit. Cell viability was assessed using PI staining and apoptotic nuclei were detected with TdT-mediated digoxigenin-dUTP nick-end labelling assay (TUNEL) assay. Key findings: Treatment of cells with 100 μM H 2O 2 resulted in a partially reversible increase in non-inactivating outward K + currents and an alteration in the steady-state activation property of the channels. The H 2O 2-induced increase in K + currents was mimicked by a PKC activator, and was blocked by the PKC inhibitor or the large conductance Ca 2+-activited K + (BK) channel blockers. The intracellular PKC levels were significantly enhanced by H 2O 2 treatment in a concentration-dependent manner. After exposure to H 2O 2, evaluation of fibroblasts survival rate and damaged cell number with TUNEL-positive nuclei revealed an increased cell injury. Blocking the K + channels with blockers significantly decreased the H 2O 2-induced human dermal fibroblasts injury. Significance: Our results revealed that H 2O 2 could enhance BK currents by PKC pathway. Increased K + currents might be related to H 2O 2-induced human dermal fibroblasts injury. The results reported here contribute to our understanding of the mechanism underlying H 2O 2-induced human dermal fibroblasts injury.
机译：目的：最近的研究表明，真皮成纤维细胞具有多种类型的电压依赖性钾离子通道，这些通道的激活可诱导细胞凋亡。在本研究中，我们旨在研究过氧化氢（H 2O 2），一种氧化应激诱导剂，是否可以调节这些通道或诱导人皮肤成纤维细胞的损伤。主要方法：使用全细胞记录研究了H 2O 2对K +电流的影响。用直接人PKC酶免疫测定试剂盒测量细胞内PKC水平。使用PI染色评估细胞活力，并使用TdT介导的洋地黄毒苷-dUTP缺口末端标记测定（TUNEL）测定检测凋亡细胞核。关键发现：用100μMH 2O 2处理细胞导致非灭活的向外K +电流部分可逆地增加，并改变了通道的稳态激活特性。 H 2 O 2诱导的K +电流增加被PKC激活剂模拟，并被PKC抑制剂或大电导的Ca 2+激活的K +（BK）通道阻滞剂阻​​止。 H 2O 2处理以浓度依赖的方式显着提高了细胞内PKC水平。暴露于H 2O 2后，用TUNEL阳性核评估成纤维细胞的存活率和受损细胞数表明细胞损伤增加。用阻滞剂阻断K +通道可显着降低H 2O 2诱导的人皮肤成纤维细胞损伤。启示：我们的结果显示H 2O 2可以通过PKC途径增强BK电流。 K +电流增加可能与H 2O 2诱导的人类皮肤成纤维细胞损伤有关。此处报道的结果有助于我们理解H 2O 2诱导的人类皮肤成纤维细胞损伤的潜在机制。

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