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首页> 外文期刊>Cell and Tissue Research >Cellular channelopathy mediated by hypergravity: IL-6-mediated Nkcc1 activation and enhanced Trpm2 expression in rat atrium
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Cellular channelopathy mediated by hypergravity: IL-6-mediated Nkcc1 activation and enhanced Trpm2 expression in rat atrium

机译:由超高起症介导的细胞通道病变:IL-6介导的NKCC1激活和提高大鼠中庭的TRPM2表达

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摘要

Although cardiac tissue is considered a target of gravitational force (g-force), the mechanism of hypergravity on the ion modulation or identification of ion transporters is still unknown. Thus, we determine the effect of hypergravity on a physical force-sensitive cytokine, IL-6 and its related channel activity to investigate rat cardiac function changes in response to accelerated g-force. Serum IL-6 levels and intracellular calcium levels of the right atrium were moderately increased under hypergravity stimulation (4g). IL-6 was involved in the modulation of sodium-potassium-chloride cotransporter (Nkcc) activity. Surprisingly, the right atrium under 4g revealed significantly enhanced Nkcc1 activity. The use of IL-6 on the NKCC1-overexpressed or native NKCC-expressing cells also showed enhanced NKCC1 activity. Hypergravity conditions were also involved in the oxidative stress activated Trpm2 channel and revealed an enhanced expression of the Trpm2 channel under 4g in the rat right atrium. In conclusion, hypergravity revealed that moderate increases in serum IL-6 and enhanced Nkcc1 activity was modulated by IL-6. In addition, enhanced Trpm2 channel expression could be involved in the increased intracellular calcium levels of the right atrium under hypergravitational force. We therefore address that enhanced physical force-sensitive cytokine and oxidative stress by the gravitational force mediate activation of the cotransporter involved in possibilities of edema and calcium loading in cardiac tissue.
机译:虽然心脏组织被认为是重力(g-力)的目标,但超重力对离子调节或识别离子转运蛋白的机制仍不清楚。因此,我们确定超重力对物理力敏感细胞因子IL-6及其相关通道活性的影响,以研究加速重力对大鼠心功能的影响。在超重力刺激(4g)下,血清IL-6水平和右心房细胞内钙水平适度升高。IL-6参与了氯化钠钾共转运蛋白(Nkcc)活性的调节。令人惊讶的是,4g以下的右心房显示Nkcc1活性显著增强。在NKCC1过度表达或天然NKCC表达细胞上使用IL-6也显示出NKCC1活性增强。超重条件也参与了氧化应激激活的Trpm2通道,并显示在4g以下大鼠右心房Trpm2通道的表达增强。总之,超重显示血清IL-6的中度升高和Nkcc1活性的增强是由IL-6调节的。此外,Trpm2通道表达增强可能与超重力作用下右心房细胞内钙水平升高有关。因此,我们研究了通过重力增强的体力敏感细胞因子和氧化应激介导共转运蛋白的激活,该共转运蛋白参与了心肌组织水肿和钙负荷的可能性。

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