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首页> 外文期刊>Journal of cellular biochemistry. >Effects of cell swelling on intracellular calcium and membrane currents in bovine articular chondrocytes.
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Effects of cell swelling on intracellular calcium and membrane currents in bovine articular chondrocytes.

机译：细胞肿胀对牛关节软骨细胞内细胞内钙和膜电流的影响。

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Chondrocytes experience a dynamic extracellular osmotic environment during normal joint loading when fluid is forced from the matrix, increasing the local proteoglycan concentration and therefore the ionic strength and osmolarity. To exist in such a challenging environment, chondrocytes must possess mechanisms by which cell volume can be regulated. In this study, we investigated the ability of bovine articular chondrocytes (BAC) to regulate cell volume during a hypo-osmotic challenge. We also examined the effect of hypo-osmotic stress on early signaling events including [Ca2+](i) and membrane currents. Changes in cell volume were measured by monitoring the fluorescence of calcein-loaded cells. [Ca2+](i) was quantified using fura-2, and membrane currents were recorded using patch clamp. BAC exhibited regulated volume decrease (RVD) when exposed to hypo-osmotic saline which was inhibited by Gd3+. Swelling stimulated [Ca2+](i) transients in BAC which were dependent on swelling magnitude. Gd3+, zero [Ca2+](o), and thapsigargin all attenuated the [Ca2+](i) response, suggesting roles for Ca2+ influx through stretch activated channels, and Ca2+ release from intracellular stores. Inward and outward membrane currents significantly increased during cell swelling and were inhibited by Gd3+. These results indicate that RVD in BAC may involve [Ca2+](i) and ion channel activation, both of which play pivotal roles in RVD in other cell types. These signaling pathways are also similar to those activated in chondrocytes subjected to other biophysical signals. It is possible, then, that these signaling events may also be involved in a mechanism by which mechanical loads are transduced into appropriate cellular responses by chondrocytes.
机译：当从基质中迫使液体进入正常关节负荷时，软骨细胞会经历动态的细胞外渗透环境，从而增加了局部蛋白聚糖的浓度，从而增加了离子强度和渗透压。为了在如此具有挑战性的环境中生存，软骨细胞必须具有调节细胞体积的机制。在这项研究中，我们调查了牛关节软骨细胞（BAC）在低渗攻击过程中调节细胞体积的能力。我们还检查了低渗压力对早期信号事件（包括[Ca2 +]（i）和膜电流）的影响。通过监测钙黄绿素加载的细胞的荧光来测量细胞体积的变化。使用fura-2定量[Ca2 +]（i），并使用膜片钳记录膜电流。当暴露于被Gd3 +抑制的低渗盐水中时，BAC表现出调节的体积减少（RVD）。溶胀刺激了BAC中的[Ca2 +]（i）瞬变，这取决于溶胀的幅度。 Gd3 +，零[Ca2 +]（o）和毒胡萝卜素都减弱了[Ca2 +]（i）响应，表明Ca2 +通过伸展激活通道流入的作用以及Ca2 +从细胞内储存的释放。在细胞肿胀期间，内向和外向膜电流显着增加，并被Gd3 +抑制。这些结果表明，BAC中的RVD可能涉及[Ca2 +]（i）和离子通道激活，这两者在其他细胞类型的RVD中起关键作用。这些信号传导途径也类似于在经受其他生物物理信号的软骨细胞中激活的那些。因此，这些信号传递事件也可能与软骨细胞将机械负荷转换为适当的细胞反应的机制有关。

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