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首页> 外文期刊>Cellular Physiology and Biochemistry >Calcium-sensing receptor activation increases cell-cell adhesion and β-cell function
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Calcium-sensing receptor activation increases cell-cell adhesion and β-cell function

机译：钙敏感受体激活可增强细胞粘附和β细胞功能

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Background/Aims: The extracellular calcium-sensing receptor (CaR) is expressed in pancreatic β-cells where it is thought to facilitate cell-to-cell communication and augment insulin secretion. However, it is unknown how CaR activation improves β-cell function. Methods: Immunocytochemistry and western blotting confirmed the expression of CaR in MIN6 β-cell line. The calcimimetic R568 (1μM) was used to increase the affinity of the CaR and specifically activate the receptor at a physiologically appropriate extracellular calcium concentration. Incorporation of 5-bromo-2'-deoxyuridine (BrdU) was used to measure cell proliferation, whilst changes in non-nutrient-evoked cytosolic calcium were assessed using fura-2- microfluorimetry. AFM-single-cell-force spectroscopy related CaR-evoked changes in epithelial (E)-cadherin expression to improved functional tethering between coupled cells. Results: Activation of the CaR over 48hr doubled the expression of E-cadherin (206±41%) and increased L-type voltage-dependent calcium channel expression by 70% compared to control. These changes produced a 30% increase in cell-cell tethering and elevated the basal-to-peak amplitude of ATP (50μM) and tolbutamide (100μM)-evoked changes in cytosolic calcium. Activation of the receptor also increased PD98059 (1-100μM) and SU1498 (1-100μM)-dependent β-cell proliferation. Conclusion: Our data suggest that activation of the CaR increases E-cadherin mediated functional tethering between β-cells and increases expression of L-type VDCC and secretagogue-evoked changes in [Ca ~(2+)] _i. These findings could explain how local changes in calcium, co-released with insulin, activate the CaR on neighbouring cells to help ensure efficient and appropriate secretory function.
机译：背景/目的：细胞外钙敏感受体（CaR）在胰腺β细胞中表达，据认为可促进细胞间通讯并增加胰岛素分泌。然而，未知CaR激活如何改善β细胞功能。方法：免疫细胞化学和Western blotting证实CaR在MIN6β细胞系中的表达。拟钙剂R568（1μM）用于增加CaR的亲和力，并在生理上适当的细胞外钙浓度下特异性激活受体。使用5-溴-2'-脱氧尿苷（BrdU）的掺入来测量细胞增殖，同时使用呋喃-2-微荧光法评估非营养素诱发的胞质钙的变化。 AFM单细胞力光谱法可引起CaR引起的上皮（E）-钙黏着蛋白表达变化，从而改善耦合细胞之间的功能性束缚。结果：与对照组相比，CaR在48小时内的激活使E-钙黏着蛋白的表达增加了一倍（206±41％），并使L型电压依赖性钙通道的表达增加了70％。这些变化使细胞-细胞束缚增加了30％，并增加了ATP（50μM）和甲苯丁酰胺（100μM）引起的胞质钙变化的基峰幅度。受体的激活还增加了PD98059（1-100μM）和SU1498（1-100μM）依赖的β细胞增殖。结论：我们的数据表明CaR的激活增加了E-钙粘蛋白介导的β细胞之间的功能性束缚，并增加了L型VDCC的表达和促分泌素引起的[Ca〜（2+）] _i变化。这些发现可以解释与胰岛素共释放的钙的局部变化如何激活邻近细胞上的CaR，以帮助确保有效和适当的分泌功能。

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