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Reactive oxygen and nitrogen species disturb Ca2+ oscillations in insulin-secreting MIN6 beta-cells

机译：活性氧和氮物质干扰胰岛素分泌性MIN6β细胞中的Ca2 +振荡

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摘要

Disturbances in pulsatile insulin secretion and Ca2+ oscillations in pancreatic -cells are early markers of diabetes, but the underlying mechanisms are still incompletely understood. Reactive oxygenitrogen species (ROS/RNS) are implicated in reduced -cell function, and ROS/RNS target several Ca2+ pumps and channels. Thus, we hypothesized that ROS/RNS could disturb Ca2+ oscillations and downstream insulin pulsatility. We show that ROS/RNS production by photoactivation of aluminum phthalocyanine chloride (AlClPc) abolish or accelerate Ca2+ oscillations in the MIN6 -cell line, depending on the amount of ROS/RNS. Application of the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) inhibitor thapsigargin modifies the Ca2+ response to high concentrations of ROS/RNS. Further, thapsigargin produces effects that resemble those elicited by moderate ROS/RNS production. These results indicate that ROS/RNS interfere with endoplasmic reticulum Ca2+ handling. This idea is supported by theoretical studies using a mathematical model of Ca2+ handling adapted to MIN6 cells. Our results suggest a putative link between ROS/RNS and disturbed pulsatile insulin secretion.
机译：胰腺细胞搏动性胰岛素分泌紊乱和Ca2 +振荡是糖尿病的早期标志，但其潜在机制仍不完全清楚。活性氧/氮物质（ROS / RNS）与细胞功能降低有关，ROS / RNS靶向多个Ca2 +泵和通道。因此，我们假设ROS / RNS可能会干扰Ca2 +振荡和下游胰岛素搏动。我们表明，通过光活化铝酞菁氯化铝（AlClPc）来产生ROS / RNS可以消除或加速MIN6-细胞系中的Ca2 +振荡，具体取决于ROS / RNS的量。肌浆/内质网Ca2 + ATPase（SERCA）抑制剂thapsigargin的应用可改变Ca2 +对高浓度ROS / RNS的反应。此外，thapsigargin产生的效果类似于中等ROS / RNS产生的效果。这些结果表明ROS / RNS干扰内质网Ca2 +处理。通过使用适用于MIN6细胞的Ca2 +处理数学模型的理论研究，此想法得到了支持。我们的结果表明ROS / RNS和脉动性胰岛素分泌紊乱之间的假定联系。

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