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首页> 外文期刊>Cellular Signalling >Characterization of voltage operated R-type Ca2+ channels in modulating somatostatin receptor subtype 2-and 3-dependent inhibition of insulin secretion from INS-1 cells
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Characterization of voltage operated R-type Ca2+ channels in modulating somatostatin receptor subtype 2-and 3-dependent inhibition of insulin secretion from INS-1 cells

机译：调节生长抑素受体亚型2-and 3依赖性胰岛素分泌的电压操作R型CA2 +通道的表征来自INS-1细胞的胰岛素分泌

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Somatostatin (SST) inhibits Ca2+ entry into pancreatic B-cells via voltage-operated Ca2+ channels (VOCCs) of L-type, leading to the suppression of insulin secretion. Activation of R-type channels increases insulin secretion. However, the role of R-type Ca2+ channels (Ca(v)2.3) in mediating the effects of SST on insulin secretion has not been so far investigated. Here, we identify the SST-receptor subtypes (SSTR) expressed on insulin-producing INS-1 cells by RT-PCR and by functional assays. The role of R-type channels in regulating [Ca2+](i) in response to SST-treatment was detected by cell fluorescence imaging and patch-clamp technique. INS-I expressed SSTR2 and SSTR3 and agonists (ag.) selective for these receptors reduced 10 nM exendin-4/20 mM glucose-stimulated insulin secretion. Surprisingly, SST and SST2-ag. transiently increased [Ca2+](i). Subsequently, these agonists led to a decrease in [Ca2+](i) below the basal levels. In contrast, SST3-ag failed to induce a transient peak of [Ca2+](i). Instead, a persistent minor suppression of [Ca2+](i) was detected from 25 min. R-type channel blocker SNX-482 altered [Ca2+](i) in SST- and SST2-ag.-treated cells. Notably, the inhibition of insulin secretion by SST and SST2-ag., but not SST3-ag. was attenuated by SNX-482. Taken together, SST and SSTR2 regulate [Ca2+](i) and insulin secretion in INS-1 cells via R-type channels. In contrast, the R-type calcium channel does not mediate the effects of SST3-ag. on insulin secretion. We conclude that R-type channels play a major role in the inhibition of insulin secretion by somatostatin in INS-1 cells. (c) 2008 Elsevier Inc. All rights reserved.
机译：生长抑素（SST）通过L型的电压操作的Ca2 +通道（Voccs）抑制Ca2 +进入胰腺B细胞，导致抑制胰岛素分泌。 R型通道的活化增加了胰岛素分泌。然而，目前还没有研究R型Ca2 +通道（Ca（v）2.3）在调解SST对胰岛素分泌的影响中的作用。这里，我们通过RT-PCR鉴定在产生胰岛素的INS-1细胞上表达的SST-受体亚型（SSTR）和功能测定。通过细胞荧光成像和贴片钳技术检测R型通道在调节[Ca2 +]（i）时的作用。 INS-I表达SSTR2和SSTR3和激动剂（AG。）对这些受体的选择性降低了10nm exendin-4 / 20mM葡萄糖刺激的胰岛素分泌。令人惊讶的是，SST和SST2-AG。瞬时增加[ca2 +]（i）。随后，这些激动剂导致基础水平以下的[Ca2 +]（i）减少。相反，SST3-AG未能诱导[CA2 +]（i）的瞬态峰。相反，从25分钟检测到[Ca2 +]（i）的持续微小抑制。 R型通道阻断器SNX-482在SST-和SST2-AG的细胞中改变[CA2 +]（I）。值得注意的是，SST和SST2-AG的抑制胰岛素分泌。但不是SST3-AG。被SNX-482衰减。一起使用的SST和SSTR2调节[Ca2 +]（I）和Ins-1细胞中的胰岛素分泌通过R型通道。相反，R型钙通道不会介导SST3-AG的效果。论胰岛素分泌。我们得出结论，R型频道在INS-1细胞中抑制胰岛素分泌抑制胰岛素分泌起作用。 （c）2008年elestvier Inc.保留所有权利。

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