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首页> 外文期刊>Cellular Signalling >Norepinephrine induces slow calcium signalling in murine brown preadipocytes through the beta-adrenoceptor/cAMP/protein kinase A pathway
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Norepinephrine induces slow calcium signalling in murine brown preadipocytes through the beta-adrenoceptor/cAMP/protein kinase A pathway

机译：去甲肾上腺素通过β-肾上腺素受体/ cAMP /蛋白激酶A途径诱导鼠棕色前脂肪细胞中的钙信号缓慢传递

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The mechanism of adrenergically activated calcium signalling in isolated murine brown preadipocytes (stromal-vascular fraction) was studied with Fura-2. Norepinephrine (NE) generated in preadipocytes a slow Ca2+-response ( similar to10 nM/min) without a burst and a maximum, whereas in mature brown adipocytes, the quick burst reached 1.5 muM [Ca2+](i). Thapsigargin, which is known to discharge Ca2+ ions from the IP3-sensitive stores, initiated a huge capacitative calcium entry in mature brown adipocytes but failed to stimulate a response in preadipocytes. The beta-selective antagonist nadolol almost completely prevented the effect of NE on [Ca2+](i), while the antagonist of alpha-adrenoceptors phentolamine caused only a similar to 25% reduction of the cellular response. Forskolin or the cell-permeable Br-cAMP caused [Ca2+](i) rise, which were even higher than with NE. The protein kinase A (PKA) inhibitor N-[2-(p-bromocynnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89) reduced and the phosphodiesterase inhibitors 3-isobutyl-1-methylxanthine (IBMX), N-cyclohexyl-N-(2-hydroxyethyl)-4-(6-(1,2-dihydro-2-oxoquinolyloxy))butyra mide (OPC-3911), 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidone (Ro 20-1724) or the protein phosphatase inhibitor okadaic acid enhanced the NE-, isoproterenol- or forskolin-initiated cellular calcium responses. It was concluded that (i) brown preadipocytes lacked a trigger mechanism of initiation of [Ca2+](i) rises and (ii) the cAMP- and protein kinase A-mediated phosphorylation played an important role in the beta-adrenoceptor-initiated calcium signalling in these cells. All these features distinguish brown adipocyte precursors from differentiated brown adipocytes, where calcium signalling is initiated exclusively via alpha(1)-adrenoceptors and the trigger mechanism. (C) 2003 Elsevier Science Inc. All rights reserved. [References: 39]
机译：用Fura-2研究了分离的鼠棕色前脂肪细胞（基质血管部分）中肾上腺素激活钙信号转导的机制。前脂肪细胞中产生的去甲肾上腺素（NE）缓慢的Ca2 +响应（类似于10 nM / min）没有爆发，并且最大，而在成熟的棕色脂肪细胞中，快速爆发达到1.5μM[Ca2 +]（i）。 Thapsigargin已知可以从IP3敏感存储中释放Ca2 +离子，它在成熟的棕色脂肪细胞中引发了巨大的电容性钙进入，但未能刺激前脂肪细胞的反应。 β选择性拮抗剂纳多洛尔几乎完全阻止了NE对[Ca2 +]（i）的影响，而α-肾上腺素受体酚妥拉明的拮抗剂仅引起细胞反应降低约25％。 Forskolin或可透过细胞的Br-cAMP引起[Ca2 +]（i）升高，甚至比NE升高。蛋白激酶A（PKA）抑制剂N- [2-（对溴氰基氨基）乙基] -5-异喹啉磺酰胺（H-89）还原，磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤（IBMX），N-环己基-N -（2-羟乙基）-4-（6-（1,2-二氢-2-氧喹啉基氧基））丁酸中和酯（OPC-3911），4-（3-丁氧基-4-甲氧基苄基）-2-咪唑啉酮（Ro 20 -1724）或蛋白磷酸酶抑制剂冈田酸增强了NE，异丙肾上腺素或福司可林引发的细胞钙反应。结论是：（i）棕色前脂肪细胞缺乏启动[Ca2 +]的触发机制（i）升高，并且（ii）cAMP和蛋白激酶A介导的磷酸化在β-肾上腺素受体引发的钙信号传导中起重要作用在这些细胞中。所有这些特征将褐色脂肪细胞前体与分化的褐色脂肪细胞区分开，在褐色脂肪细胞中，钙信号传导仅通过alpha（1）-肾上腺素能受体和触发机制启动。 （C）2003 Elsevier Science Inc.保留所有权利。 [参考：39]

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