Fine-tuning of eTRPM8 expression and activity conditions keratinocyte fate

IF 3.3 3区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Channels Pub Date : 2016-04-20 DOI:10.1080/19336950.2016.1168551

G. Bidaux, Anne-sophie Borowiec, N. Prevarskaya, D. Gordienko

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引用次数: 15

Abstract

ABSTRACT Recently, we reported the cloning and characterization of short isoform of the icilin-activated cold receptor TRPM8 channel in keratinocytes, dubbed eTRPM8. We demonstrated that eTRPM8 via fine tuning of the endoplasmic reticulum (ER) – mitochondria Ca2+ shuttling regulates mitochondrial ATP and superoxide (O2•-) production and, thereby, mediates control of epidermal homeostasis by mild cold. Here, we provide additional information explaining why eTRPM8 suppression and TRPM8 stimulation both inhibit keratinocyte growth. We also demonstrate that stimulation of eTRPM8 with icilin may give rise to sustained oscillatory responses. Furthermore, we show that ATP-induced cytosolic and mitochondrial Ca2+ responses are attenuated by eTRPM8 suppression. This suggests positive interplay between eTRPM8 and purinergic signaling pathways, what may serve to facilitate the ER-mitochondria Ca2+ shuttling. Finally, we demonstrate that cold (25°C) induces eTRPM8-dependent superoxide-mediated necrosis of keratinocytes. Altogether, these results are in line with our model of eTRPM8-mediated cold-dependent balance between keratinocyte proliferation and differentiation.

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微调eTRPM8的表达和活性条件角质细胞的命运

最近，我们报道了角化细胞中青霉素激活的冷受体TRPM8通道的短异构体的克隆和表征，称为eTRPM8。我们证明了eTRPM8通过内质网(ER) -线粒体Ca2+穿梭的微调调节线粒体ATP和超氧化物(O2•-)的产生，从而介导轻度寒冷对表皮稳态的控制。在这里，我们提供了额外的信息来解释为什么抑制TRPM8和刺激TRPM8都会抑制角化细胞的生长。我们还证明，用icilin刺激eTRPM8可能会引起持续的振荡反应。此外，我们发现atp诱导的细胞质和线粒体Ca2+反应被eTRPM8抑制减弱。这表明eTRPM8和嘌呤能信号通路之间存在积极的相互作用，这可能有助于促进er线粒体Ca2+穿梭。最后，我们证明低温(25°C)诱导etrpm8依赖性超氧化物介导的角质形成细胞坏死。总之，这些结果与我们的模型一致，即etrpm8介导的角化细胞增殖和分化之间的冷依赖平衡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Channels 生物-生化与分子生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Channels is an open access journal for all aspects of ion channel research. The journal publishes high quality papers that shed new light on ion channel and ion transporter/exchanger function, structure, biophysics, pharmacology, and regulation in health and disease. Channels welcomes interdisciplinary approaches that address ion channel physiology in areas such as neuroscience, cardiovascular sciences, cancer research, endocrinology, and gastroenterology. Our aim is to foster communication among the ion channel and transporter communities and facilitate the advancement of the field.