Article ID Journal Published Year Pages File Type
2048056 FEBS Letters 2013 6 Pages PDF
Abstract

•Short heat shock decreased the endocytotic activity of human dendritic cells (DCs).•Heat shock-induced robust membrane currents in DCs.•These effects were mediated by TRPV2 ion channels.

Our goal was to investigate the effect of heat shock on human monocyte-derived dendritic cells (DCs) and to dissect the role of thermosensitive transient receptor potential (TRP) channels in the process. We provide evidence that a short heat shock challenge (43 °C) decreased the endocytotic activity of the DCs and that this effect could be alleviated by the RNAi-mediated knockdown of TRPV2 but, importantly, not by the pharmacological (antagonists) or molecular (RNAi) suppression of TRPV1 and TRPV4 activities/levels. Likewise, the heat shock-induced robust membrane currents were selectively and markedly inhibited by TRPV2 “silencing” whereas modulation of TRPV1 and TRPV4 activities, again, had no effect. These intriguing data introduce TRPV2-coupled signaling as a key player in mediating the cellular actions of heat shock on DCs.

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