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Am J Physiol Cell Physiol 297: C188-C197, 2009. First published May 13, 2009; doi:10.1152/ajpcell.00052.2009
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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Identification of the large-conductance background K+ channel in mouse B cells as TREK-2

Haifeng Zheng,1 Joo Hyun Nam,1 Bo Pang,1 Dong Hoon Shin,1 Ji Seon Kim,1,4 Yang-Sook Chun,1,4 Jong-Wan Park,2,4 Hyowon Bang,5 Woo Kyung Kim,6 Yung E. Earm,1 and Sung Joon Kim1,3,4

1Department of Physiology, 2Department of Pharmacology, 3Kidney Research Institute, 4Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul; 5Department of Physiology, Chung-Ang University College of Medicine, Seoul; and 6Department of Internal Medicine, Dongguk University College of Medicine, Kyungpook, Korea

Submitted 28 January 2009 ; accepted in final form 10 May 2009

Mouse B cells and their cell line (WEHI-231) express large-conductance background K+ channels (LKbg) that are activated by arachidonic acids, characteristics similar to TREK-2. However, there is no evidence to identify the molecular nature of LKbg; some properties of LKbg were partly different from the reported results of TREK type channels. In this study, we compared the properties of cloned TREK-2 and LKbg in terms of their sensitivities to ATP, phosphatidylinositol 4,5-bisphosphate (PIP2), intracellular pH (pHi), and membrane stretch. Similar to the previous findings of LKbg, TREK-2 showed spontaneous activation after membrane excision (i-o patch) and were inhibited by MgATP or by PIP2. The inhibition by MgATP was prevented by wortmannin, suggesting membrane-delimited regulation of TREKs by phosphoinositide (PI) kinase. The same was observed with the property of LKbg; the activation of TREK-2 by membrane stretch was suppressed by U73122 [GenBank] (PLC inhibitor). As with the known properties of TREK-2, LKbg were activated by acidic pHi and inhibited by PKC activator. Finally, we confirmed the expression of TREK-2 in WEHI-231 by using RT-PCR and immunoblot analyses. The amplitude of background K+ current and the TREK-2 expression in WEHI-231 were commonly decreased by genetic knockdown of TREK-2 using small interfering RNA. The downregulation of TREK-2 attenuated Ca2+-influx induced by arachidonic acid in WEHI-231. As a whole, these results strongly indicate that TREK-2 encodes LKbg in mouse B cells. We also newly suggest that the low activity of TREK-2 in intact cells is due to the inhibition by intrinsic PIP2.

K2P channel; arachidonic acid; PI kinase; membrane stretch; immune cells


Address for reprint requests and other correspondence: S. J. Kim, Dept. of Physiology, Seoul National Univ. College of Medicine, 103 Daehangno, Jongno-gu, Seoul 110-799, Korea (E-mail: sjoonkim{at}snu.ac.kr)






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