Dexamethasone activates transient receptor potential canonical 4 (TRPC4) channels via Rasd1 small GTPase pathway

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• 作者：Jinhong Wie ; Jinsung Kim ; Kotdaji Ha…
• 关键词：TRPC4 ; Small G protein ; Rasd1 ; GPCR ; Dexamethasone ; Insulin
• 刊名：Pfl篓鹿gers Archiv - European Journal of Physiology
• 出版年：2015
• 出版时间：October 2015
• 年：2015
• 卷：467
• 期：10
• 页码：2081-2091
• 全文大小：2,410 KB
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• 作者单位：Jinhong Wie (1)
  Jinsung Kim (1) (2)
  Kotdaji Ha (1)
  Yin Hua Zhang (1)
  Ju-Hong Jeon (1)
  Insuk So (1)
  
  1. Department of Physiology, Seoul National University College of Medicine, Seoul, 110-799, Republic of Korea
  2. Catholic University of Korea, College of Medicine, Seoul, 137-701, Republic of Korea
  
• 刊物主题：Human Physiology;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-2013

文摘

Canonical transient receptor potential 4 (TRPC4) channels are calcium-permeable, nonselective cation channels that are widely distributed in mammalian cells. It is generally speculated that TRPC4 channels are activated by G_q/11-PLC pathway or directly activated by G_i/o proteins. Although many mechanistic studies regarding TRPC4 have dealt with heterotrimeric G proteins, here, we first report the functional relationship between TRPC4 and small GTPase, Rasd1. Rasd1 selectively activated TRPC4 channels, and it was the only Ras protein among Ras protein family that can activate TRPC4 channels. For this to occur, it was found that certain population of functional Gα_i1 and Gα_i3 proteins are essential. Meanwhile, dexamethasone, a synthetic glucocorticoid and anti-inflammatory drug was known to increase messenger RNA (mRNA) level of Rasd1 in pancreatic β-cells. We have found that dexamethasone triggers TRPC4-like cationic current in INS-1 cells via increasing protein expression level of Rasd1. This relationship among dexamethasone, Rasd1, and TRPC4 could suggest a new therapeutic agent for hospitalized diabetes mellitus (DM) patients with prolonged dexamethasone prescription. Keywords TRPC4 Small G protein Rasd1 GPCR Dexamethasone Insulin