Activation of TRPV4 channel in pancreatic INS-1E beta cells enhances glucose-stimulated insulin secretion via calcium-dependent mechanisms

被引：24
作者：
Skrzypski, M. [1 ,2 ]
Kakkassery, M. [1 ]
Mergler, S. [3 ]
Groetzinger, C. [1 ]
Khajavi, N. [3 ]
Sassek, M. [2 ]
Szczepankiewicz, D. [2 ]
Wiedenmann, B. [1 ]
Nowak, K. W. [2 ]
Strowski, M. Z. [1 ]
机构：
[1] Charite, Dept Gastroenterol & Hepatol, Interdisciplinary Ctr Metab Endocrinol Diabet & M, D-13353 Berlin, Germany
[2] Poznan Univ Life Sci, Dept Anim Physiol & Biochem, PL-60637 Poznan, Poland
[3] Charite, Dept Ophthalmol, D-13353 Berlin, Germany
来源：
FEBS LETTERS | 2013年 / 587卷 / 19期
关键词：
Beta cell; Calcium; INS-1E; Insulin secretion; TRP; TRPV4; NONSELECTIVE CATION CHANNEL; ION-CHANNEL; RECEPTOR; SENSITIVITY; METABOLISM; ISLETS;
D O I：
10.1016/j.febslet.2013.08.025
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Transient receptor potential channel vanilloid type 4 (TRPV4) is a Ca2+- and Mg2+-permeable cation channel that influences oxidative metabolism and insulin sensitivity. The role of TRPV4 in pancreatic beta cells is largely unknown. Here, we characterize the role of TRPV4 in controlling intracellular Ca2+ and insulin secretion in INS-1E beta cells. Osmotic, thermal or pharmacological activation of TRPV4 caused a rapid rise of intracellular Ca2+ and enhanced glucose-stimulated insulin secretion. In the presence of the TRPV channel blocker ruthenium red (RuR) or after suppression of TRPV4 protein production, TRPV4 activators failed to increase [Ca2+]i and insulin secretion in INS-1E cells. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
引用
收藏
页码：3281 / 3287
页数：7
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