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      Lysophosphatidylinositol-induced activation of the cation channel TRPV2 triggers glucagon-like peptide-1 secretion in enteroendocrine L cells

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          Abstract

          The lysophosphatidylinositol (LPI) has crucial roles in multiple physiological processes, including insulin exocytosis from pancreatic islets. However, the role of LPI in secretion of glucagon-like peptide-1 (GLP-1), a hormone that enhances glucose-induced insulin secretion, is unclear. Here, we used the murine enteroendocrine L cell line GLUTag and primary murine small intestinal cells to elucidate the mechanism of LPI-induced GLP-1 secretion. Exogenous LPI addition increased intracellular Ca 2+ concentrations ([Ca 2+] i ) in GLUTag cells and induced GLP-1 secretion from both GLUTag and acutely prepared primary intestinal cells. The [Ca 2+] i increase was suppressed by an antagonist for G protein-coupled receptor 55 (GPR55) and by silencing of GPR55 expression, indicating involvement of G q and G 12/13 signaling pathways in the LPI-induced increased [Ca 2+] i levels and GLP-1 secretion. However, GPR55 agonists did not mimic many of the effects of LPI. We also found that phospholipase C inhibitor and Rho-associated kinase inhibitor suppressed the [Ca 2+] i increase and that LPI increased the number of focal adhesions, indicating actin reorganization. Of note, blockage or silencing of transient receptor potential cation channel subfamily V member 2 (TRPV2) channels suppressed both the LPI-induced [Ca 2+] i increase and GLP-1 secretion. Furthermore, LPI accelerated TRPV2 translocation to the plasma membrane, which was significantly suppressed by a GPR55 antagonist. These findings suggest that TRPV2 activation via actin reorganization induced by G q and G 12/13 signaling is involved in LPI-stimulated GLP-1 secretion in enteroendocrine L cells. Because GPR55 agonists largely failed to mimic the effects of LPI, its actions on L cells are at least partially independent of GPR55 activation.

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          Author and article information

          Journal
          J Biol Chem
          J. Biol. Chem
          jbc
          jbc
          JBC
          The Journal of Biological Chemistry
          American Society for Biochemistry and Molecular Biology (11200 Rockville Pike, Suite 302, Rockville, MD 20852-3110, U.S.A. )
          0021-9258
          1083-351X
          30 June 2017
          22 May 2017
          : 292
          : 26
          : 10855-10864
          Affiliations
          From the []Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo 153-8902, Japan,
          [§ ]Cell Signaling Group, Waseda Bioscience Research Institute in Singapore (WABIOS), Singapore 138667, Singapore,
          []Comprehensive Research Organization, Waseda University, Tokyo 162-0041, Japan, and
          []National Research Institute for Child Health and Development, Tokyo 157-8535, Japan
          Author notes
          [1 ] To whom correspondence should be addressed: Dept. of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, 3-8-1 Komaba, Meguro, Tokyo 153-8902, Japan. Tel./Fax: 81-3-5465-8208; E-mail: takatsuboi@ 123456bio.c.u-tokyo.ac.jp .

          Edited by Henrik G. Dohlman

          Article
          PMC5491772 PMC5491772 5491772 M117.788653
          10.1074/jbc.M117.788653
          5491772
          28533434
          b7323bdf-02bc-4082-bb08-071534c92b95
          © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
          History
          : 28 March 2017
          : 17 May 2017
          Funding
          Funded by: Ministry of Education, Culture, Sports, Science, and Technology , open-funder-registry 10.13039/501100001700;
          Award ID: 26460289
          Award ID: 26291018
          Categories
          Signal Transduction

          cell signaling,exocytosis,G protein-coupled receptor (GPCR),hormone,imaging,transient receptor potential channels (TRP channels)

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