論文

査読有り
2011年4月

A fundamental role for NO-PLC signaling pathway in mediating intracellular Ca2+ oscillation in pancreatic acini

NITRIC OXIDE-BIOLOGY AND CHEMISTRY
  • Amira Moustafa
  • ,
  • Kentaro Q. Sakamoto
  • ,
  • Yoshiaki Habara

24
3
開始ページ
139
終了ページ
150
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.niox.2011.02.001
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

The aim of the present study was to investigate the possible interaction between intracellular Ca2+ and nitric oxide (NO) in rat pancreatic acinar cells, especially intracellular signaling events. (1) Nitric oxide donors SNP (0.1-100 mu M) and NOR-3 (50-400 mu M) induced Ca2+ oscillations in fluo-4-loaded acini, that appeared to be analogous to what we usually observe in acini stimulated with physiological secretagogues such as CCK-8 and this oscillations were abolished in the presence of carboxy-PTIO. (2) The NO donors-evoked Ca2+ oscillations were not abolished even in the absence of extracellular Ca2+ but totally disappeared when cells were pretreated with thapsigargin, a sarcoplasmic-endoplasmic reticulum Ca2+ ATPase (SERCA) inhibitor. (3) Inhibition of guanylate cyclase with 1 H-[1,2,4] oxadiazolo [4,3-a] quinoxaline-1-one (ODQ) attenuated Ca2+ oscillations evoked by SNP in the absence of extracellular Ca2+ (4) Inhibitors of phospholipase C activity, U73122 and the IP3R blocker xestospongin C, both abolished the SNP-induced Ca2+ response. (5) Furthermore, we found that both CCK-8 and carbachol (CCh) induced NO production in DAF-2-loaded acinar cells and that an inhibitor of NO synthase, N-G-monomethyl-L-arginine (L-NMMA), significantly reduced CCK-8-induced Ca2+ oscillation. These results indicate that NO mobilizes Ca2+ from internal stores through activation of guanylate cyclase and resultant cGMP production. In addition, PLC activation of IP3 production is also suggested to be involved in Ca2+ mobilization via IP3 receptors. This suggests the presence of cross-talk between Ca2+ and NO in pancreatic acini and this cascade may, at least partially, participate in physiological secretagogue-evoked Ca2+ dynamics in pancreatic acinar cells. (C) 2011 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.niox.2011.02.001
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21335096
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000289825600004&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.niox.2011.02.001
  • ISSN : 1089-8603
  • PubMed ID : 21335096
  • Web of Science ID : WOS:000289825600004

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