Am J Physiol Cell Physiol Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 284: C506-C510, 2003; doi:10.1152/ajpcell.00384.2002
0363-6143/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kawanabe, Y.
Right arrow Articles by Masaki, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawanabe, Y.
Right arrow Articles by Masaki, T.
Vol. 284, Issue 2, C506-C510, February 2003

Role of phosphoinositide 3-kinase in the nonselective cation channel activation by endothelin-1/endothelinB receptor

Yoshifumi Kawanabe1,2, Nobuo Hashimoto1, and Tomoh Masaki2

Departments of 1 Neurosurgery and 2 Pharmacology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto 606-8507, Japan

We recently demonstrated that endothelin-1 (ET-1) activates two types of Ca2+-permeable nonselective cation channel (designated NSCC-1 and NSCC-2) in Chinese hamster ovarian cells expressing endothelinB receptor (CHO-ETBR). These channels can be discriminated using the Ca2+ channel blockers, LOE 908 and SK&F 96365. LOE 908 is a blocker of NSCC-1 and NSCC-2, whereas SK&F 96365 is a blocker of NSCC-2. In this study, we investigated the possible role of phosphoinositide 3-kinase (PI3K) in the ET-1-induced activation of NSCCs in CHO-ETBR using wortmannin and LY-294002, inhibitors of PI3K. ET-1-induced Ca2+ influx was partially inhibited in CHO-ETBR pretreated with wortmannin or LY-294002. In contrast, addition of wortmannin or LY-294002 after stimulation with ET-1 did not suppress Ca2+ influx. The Ca2+ channels activated by ET-1 in wortmannin- or LY-294002-treated CHO-ETBR were sensitive to LOE 908 and resistant to SK&F 96365. In conclusion, NSCC-2 is stimulated by ET-1 via PI3K-dependent cascade, whereas NSCC-1 is stimulated independently of the PI3K pathway. Moreover, PI3K seems to be required for the initiation of the Ca2+ entry through NSCC-2 but not for its maintenance.

endothelin-1; endothelinB receptor; phosphoinositide 3-kinase; nonselective cation channel


This article has been cited by other articles:


Home page
 FASEB J.Home page
N. S. Dawson, D. C. Zawieja, M. H. Wu, and H. J. Granger
Signaling pathways mediating VEGF165-induced calcium transients and membrane depolarization in human endothelial cells
FASEB J, May 1, 2006; 20(7): 991 - 993.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
Y. Kawanabe, N. Hashimoto, and T. Masaki
Characterization of G proteins involved in activation of nonselective cation channels and arachidonic acid release by norepinephrine/{alpha}1A-adrenergic receptors
Am J Physiol Cell Physiol, March 1, 2004; 286(3): C596 - C600.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
Y. Kawanabe, N. Hashimoto, and T. Masaki
Effects of nonselective cation channels and PI3K on endothelin-1-induced PYK2 tyrosine phosphorylation in C6 glioma cells
Am J Physiol Cell Physiol, September 1, 2003; 285(3): C539 - C545.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online