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


     

Am J Physiol Cell Physiol 286: C213-C221, 2004. First published October 8, 2003; doi:10.1152/ajpcell.00346.2003
0363-6143/04 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
286/2/C213    most recent
00346.2003v1
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 ISI 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 ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Huang, L.
Right arrow Articles by Li, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Huang, L.
Right arrow Articles by Li, M.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

[Ca2+]i regulates trafficking of Cav1.3 ({alpha}1D Ca2+ channel) in insulin-secreting cells

Luping Huang,1,* Arin Bhattacharjee,2,* James T. Taylor,1 Min Zhang,3 Brian M. Keyser,1 Luis Marrero,4 and Ming Li1

1Departments of Pharmacology, Tulane University Health Sciences Center and 4Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112; 2Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520; and 3Department of Pharmacology, Medical College of Virginia, Richmond, Virginia 23298

Submitted 12 August 2003 ; accepted in final form 25 September 2003

Chronic exposure of pancreatic {beta}-cells to high concentrations of glucose impairs the insulin secretory response to further glucose stimulation. This phenomenon is referred to as glucose desensitization. It has been shown that glucose desensitization is associated with abnormal elevation of {beta}-cell basal intracellular free Ca2+ concentration ([Ca2+]i). We have investigated the relationship between the basal intracellular free Ca2+ and the L-type (Cav1.3) Ca2+ channel translocation in insulin-secreting cells. Glucose stimulation or membrane depolarization induced a nifedipine-sensitive Ca2+ influx, which was attenuated when the basal [Ca2+]i was elevated. Using voltage-clamp techniques, we found that changing [Ca2+]i could regulate the amplitude of the Ca2+ current. This effect was attenuated by drugs that interfere with the cytoskeleton. Immunofluorescent labeling of Cav1.3 showed an increase in the cytoplasmic distribution of the channels under high [Ca2+]i conditions by deconvolution microscopy. The [Ca2+]i-dependent translocation of Cav1.3 channel was also demonstrated by Western blot analysis of biotinylation/NeutrAvidin-bead-eluted surface proteins in cells preincubated at various [Ca2+]i. These results suggest that Cav1.3 channel trafficking is involved in glucose desensitization of pancreatic {beta}-cells.

internalization; intracellular free calcium; glucose desensitization


Address for reprint requests and other correspondence: M. Li, Depts. of Pharmacology SL-83, 1430 Tulane Ave., New Orleans, LA 70112 (E-mail: mli{at}tulane.edu).




This article has been cited by other articles:


Home page
 J. Physiol.Home page
E. L. Morgan, O. J. Mace, J. Affleck, and G. L. Kellett
Apical GLUT2 and Cav1.3: regulation of rat intestinal glucose and calcium absorption
J. Physiol., April 15, 2007; 580(2): 593 - 604.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
O. J. Mace, E. L. Morgan, J. A. Affleck, N. Lister, and G. L. Kellett
Calcium absorption by Cav1.3 induces terminal web myosin II phosphorylation and apical GLUT2 insertion in rat intestine
J. Physiol., April 15, 2007; 580(2): 605 - 616.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
J. T. Taylor, L. Huang, B. M. Keyser, H. Zhuang, C. W. Clarkson, and M. Li
Role of high-voltage-activated calcium channels in glucose-regulated {beta}-cell calcium homeostasis and insulin release
Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E900 - E908.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
S.-N. Yang and P.-O. Berggren
{beta}-Cell CaV channel regulation in physiology and pathophysiology
Am J Physiol Endocrinol Metab, January 1, 2005; 288(1): E16 - E28.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
L. Huang, B. M. Keyser, T. M. Tagmose, J. B. Hansen, J. T. Taylor, H. Zhuang, M. Zhang, D. S. Ragsdale, and M. Li
NNC 55-0396 [(1S,2S)-2-(2-(N-[(3-Benzimidazol-2-yl)propyl]-N-methylamino)ethyl)-6-fluoro-1,2,3,4-tetrahydro-1-isopropyl-2-naphtyl cyclopropanecarboxylate dihydrochloride]: A New Selective Inhibitor of T-Type Calcium Channels
J. Pharmacol. Exp. Ther., April 1, 2004; 309(1): 193 - 199.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the American Physiological Society.