Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Logo for

J. Cell Sci. 116 (7): 1269-1277

Research Article

Microtubule-dependent redistribution of the type-1 inositol 1,4,5-trisphosphate receptor in A7r5 smooth muscle cells

Elke Vermassen1, Kristel Van Acker1, Wim G. Annaert2, Bernard Himpens1, Geert Callewaert1, Ludwig Missiaen1, Humbert De Smedt1, and Jan B. Parys1,*

1 Laboratory of Physiology, CME/VIB04, K.U. Leuven Campus Gasthuisberg O/N, Herestraat 49, B-3000 Leuven, Belgium
2 Laboratory for Neuronal Membrane Trafficking, CME/VIB04, K.U. Leuven Campus Gasthuisberg O/N, Herestraat 49, B-3000 Leuven, Belgium

* Author for correspondence (e-mail: Jan.Parys{at}

Accepted for publication 7 January 2003.

Abstract: In A7r5 vascular smooth muscle cells, the two expressed inositol 1,4,5-trisphosphate receptor (IP3R) isoforms were differentially localized. IP3R1 was predominantly localized in the perinuclear region, whereas IP3R3 was homogeneously distributed over the cytoplasm. Prolonged stimulation (1-5 hours) of cells with 3 µM argininevasopressin induced a redistribution of IP3R1 from the perinuclear region to the entire cytoplasm, whereas the localization of IP3R3 appeared to be unaffected. The redistribution process occurred independently of IP3R downregulation. No structural changes of the endoplasmic reticulum were observed, but SERCA-type Ca2+ pumps redistributed similarly to IP3R1. The change in IP3R1 localization induced by arginine-vasopressin could be blocked by the simultaneous addition of nocodazole or taxol and depended on Ca2+ release from intracellular stores since Ca2+-mobilizing agents such as thapsigargin and cyclopiazonic acid could induce the redistribution. Furthermore, various protein kinase C inhibitors could inhibit the redistribution of IP3R1, whereas the protein kinase C activator 1-oleoyl-2-acetyl-sn-glycerol induced the redistribution. Activation of protein kinase C also induced an outgrowth of the microtubules from the perinuclear region into the cytoplasm, similar to what was seen for the redistribution of IP3R1. Finally, blocking vesicular transport at the level of the intermediate compartment inhibited the redistribution. Taken together, these findings suggest a role for protein kinase C and microtubuli in the redistribution of IP3R1, which probably occurs via a mechanism of vesicular trafficking.

Key Words: Calcium stores • Calcium • Cytoskeleton • Protein kinase C • Intracellular calcium channel

Facilitated Hyperpolarization Signaling in Vascular Smooth Muscle-overexpressing TRIC-A Channels.
S. Tao, D. Yamazaki, S. Komazaki, C. Zhao, T. Iida, S. Kakizawa, Y. Imaizumi, and H. Takeshima (2013)
J. Biol. Chem. 288, 15581-15589
   Abstract »    Full Text »    PDF »
CRACing the Cluster: Functionally Active Orai1 Channels in the Absence of Clustering With STIM1.
K. A. Smith and J. X.- J. Yuan (2012)
Circ. Res. 111, 9-11
   Full Text »    PDF »
Inositol trisphosphate receptors in smooth muscle cells.
D. Narayanan, A. Adebiyi, and J. H. Jaggar (2012)
Am J Physiol Heart Circ Physiol 302, H2190-H2210
   Abstract »    Full Text »    PDF »
An update on nuclear calcium signalling.
M. D. Bootman, C. Fearnley, I. Smyrnias, F. MacDonald, and H. L. Roderick (2009)
J. Cell Sci. 122, 2337-2350
   Abstract »    Full Text »    PDF »
Protein kinase C delta stimulates antigen presentation by Class II MHC in murine dendritic cells.
M. Majewski, T. O. Bose, F. C. M. Sille, A. M. Pollington, E. Fiebiger, and M. Boes (2007)
Int. Immunol. 19, 719-732
   Abstract »    Full Text »    PDF »
Cell++--simulating biochemical pathways.
C. Sanford, M. L.K. Yip, C. White, and J. Parkinson (2006)
Bioinformatics 22, 2918-2925
   Abstract »    Full Text »    PDF »
Inositol 1,4,5-trisphosphate supports the arrhythmogenic action of endothelin-1 on ventricular cardiac myocytes.
A. Proven, H. L. Roderick, S. J. Conway, M. J. Berridge, J. K. Horton, S. J. Capper, and M. D. Bootman (2006)
J. Cell Sci. 119, 3363-3375
   Abstract »    Full Text »    PDF »
Cluster Formation of Inositol 1,4,5-Trisphosphate Receptor Requires Its Transition to Open State.
Y. Tateishi, M. Hattori, T. Nakayama, M. Iwai, H. Bannai, T. Nakamura, T. Michikawa, T. Inoue, and K. Mikoshiba (2005)
J. Biol. Chem. 280, 6816-6822
   Abstract »    Full Text »    PDF »
Translational Mobility of the Type 3 Inositol 1,4,5-Trisphosphate Receptor Ca2+ Release Channel in Endoplasmic Reticulum Membrane.
M. Ferreri-Jacobia, D.-O. D. Mak, and J. K. Foskett (2005)
J. Biol. Chem. 280, 3824-3831
   Abstract »    Full Text »    PDF »
Distinct Roles of Inositol 1,4,5-Trisphosphate Receptor Types 1 and 3 in Ca2+ Signaling.
M. Hattori, A. Z. Suzuki, T. Higo, H. Miyauchi, T. Michikawa, T. Nakamura, T. Inoue, and K. Mikoshiba (2004)
J. Biol. Chem. 279, 11967-11975
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882