Endoplasmic reticulum Ca2+-ATPase pump is up-regulated in calcium-transporting dental enamel cells: a non-housekeeping role for SERCA2b

2001 ◽  
Vol 358 (1) ◽  
pp. 217-224 ◽  
Author(s):  
Isobel K. FRANKLIN ◽  
Robert A. WINZ ◽  
Michael J. HUBBARD

Dental enamel-forming cells face a major challenge to avoid the cytotoxic effects of excess calcium. We have characterized sarcoplasmic/endoplasmic reticulum calcium-ATPase pumps (SERCA) in rat enamel cells to address the proposal that non-mitochondrial calcium stores play a dominant role in transcellular calcium transport. A single major isoform, SERCA2b, was detected during the protein-secretory and calcium-transport stages of enamel formation using reverse-transcriptase PCR, cDNA cloning, Northern analysis and immunoblotting. Most importantly, SERCA2b exhibited a specific 3-fold up-regulation to high expression levels during calcium transport, as determined by quantitative immunoblotting and ATPase assays. Sensitivity of the calcium-dependent ATPase to thapsigargin and three other SERCA inhibitors was characterized. These findings indicate that enamel cells are well-equipped to sequester calcium in endoplasmic reticulum stores and so protect against calcium toxicity, associate SERCA with transcellular calcium transport for the first time, and establish SERCA2b as a molecular and pharmacological target for future investigations of calcium transcytosis. The observed physiological regulation in enamel cells contradicts the widespread perception that SERCA2b is restricted to general housekeeping duties.

2008 ◽  
Vol 294 (6) ◽  
pp. F1279-F1286 ◽  
Author(s):  
Kimberly H. Weber ◽  
Eun Kyung Lee ◽  
Uma Basavanna ◽  
Sabina Lindley ◽  
Roy C. Ziegelstein ◽  
...  

We previously found that polycystin-1 accelerated the decay of ligand-activated cytoplasmic calcium transients through enhanced reuptake of calcium into the endoplasmic reticulum (ER; Hooper KM, Boletta A, Germino GG, Hu Q, Ziegelstein RC, Sutters M. Am J Physiol Renal Physiol 289: F521–F530, 2005). Calcium flux across the ER membrane is determined by the balance of active uptake and passive leak. In the present study, we show that polycystin-1 inhibited calcium leak across the ER membrane, an effect that would explain the capacity of this protein to accelerate clearance of calcium from the cytoplasm following a calcium release response. Calcium leak was detected by measurement of the accumulation of calcium in the cytoplasm following treatment with thapsigargin. Heterologous polycystin-1, stably expressed in Madin-Darby canine kidney cells, attenuated the thapsigargin-induced calcium peak with no effect on basal calcium stores, mitochondrial calcium uptake, or extrusion of calcium across the plasma membrane. The capacity of polycystin-1 to limit the rate of decay of ER luminal calcium following inhibition of the pump was shown indirectly using the calcium ionophore ionomycin, and directly by loading the ER with a low-affinity calcium indicator. We conclude that disruption of ER luminal calcium homeostasis may contribute to the cyst phenotype in autosomal dominant polycystic kidney disease.


2005 ◽  
Vol 167 (1) ◽  
pp. 233-242 ◽  
Author(s):  
Jean-Philippe Brouland ◽  
Pascal Gélébart ◽  
Tünde Kovàcs ◽  
Jocelyne Enouf ◽  
Johannes Grossmann ◽  
...  

1998 ◽  
Vol 5 ◽  
pp. 135
Author(s):  
V. Pinelis ◽  
D. Fajuk ◽  
L. Khaspekov ◽  
T. Storozhevykh ◽  
N. Vinskaya ◽  
...  

2004 ◽  
Vol 322 (4) ◽  
pp. 1223-1236 ◽  
Author(s):  
Béla Papp ◽  
Jean-Philippe Brouland ◽  
Pascal Gélébart ◽  
Tünde Kovàcs ◽  
Christine Chomienne

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