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1 Department of Cellular and Molecular Biology, Toronto General Hospital Research Institute, Toronto, ON, Canada
2 Department of Heart and Stroke Richard Lewar Centre of Excellence, University of Toronto, Toronto, ON, Canada
3 Department of Cellular and Molecular Biology, Toronto General Hospital Research Institute, Toronto, ON, Canada; Department of Heart and Stroke Richard Lewar Centre of Excellence, University of Toronto, Toronto, ON, Canada
4 Department of Heart and Stroke Richard Lewar Centre of Excellence, University of Toronto, Toronto, ON, Canada; Department of Medicine, University of Toronto, Toronto, ON, Canada
5 Department of Medicine, University of Toronto, Toronto, ON, Canada
6 Department of Heart and Stroke Richard Lewar Centre of Excellence, University of Toronto, Toronto, ON, Canada; Department of Medicine, University of Toronto, Toronto, ON, Canada; Department of Medicine, University of Toronto, Toronto, ON, Canada
* To whom correspondence should be addressed. E-mail: mansoor.husain{at}utoronto.ca.
Calcineurin mediates repression of plasma membrane Ca2+ ATPase-4 {PMCA4} expression in neurons, while c-Myb is known to repress PMCA1 expression in vascular smooth muscle cells {VSMC}. Here we describe a novel mouse VSMC line (MOVAS) in which 45Ca efflux rates decreased 50%, Fura2AM-based intracellular Ca2+ concentrations {[Ca2+]i} increased 2 fold, and real-time RT-PCR and Western blot revealed a ~ 40% decrease in PMCA4 expression levels from G0 to G1/S in the cell cycle, where PMCA4 constituted ~20% of total PMCA protein. Although calcineurin activity increased 5-fold as MOVAS progressed from G0 to G1/S, inhibition of this increase with either BAPTA or retroviral transduction with peptide inhibitors of calcineurin (CAIN), or its downstream target NFAT (VIVIT), had no effect on the repression of PMCA4 mRNA expression at G1/S. By contrast, Ca2+-independent activity of the calmodulin-dependent protein kinase-II {CaMK-II} increased 8 fold as MOVAS progressed from G0 to G1/S, and treatment with an inhibitor of CaMK-II (KN-93) or transduction of a c-Myb neutralizing antibody significantly alleviated the G1/S-associated repression of PMCA4. These data show that G1/S-specific PMCA4 repression in proliferating VSMC is brought about by c-Myb and CaMK-II, and that calcineurin may regulate cell cycle-associated [Ca2+]i through alternate targets.
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