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Am J Physiol Heart Circ Physiol 296: H910-H916, 2009. First published February 13, 2009; doi:10.1152/ajpheart.00984.2008
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Translocon closure to Ca²⁺ leak in proliferating vascular smooth muscle cells

¹Multidisciplinary Cardiovascular Research Centre and ²Institute of Membrane and Systems Biology, Faculty of Biological Sciences, and ³Faculty of Medicine and Health, University of Leeds, and ⁴Department of Cardiac Surgery, Leeds General Infirmary, Great George Street, Leeds, United Kingdom; and ⁵Clinical Physiology Department, Faculty of Medicine, Menoufiya University, Menoufiya, Egypt

Submitted 10 September 2008 ; accepted in final form 10 February 2009

Vascular smooth muscle cells have a proliferative phenotype that is important in vascular development, adaptation, and disease. Intracellular calcium handling is thought to play pivotal roles in determining the properties of these cells, and thus previously unrecognized mechanisms for transmembrane calcium movement are of potential interest. An unsolved question is the mechanism of constitutive (passive) calcium leak from the intracellular stores. Studies of other cell types have suggested that the translocon is a calcium leak pathway. Here we investigated the contribution of the translocon in proliferating vascular smooth muscle cells. Calcium leak into the cytoplasm was measured using fura-2, and protein synthesis was measured using radioactive methionine. Puromycin, emetine, and anisomycin are chemicals that inhibit protein synthesis, acting via the translocon; all three agents strongly inhibited protein synthesis in the smooth muscle cells within 1 h. Puromycin, which opens the translocon, evoked a transient increase in cytoplasmic calcium that was similar in amplitude to the calcium rise evoked by thapsigargin. The puromycin effect was abolished by thapsigargin. The treatment of cells for 1 h with emetine or anisomycin, which close the translocon, inhibited the calcium release evoked by puromycin but not the calcium release evoked by extracellular ATP, endothelin-1, or the calcium ionophore ionomycin. Thapsigargin-evoked calcium rises were slightly suppressed by emetine but unaffected by puromycin or anisomycin. The data suggest that the translocon has the capacity to act as a calcium leak pathway in the ribosomal endoplasmic reticulum but that it is normally closed and lacks relevance to physiological calcium leak mechanisms.

calcium stores; blood vessels; remodeling

This article has been cited by other articles:

				J.-P. Savineau Is the translocon a crucial player of the calcium homeostasis in vascular smooth muscle cell? Am J Physiol Heart Circ Physiol, April 1, 2009; 296(4): H906 - H907. [Full Text] [PDF]