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The non-excitable smooth muscle: calcium signaling and phenotypic switching during vascular disease House SJ; Potier M; Bisaillon J; Singer HA; Trebak MPflugers Arch 2008[Aug]; 456 (5): 769-85Calcium (Ca(2+)) is a highly versatile second messenger that controls vascular smooth muscle cell (VSMC) contraction, proliferation, and migration. By means of Ca(2+) permeable channels, Ca(2+) pumps and channels conducting other ions such as potassium and chloride, VSMC keep intracellular Ca(2+) levels under tight control. In healthy quiescent contractile VSMC, two important components of the Ca(2+) signaling pathways that regulate VSMC contraction are the plasma membrane voltage-operated Ca(2+) channel of the high voltage-activated type (L-type) and the sarcoplasmic reticulum Ca(2+) release channel, Ryanodine Receptor (RyR). Injury to the vessel wall is accompanied by VSMC phenotype switch from a contractile quiescent to a proliferative motile phenotype (synthetic phenotype) and by alteration of many components of VSMC Ca(2+) signaling pathways. Specifically, this switch that culminates in a VSMC phenotype reminiscent of a non-excitable cell is characterized by loss of L-type channels expression and increased expression of the low voltage-activated (T-type) Ca(2+) channels and the canonical transient receptor potential (TRPC) channels. The expression levels of intracellular Ca(2+) release channels, pumps and Ca(2+)-activated proteins are also altered: the proliferative VSMC lose the RyR3 and the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase isoform 2a pump and reciprocally regulate isoforms of the ca(2+)/calmodulin-dependent protein kinase II. This review focuses on the changes in expression of Ca(2+) signaling proteins associated with VSMC proliferation both in vitro and in vivo. The physiological implications of the altered expression of these Ca(2+) signaling molecules, their contribution to VSMC dysfunction during vascular disease and their potential as targets for drug therapy will be discussed.|*Phenotype[MESH]|Animals[MESH]|Calcium Channels/metabolism[MESH]|Calcium Signaling/*physiology[MESH]|Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism[MESH]|Calcium/*metabolism[MESH]|Inositol 1,4,5-Trisphosphate Receptors/metabolism[MESH]|Muscle Contraction/physiology[MESH]|Muscle, Smooth/cytology/*physiology[MESH]|Myocytes, Smooth Muscle/*physiology[MESH]|Plasma Membrane Calcium-Transporting ATPases/metabolism[MESH]|Potassium Channels/metabolism[MESH]|Ryanodine Receptor Calcium Release Channel/metabolism[MESH]|Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism[MESH]|TRPC Cation Channels/metabolism[MESH]|Vascular Diseases/*physiopathology[MESH] |
