Ca2+/Calmodulin-Dependent Protein Kinase II Signaling in Vascular Smooth Muscle

Ca2+/calmodulin‐dependent protein kinase II function in vascular remodelling

“…Pharmacological inhibition of CaMKII activity (Rokolya & Singer, 2000) or siRNA mediated suppression of CaMKIIδ isoforms (Kim et al 2000) results in net inhibition of tonic contractile responses in arterial smooth muscle, although the targets are not yet clear. A discussion of CaMKII function and potential targets in differentiated VSM can be found in recent reviews (House et al 2008 b ; Kim et al 2008). Future studies in arterial tissues from genetically engineered mice lacking genes for either CaMKIIδ (Backs et al 2009) or γ (Backs et al 2010) hold promise for more completely characterizing CaMKII isoform‐dependent functions and substrates in differentiated VSM.…”

“… Model of CaMKII function in vascular smooth muscle phenotype switching Differentiated VSM express primarily CaMKII γ isoforms that participate in Ca 2+ homeostasis and modulation of contractile function in response to ligands such as angiotensin II (AII), noradrenaline (NA), or endothelin ‐1 (ET‐1) (House et al 2008 b ; Kim et al 2008). Upon cell culture or injury, VSM cells transition to a synthetic phenotype, a process that includes changes in expression of diverse Ca 2+ signalling proteins, including voltage gated Ca 2+ channels (VGCC), STIM1/Orai1 store operated channels, and specific TRPC channels including TRPC6.…”