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Review
. 2006 May 26;98(10):1240-3.
doi: 10.1161/01.RES.0000225860.41648.63.

Ca2+, calmodulin, and cyclins in vascular smooth muscle cell cycle

Vera V Koledova, Raouf A Khalil
Review

Ca2+, calmodulin, and cyclins in vascular smooth muscle cell cycle

Vera V Koledova et al. Circ Res. .
No abstract available

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Figures

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Agonist (A)-receptor (R) interaction increases the hydrolysis of phosphatidylinositol 4,5- bisphosphate (PIP2) and IP3 production in VSM. IP3 stimulates Ca2+ release from the sarcoplasmic reticulum (SR). Also, extracellular Ca2+ enters VSMC through Ca2+ channels. Ca2+ binds calmodulin (CaM), which could activate myosin light chain (MLC) kinase and initiate contraction, or regulate the activity of K+ channels, Ca2+ release channels, Ca2+ pumps, and CaM kinase II. During vascular injury, VSMC transforms into undifferentiated phenotype and enters a cell cycle which consists of G1, growth and preparation of the chromosomes for replication; S, synthesis of DNA; G2, preparation for mitosis; and M, mitosis. Ca2+/CaM increases the activity of cyclin E/CDK2 and stimulates G1/S transition, and thereby promotes VSM growth and proliferation.
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