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(Circulation Research. 2006;98:1240.)
© 2006 American Heart Association, Inc.

Editorials

Ca²⁺, Calmodulin, and Cyclins in Vascular Smooth Muscle Cell Cycle

Vera V. Koledova, Raouf A. Khalil

From the Division of Vascular Surgery, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass.

Correspondence to Raouf A Khalil, MD, PhD, Harvard Medical School, Brigham and Women’s Hospital, Division of Vascular Surgery, NRB 435, 77 Ave Louis Pasteur, Boston, MA 02115. E-mail raouf_khalil@hms.harvard.edu

See related article, pages 1273–1281

Key Words: calcium • calmodulin • cell cycle • cyclins • vascular smooth muscle

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Ca²⁺ is a major determinant of many biochemical processes in various cell types, from the beginning of new life and egg fertilization to the end of life and cell death.¹ In vascular smooth muscle (VSM), physiological resting levels of intracellular free Ca²⁺ concentration ([Ca²⁺]_i) in the nanomolar range are necessary to maintain basal vascular tone.^2–4 VSM activation is associated with an increase in [Ca²⁺]_i in the micromolar range,^2–4 and large increases in VSM [Ca²⁺]_i have been identified in excessive vasoconstriction disorders such as hypertension and coronary vasospasm.^2,5 Activation of surface membrane receptors in VSM triggers increases in [Ca²⁺]_i attributable to Ca²⁺ release from the intracellular stores in the sarcoplasmic reticulum and Ca²⁺ entry from the extracellular space through Ca²⁺ channels (see Figure). Ca²⁺ then activates specific protein kinases and phosphatases that are involved in VSM contraction and relaxation.^2,3,6 Ca²⁺ may also function as a second messenger to activate other signaling pathways such as cytosolic phospholipase A2, phospholipase C, protein kinase C and phosphodiesterase.^6–8 An increase in [Ca²⁺]_i could also modulate plasma membrane channels and pumps such as Ca²⁺-activated K⁺ channels and the plasma membrane CaATPase (PMCA).^9,10 Additionally, Ca²⁺ may affect sarcoplasmic reticulum channels and pumps such as the inositol 1,4,5-trisphosphate (IP₃) receptor, the ryanodine-sensitive receptor and intracellular Ca²⁺ release channels, and the Ca²⁺ uptake pump (SERCA).^11,12

View larger version (27K): [in this window] [in a new window]   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 . . . [Full Text of this Article]

Related Article:

A Calmodulin-Binding Site on Cyclin E Mediates Ca²⁺-Sensitive G₁/S Transitions in Vascular Smooth Muscle Cells

Jaehyun Choi, Andrew Chiang, Nicolas Taulier, Robert Gros, Asif Pirani, and Mansoor Husain
Circ. Res. 2006 98: 1273-1281. [Abstract] [Full Text] [PDF]

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