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(Circulation Research. 2002;90:936.)
© 2002 American Heart Association, Inc.

Editorials

To Move or Not To Move?

Cytochrome P450 Products and Cell Migration

Ingrid Fleming

From the Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.G.-Universität, Frankfurt am Main, Germany.

Correspondence to Ingrid Fleming, Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.G.-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany.

Key Words: epoxyeicosatrienoic acid • migration • proliferation

Over the last 5 to 8 years, researchers have begun to appreciate the prominent role played by cytochrome P450 (CYP) enzymes in the regulation of vascular tone, homeostasis, and blood pressure. For example, interfering with CYP genes markedly affects blood pressure in mice,¹ and numerous reports have demonstrated that CYP expression is altered in genetic and experimental models of hypertension (for a recent review, see Moreno et al²).

Vascular CYP enzymes can be divided into two classes, the epoxygenases, which metabolize arachidonic acid to a series of regiospecific and stereospecific epoxides (5,6-, 8,9-, 11,12- and 14,15-epoxyeicosatrienoic acids or EETs), which are potent vasodilators, and the -hydroxylases, which generate the vasoconstrictor eicosanoid, 20-hydroxyeicosatetraenoic acid (20-HETE). 20-HETE is thought to mediate the myogenic response as well as the contraction induced by a number of contractile agonists and is generally assumed to augment basal blood pressure.³ EETs, on the other hand, are potent vasodilators and play a central role in the nitric oxide– and prostacyclin-independent relaxation of coronary, renal, and cerebral arteries. Although identified as potential endothelium-derived hyperpolarizing factors (EDHFs), it is now appreciated that EETs regulate much more than vascular tone and are in fact intracellular signal transduction molecules that have a central function in the regulation of vascular homeostasis.⁴

The effects of EETs can be attributed to their ability to activate a number of signal transduction pathways (in addition to those responsible for the activation of Ca²⁺-dependent K⁺ channels and hyperpolarization) in endothelial as well as vascular smooth muscle . . . [Full Text of this Article]

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