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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:12.)
© 2007 American Heart Association, Inc.

Editorials

Nox 4 Regulation of Vascular Smooth Muscle Cell Differentiation Marker Gene Expression

Hamid Deliri; Coleen A. McNamara

From the Cardiovascular Division/Department of Medicine and the Cardiovascular Research Center, University of Virginia Health System, Charlottesville.

Correspondence to Hamid Deliri, MD, Cardiovascular Division/Department of Medicine, 415 Lane Road, MR5 Building, Room G231, PO Box 801394, University of Virginia Health System, Cardiovascular Research Department, Charlottesville, VA 22908. E-mail hd2d@virginia.edu

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

Vascular smooth muscle cells (VSMCs) undergo phenotypic switching in response to vascular injury. A hallmark feature of VSMC phenotypic switching is altered expression of VSMC-selective genes that define the contractile phenotype, including SM-actin, SMC myosin heavy chain (SM-MHC), Calponin, SM22, and H-caldesmon.¹ Although expression of no single marker is specific for SMC lineage, SM-MHC appears to be the most specific marker to date.^2,3 After acute vascular injury of an intact blood vessel, the expression of SMC differentiation markers are transiently decreased 7 days after vascular injury, when VSMCs are proliferating and migrating into the neointima.^4,5 Expression of SMC marker proteins is largely regulated at the gene transcription level in vitro and in vivo.^4,6 Transcriptional regulation of many of these contractile proteins involves the transcription factor serum response factor (SRF), which binds CArG cis regulatory elements. Recent studies have shown that myocardin and myocardin-related factors (MRTFA, MRTFB or MKL1, MKL2) function as SRF coactivators and are required for SRF:CArG-dependent regulation of VSMC-selective genes. SRF activity itself is also regulated by posttranscriptional mechanisms such as phosphorylation and alternative splicing.⁶

See page 42

Reactive oxygen species (ROS), like superoxide anions and hydrogen peroxide, have been implicated in a variety of processes involved in vascular lesion formation such as proliferation, differentiation, and apoptosis.^7,8 Classically described as microcidal byproducts of oxidative metabolism, they also function as intracellular second messengers in minute concentrations that can activate cellular signaling cascades. In their role as intracellular second messengers, ROS can activate ß-subunit of G proteins, . . . [Full Text of this Article]

Related Article:

Nox4 Is Required for Maintenance of the Differentiated Vascular Smooth Muscle Cell Phenotype

Roza E. Clempus, Dan Sorescu, Anna E. Dikalova, Lily Pounkova, Patricia Jo, George P. Sorescu, Bernard Lassègue, and Kathy K. Griendling
Arterioscler Thromb Vasc Biol 2007 27: 42-48. [Abstract] [Full Text] [PDF]

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