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

Nox 4 Regulation of Vascular Smooth Muscle Cell Differentiation Marker Gene Expression Editorial Nox 4 Regulation of Vascular Smooth Muscle Cell Differentiation Marker Gene Expression Hamid Deliri, Coleen A. McNamara ascular smooth muscle cells (VSMCs) undergo phe- Intracellular gp91phox-related NAD(P)H oxidase (Nox) is notypic switching in response to vascular injury. A a family of enzymes that generate ROS in a controlled Vhallmark feature of VSMC phenotypic switching is manner. In the mouse, the Nox family includes Nox 1, Nox 2, altered expression of VSMC-selective genes that define the Nox 3, and Nox 4. In humans the Nox family consists of contractile phenotype, including SM-actin, SMC myosin Nox1 to Nox5 and the dual oxidases Duox 1 and Duox 2. heavy chain (SM-MHC), Calponin, SM22, and Nox 1 and Nox 4 are both expressed in human and rodent 1 7 H-caldesmon. Although expression of no single marker is aortic VSMCs. Nox 1, the first identified mammalian homo- specific for SMC lineage, SM-MHC appears to be the most logue of gp91phox, is involved in signal transduction leading 2,3 specific marker to date. After acute vascular injury of an to hypertrophy and cell proliferation. Nox 1 can form a intact blood vessel, the expression of SMC differentiation complex with p22phox which enhances its stability and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

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

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ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/01.ATV.0000254154.43871.50
pmid
17185622
Publisher site
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Abstract

Editorial Nox 4 Regulation of Vascular Smooth Muscle Cell Differentiation Marker Gene Expression Hamid Deliri, Coleen A. McNamara ascular smooth muscle cells (VSMCs) undergo phe- Intracellular gp91phox-related NAD(P)H oxidase (Nox) is notypic switching in response to vascular injury. A a family of enzymes that generate ROS in a controlled Vhallmark feature of VSMC phenotypic switching is manner. In the mouse, the Nox family includes Nox 1, Nox 2, altered expression of VSMC-selective genes that define the Nox 3, and Nox 4. In humans the Nox family consists of contractile phenotype, including SM-actin, SMC myosin Nox1 to Nox5 and the dual oxidases Duox 1 and Duox 2. heavy chain (SM-MHC), Calponin, SM22, and Nox 1 and Nox 4 are both expressed in human and rodent 1 7 H-caldesmon. Although expression of no single marker is aortic VSMCs. Nox 1, the first identified mammalian homo- specific for SMC lineage, SM-MHC appears to be the most logue of gp91phox, is involved in signal transduction leading 2,3 specific marker to date. After acute vascular injury of an to hypertrophy and cell proliferation. Nox 1 can form a intact blood vessel, the expression of SMC differentiation complex with p22phox which enhances its stability and

Journal

Arteriosclerosis, Thrombosis, and Vascular Biology – Wolters Kluwer Health

Published: Jan 1, 2007

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