SOXF: redox mediators of vascular smooth muscle cell growth

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SOXF: redox mediators of vascular smooth muscle cell growth.

O xidative stress and the production of intracellular reactive oxygen species (ROS), such as superoxide (O2 ), hydrogen peroxide (H2O2), and hydroxyl radical (OH), have been implicated in the pathogenesis of cardiovascular disease, in part by promoting vascular smooth muscle proliferation. Within the vessel wall, ROS are generated by several mechanisms, including vascular NAD(P)H oxidases. 6 RO...

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Experiments were performed to determine the role of reactive oxygen species (ROS) in regulating vascular smooth muscle cell (VSMC) phenotype. After quiescence, cultured human VSMCs increased their expression of differentiation proteins (alpha-actin, calponin, and SM1 and SM2 myosin), but not beta-actin. ROS activity, determined using the H(2)O(2)-sensitive probe dichlorodihydrofluorescein (DCF)...

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Control of Vascular Smooth Muscle Cell Growth by Connexin 43

Connexin 43 (Cx43), the principal gap junction protein in vascular smooth muscle cells (VSMCs), regulates movement of ions and other signaling molecules through gap junction intercellular communication (GJIC) and plays important roles in maintaining normal vessel function; however, many of the signaling mechanisms controlling Cx43 in VSMCs are not clearly described. The goal of this study was t...

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Regulation of vascular smooth muscle cell growth by aldose reductase.

Aldose reductase (AR) is a broad-specificity aldo-keto reductase with wide species and tissue distribution. The enzyme has been implicated in the development of pleiotropic complications of long-term diabetes. However, the euglycemic function of the enzyme remains unclear. To examine its potential role in cell growth, changes in AR mRNA and protein were measured in human aortic smooth muscle ce...

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Vascular smooth muscle growth: autocrine growth mechanisms.

Vascular smooth muscle cells (VSMC) exhibit several growth responses to agonists that regulate their function including proliferation (hyperplasia with an increase in cell number), hypertrophy (an increase in cell size without change in DNA content), endoreduplication (an increase in DNA content and usually size), and apoptosis. Both autocrine growth mechanisms (in which the individual cell syn...

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ژورنال

عنوان ژورنال: Heart

سال: 2004

ISSN: 0007-0769

DOI: 10.1136/hrt.2003.029371