Redox Regulation of Vascular Smooth Muscle Cell Differentiation

@article{Su2001RedoxRO,
  title={Redox Regulation of Vascular Smooth Muscle Cell Differentiation},
  author={B. Su and S. Mitra and H. Gregg and S. Flavahan and M. Chotani and K. Clark and P. Goldschmidt-Clermont and N. Flavahan},
  journal={Circulation Research: Journal of the American Heart Association},
  year={2001},
  volume={89},
  pages={39-46}
}
  • B. Su, S. Mitra, +5 authors N. Flavahan
  • Published 2001
  • Biology, Medicine
  • Circulation Research: Journal of the American Heart Association
Abstract— 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 (&agr;-actin, calponin, and SM1 and SM2 myosin), but not &bgr;-actin. ROS activity, determined using the H2O2-sensitive probe dichlorodihydrofluorescein (DCF), remained high in quiescent cells and was inhibited by catalase (3000 U/mL) or by N… Expand
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References

SHOWING 1-10 OF 57 REFERENCES
Redox control of vascular smooth muscle proliferation.
TLDR
High levels of oxidative stress are apparently involved in the pathogenesis of vascular diseases such as hypertension and atherosclerosis, along with abnormal vascular growth after balloon injury, so the pathways responsible for oxidative stress, as well as the antioxidant defenses in the vessel wall, may provide novel therapeutic targets. Expand
Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II-induced vascular hypertrophy.
TLDR
Data indicate that AT1 receptor-mediated production of superoxide generated by the NADH/NADPH oxidase is followed by an increase in intracellular H2O2, suggesting a specific role for these oxygen species and scavenging systems in modifying the intrACEllular redox state in vascular growth. Expand
Differential activation of mitogen-activated protein kinases by H2O2 and O2- in vascular smooth muscle cells.
TLDR
Compared the effects of H2O2 and O2- on cultured rat aortic vascular smooth muscle cell growth and signal transduction and the activity of mitogen-activated protein kinase was measured by changes in mobility on Western blot and by phosphorylation of myelin basic protein. Expand
Expression of smooth muscle-specific alpha-isoactin in cultured vascular smooth muscle cells: relationship between growth and cytodifferentiation
TLDR
It is demonstrated that cultured vascular SMCs undergo differential expression of isoactins in relation to their growth state and indicate that growth arrest promotes cytodifferentiation in these cells. Expand
Molecular control of vascular smooth muscle cell differentiation.
  • G. Owens
  • Biology, Medicine
  • Acta physiologica Scandinavica
  • 1998
TLDR
Key questions include determination of mechanisms that control the coordinate expression of genes required for the differentiated function of the smooth muscle cell, and determination as to how these regulatory processes are influenced by local environmental cues known to be important to control of smooth muscle differentiation. Expand
Vascular Cell Adhesion Molecule-1 Gene Expression during Human Smooth Muscle Cell Differentiation Is Independent of NF-κB Activation*
TLDR
Findings suggest that in contrast to TNF-α activation, NF-κB is not involved in VCAM-1 gene expression during SMC differentiation. Expand
Platelet-derived growth factor-BB-induced suppression of smooth muscle cell differentiation.
TLDR
This study focused on the expression of two other SM-specific proteins, SM myosin heavy chain (SM-MHC) and SMalpha TM, to determine whether the actions of PDGF-BB were specific to SM alpha-actin or represented a global ability of PD GF-BB to inhibit expression of cell- specific proteins characteristic of differentiated SMCs. Expand
NAD(P)H oxidase: role in cardiovascular biology and disease.
TLDR
Vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix and have been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis. Expand
Components of the Protein Synthesis and Folding Machinery Are Induced in Vascular Smooth Muscle Cells by Hypertrophic and Hyperplastic Agents
TLDR
Hyperplastic and hypertrophic growth were accompanied by similar changes in protein expression, suggesting that both types of growth require up-regulation of the protein synthesis and folding machinery. Expand
A novel role for the cyclin-dependent kinase inhibitor p27(Kip1) in angiotensin II-stimulated vascular smooth muscle cell hypertrophy.
TLDR
Angiotensin II stimulation of quiescent cells in which p27(Kip1) levels are high results in hypertrophy but promotes hyperplasia when levels of p 27(KIP1) are low, as in the presence of other growth factors. Expand
...
1
2
3
4
5
...