Journal ArticleDOI
Vascular Smooth Muscle Growth: Autocrine Growth Mechanisms
TLDR
The temporal and spatial coordination of events are shown to modulate the environment in which other growth factors initiate cell cycle events, which provides another level of complexity in VSMC growth mechanisms.Abstract:
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 synthesizes and/or secretes a substance that stimulates that same cell type to undergo a growth response) and paracrine growth mechanisms (in which the individual cells responding to the growth factor synthesize and/or secrete a substance that stimulates neighboring cells of another cell type) are important in VSMC growth. In this review I discuss the autocrine and paracrine growth factors important for VSMC growth in culture and in vessels. Four mechanisms by which individual agonists signal are described: direct effects of agonists on their receptors, transactivation of tyrosine kinase-coupled receptors, generation of reactive oxygen species, and induction/secretion of other growth and survival factors. Additional growth effects mediated by changes in cell matrix are discussed. The temporal and spatial coordination of these events are shown to modulate the environment in which other growth factors initiate cell cycle events. Finally, the heterogeneous nature of VSMC developmental origin provides another level of complexity in VSMC growth mechanisms.read more
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Journal ArticleDOI
Uric acid stimulates vascular smooth muscle cell proliferation and oxidative stress via the vascular renin-angiotensin system.
TL;DR: The hypothesis that uric acid stimulates vascular smooth muscle cell (VSMC) proliferation and oxidative stress by stimulating the vascular renin–angiotensin system (RAS) is tested, and this stimulation may be mediated by the MAP kinase pathway.
Journal ArticleDOI
Redox compartmentalization in eukaryotic cells.
Young-Mi Go,Dean P. Jones +1 more
TL;DR: In this paper, the redox control networks of eukaryotic cells have been investigated and further elucidation of these networks within compartments will improve the mechanistic understanding of cell functions and their disruption in disease.
Journal ArticleDOI
Carbon monoxide suppresses arteriosclerotic lesions associated with chronic graft rejection and with balloon injury
Leo E. Otterbein,Brian S. Zuckerbraun,Manabu Haga,Fang Liu,Ruiping Song,Anny Usheva,Christina Stachulak,Natalya Bodyak,R. Neal Smith,Eva Csizmadia,Shivraj Tyagi,Yorihiro Akamatsu,Richard J Flavell,Timothy R. Billiar,Edith Tzeng,Fritz H. Bach,Augustine M.K. Choi,Miguel P. Soares,Miguel P. Soares +18 more
TL;DR: Findings demonstrate a protective role for CO in vascular injury and support its use as a therapeutic agent.
Journal ArticleDOI
Pivotal role of a gp91(phox)-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice.
TL;DR: A gp91phox-containing NADPH oxidase plays an important role in the development of angiotensin II-induced cardiac hypertrophy, independent of changes in blood pressure.
Journal ArticleDOI
Matrix metalloproteinases regulate migration, proliferation, and death of vascular smooth muscle cells by degrading matrix and non-matrix substrates
TL;DR: It is concluded that MMPs influence VSMC behaviour by cleaving both matrix and non-matrix substrates, and regulate migration, proliferation and survival of VSMC.
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