scholarly journals Calmodulin Expression Distinguishes the Smooth Muscle Cell Population of Human Carotid Plaque

2013 ◽  
Vol 183 (3) ◽  
pp. 996-1009 ◽  
Author(s):  
Matteo Coen ◽  
Giovanna Marchetti ◽  
Patricia M. Palagi ◽  
Carlotta Zerbinati ◽  
Giuseppe Guastella ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Population ◽  
Muscle Cell ◽  
Carotid Plaque ◽  
Human Carotid

Heterogeneous Smooth Muscle Cell Population Derived from Small and Larger Arteries

1998 ◽  
Vol 55 (1) ◽  
pp. 14-28 ◽  
Author(s):  
Akihiro Nakamura ◽  
Shogen Isoyama ◽  
Tsutomu Watanabe ◽  
Mitsuyasu Katoh ◽  
Takashi Sawai
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Population ◽  
Muscle Cell

Atherosclerosis Resistance in Rats Correlates with Lack of Expansion of an Immature Smooth Muscle Cell Population

1996 ◽  
Vol 33 (6) ◽  
pp. 442-453 ◽  
Author(s):  
B. Amore ◽  
A. Chiavegato ◽  
T. Paulon ◽  
P. Pauletto ◽  
S. Sartore
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Population ◽  
Muscle Cell

scholarly journals Cigarette Smoke Extract Promotes Human Vascular Smooth Muscle Cell Proliferation and Survival through ERK1/2- and NF-κB–Dependent Pathways

2010 ◽  
Vol 10 ◽  
pp. 2139-2156 ◽  
Author(s):  
Qing-wen Chen ◽  
Lars Edvinsson ◽  
Cang-Bao Xu
Keyword(s):  
Cardiovascular Disease ◽  
Cell Proliferation ◽  
Cell Death ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cell ◽  
Cigarette Smoke ◽  
Cell Population ◽  
Muscle Cell ◽  
Smoke Particles

Tobacco use is one of the major risk factors of cardiovascular disease. The underlying molecular mechanisms that link cigarette smoke to cardiovascular disease remain unclear. The present study was designed to examine the effects of dimethyl sulfoxide (DMSO)–soluble smoke particles (DSPs) on human aortic smooth muscle cell (HASMC) cultures, and to explore the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) and nuclear factor-κB (NF-κB) signal mechanisms involved. Serum-starved HASMCs were treated with DSPs for up to 48 h. DSPs promoted cell proliferation in a concentration-dependent manner from 0.05 to 0.2 ?l/ml. Activation of ERK1/2 and NF-κB was seen after exposure to DSPs. This occurred in parallel with the increase in cell population, bromodeoxyuridine incorporation, and cyclinD1/cyclin-dependent kinase 4 expression. Blocking phosphorylation of ERK1/2 by MAPK inhibitors U0126 and PD98059, and inhibiting activation of NF-κB by IκB (IκB) kinase inhibitors wedelolactone or IMD-0354, abolished the DSP effects. However, either a p38 inhibitor (SB203580) or an inhibitor of lipopolysaccharide (polymyxin B), or nicotinic receptor blockers (mecamylamine and α-bungarotoxin), did not inhibit a DSP-induced increase in the cell population. DSPs increased the expression of intercellular adhesion molecule 1 and the release of interleukin-6 in HASMCs, both of which were inhibited by ERK1/2 or NF-κB pathway inhibitors. Furthermore, cell apoptosis and necrosis were found in serum-starved HASMCs. DSPs decreased cell death and increased B-cell leukemia/lymphoma 2 expression. Blocking phosphorylation of ERK1/2 or NF-κB attenuated DSP-induced cell death inhibition. Cigarette smoke particles stimulate HASMC proliferation and inhibit cell death. The intracellular signal mechanisms behind this involve activation of ERK1/2 and NF-κB pathways.

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