Modulation of low-density lipoprotein binding by cyclic AMP in human vascular smooth muscle cells and skin fibroblasts

1988 ◽  
Vol 16 (6) ◽  
pp. 1008-1009
Author(s):  
ALIYA MIDDLETON ◽  
NICOLA BONSER ◽  
BRUCE MIDDLETON
Keyword(s):  
Smooth Muscle ◽  
Cyclic Amp ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Low Density ◽  
Lipoprotein Binding

Atherosclerosis and thrombosis

2015 ◽  
Author(s):  
Lina Badimon ◽  
Gemma Vilahur
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Low Density ◽  
Atherosclerosis Progression

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

Chemotactic response of vascular smooth muscle cells to acetoacetylated low-density lipoprotein

1988 ◽  
Vol 4 (2) ◽  
pp. 100-103 ◽  
Author(s):  
Michitaka Naito ◽  
Toshio Hayashi ◽  
Chiaki Funaki ◽  
Masafumi Kuzuya ◽  
Kanichi Asai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Chemotactic Response ◽  
Low Density
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