Nicotine Induces Pro-inflammatory Response in Aortic Vascular Smooth Muscle Cells Through a NFκB/Osteopontin Amplification Loop-Dependent Pathway

Inflammation ◽  
2011 ◽  
Vol 35 (1) ◽  
pp. 342-349 ◽  
Author(s):  
Yongyi Wang ◽  
Fei Zhang ◽  
Wengang Yang ◽  
Song Xue
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Amplification Loop ◽  
Dependent Pathway

NOR-1 modulates the inflammatory response of vascular smooth muscle cells by preventing nfkb activation

2015 ◽  
Vol 241 (1) ◽  
pp. e43
Author(s):  
I. Martí Pàmies ◽  
R. Rodriguez-Calvo ◽  
O. Calvayrac ◽  
J. Alonso ◽  
B. Ferrán ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nfkb Activation

Exendin-4 alleviates angiotensin II-induced senescence in vascular smooth muscle cells by inhibiting Rac1 activation via a cAMP/PKA-dependent pathway

2014 ◽  
Vol 307 (12) ◽  
pp. C1130-C1141 ◽  
Author(s):  
Liang Zhao ◽  
Ai Q. Li ◽  
Teng F. Zhou ◽  
Meng Q. Zhang ◽  
Xiao M. Qin
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Therapeutic Potential ◽  
Muscle Cells ◽  
Premature Senescence ◽  
Ang Ii ◽  
Age Related ◽  
Dependent Pathway

Vascular aging has been implicated in the progression of diabetes and age-related cardiovascular disorders. Glucagon-like peptide-1 (GLP-1) is an incretin hormone capable of cytoprotective actions in addition to its glucose-lowering effect. The present study was undertaken to examine whether Exendin-4, a specific ligand for the GLP-1 receptor, could prevent angiotensin (ANG) II-induced premature senescence in vascular smooth muscle cells (VSMCs) and to determine the underlying mechanism involved. Senescence-associated β-galactosidase (SA β-gal) assay showed that ANG II induced premature senescence of VSMCs. Pretreatment with Exendin-4 significantly attenuated ANG II-induced generation of H2O2 and the subsequent VSMC senescence. These effects were, however, reversed in the presence of exendin fragment 9–39, a GLP-1 receptor antagonist, or PKI14-22. Moreover, a marked increase in the levels of p53 and p21 induced by ANG II was blunted by the treatment with Exendin-4. Nevertheless, Exendin-4 failed to decrease ANG II-induced expression of NAD(P)H oxidase 1 (Nox1), NAD(P)H oxidase 4 (Nox4), p22phox, or p47phox in VSMCs. Mechanistically, Exendin-4 blocked ANG II-induced Rac1 activation through the cAMP/PKA signaling cascade. Specifically, NSC23766, a Rac1 inhibitor, abrogated the suppressive effects of Exendin-4 on ANG II-induced premature senescence and H2O2 generation, respectively. Thus Exendin-4 confers resistance to ANG II-induced superoxide anion generation from NAD(P)H oxidase and the resultant VSMC senescence by inhibiting Rac1 activation via a cAMP/PKA-dependent pathway. These findings demonstrate that GLP-1 as well as its analogs (GLP-1-related reagents) may hold therapeutic potential in the treatment of diabetes with cardiovascular disease.

β-amyloid context intensifies vascular smooth muscle cells induced inflammatory response and de-differentiation

Aging Cell ◽  
2013 ◽  
Vol 12 (3) ◽  
pp. 358-369 ◽  
Author(s):  
Amélie Vromman ◽  
Nesrine Trabelsi ◽  
Clotilde Rouxel ◽  
Gilbert Béréziat ◽  
Isabelle Limon ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inflammatory Response ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Β Amyloid

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.

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