Consequences of postnatal vascular smooth muscle EGFR deletion on acute angiotensin II action

2015 ◽  
Vol 130 (1) ◽  
pp. 19-33 ◽  
Author(s):  
Barbara Schreier ◽  
Mirja Hünerberg ◽  
Sindy Rabe ◽  
Sigrid Mildenberger ◽  
Daniel Bethmann ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Vascular Smooth Muscle ◽  
Egf Receptor ◽  
Ang Ii ◽  
Basal Blood Pressure ◽  
Epidermal Growth

In the present study we demonstrate that the epidermal growth factor (EGF) receptor (EGFR) in vascular smooth muscle cells (VSMC) is involved in basal blood pressure homoeostasis, acute pressure response to angiotensin II (Ang II) but not endothelin-1 and contributes to maturation-related remodelling.

Contribution of epidermal growth factor receptor transactivation in angiotensin II-induced enhanced expression of Gi protein and proliferation in A10 vascular smooth muscle cellsThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research.

2009 ◽  
Vol 87 (12) ◽  
pp. 1037-1045 ◽  
Author(s):  
Yessica-Haydee Gomez Sandoval ◽  
Louis-Olivier Lévesque ◽  
Madhu B. Anand-Srivastava
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Egfr Inhibitor ◽  
Ang Ii ◽  
Enhanced Expression ◽  
Epidermal Growth

We have recently shown that vasoactive peptides such as angiotensin II (Ang II) and endothelin-1 (ET-1) increased the expression of Gi proteins and proliferation of A10 vascular smooth muscle cells (VSMC) through MAP kinase / PI3 kinase pathways. The present study was undertaken to examine the implication of growth factor receptor activation in Ang II-induced enhanced expression of Gi proteins and proliferation of A10 VSMC and to further investigate the underlying mechanisms responsible for these increases. Cell proliferation was determined by [3H]thymidine incorporation, and the expression of Gi proteins and the phosphorylation of ERK1/2 and epidermal growth factor receptor (EGFR) was determined by Western blotting. Treatment of A10 VSMC with Ang II enhanced the expression of Gi proteins, which was attenuated by Ang II AT1 receptor antagonist but not by AT2 receptor antagonist. The inhibitor of EGFR also attenuated the enhanced expression of Gi proteins induced by Ang II to control levels. In addition, Ang II enhanced the phosphorylation of EGFR in A10 VSMC, and this was restored to control levels by the EGFR inhibitor and antioxidants. Furthermore, Ang II also augmented the proliferation and ERK1/2 phosphorylation of A10 VSMC, which were restored to control levels by the EGFR inhibitor. These data suggest that the Ang II-induced increase in oxidative stress transactivates EGFR, which through MAP kinase signaling may contribute to the enhanced expression of Gi proteins and thereby to the increased proliferation of A10 VSMC.

scholarly journals Angiotensin II, Hypercholesterolemia, and Vascular Smooth Muscle Cells: A Perfect Trio for Vascular Pathology

2020 ◽  
Vol 21 (12) ◽  
pp. 4525
Author(s):  
Amanda St. Paul ◽  
Cali B. Corbett ◽  
Rachael Okune ◽  
Michael V. Autieri
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Vascular Diseases ◽  
Reduce Blood Pressure ◽  
Vascular Pathology ◽  
Lipid Lowering ◽  
Ang Ii

Cardiovascular disease is the leading cause of morbidity and mortality in the Western and developing world, and the incidence of cardiovascular disease is increasing with the longer lifespan afforded by our modern lifestyle. Vascular diseases including coronary heart disease, high blood pressure, and stroke comprise the majority of cardiovascular diseases, and therefore represent a significant medical and socioeconomic burden on our society. It may not be surprising that these conditions overlap and potentiate each other when we consider the many cellular and molecular similarities between them. These intersecting points are manifested in clinical studies in which lipid lowering therapies reduce blood pressure, and anti-hypertensive medications reduce atherosclerotic plaque. At the molecular level, the vascular smooth muscle cell (VSMC) is the target, integrator, and effector cell of both atherogenic and the major effector protein of the hypertensive signal Angiotensin II (Ang II). Together, these signals can potentiate each other and prime the artery and exacerbate hypertension and atherosclerosis. Therefore, VSMCs are the fulcrum in progression of these diseases and, therefore, understanding the effects of atherogenic stimuli and Ang II on the VSMC is key to understanding and treating atherosclerosis and hypertension. In this review, we will examine studies in which hypertension and atherosclerosis intersect on the VSMC, and illustrate common pathways between these two diseases and vascular aging.

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