scholarly journals Local Angiotensin Pathways in Human Carotid Atheroma: Towards a Systems Biology Approach

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Giampiero Bricca ◽  
Liliana Legedz ◽  
Ali Nehme ◽  
Hanène Ayari ◽  
Christian Paultre ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Systems Biology ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Concomitant Increase ◽  
Glucocorticoid Signaling ◽  
Human Carotid

We will summarize the data we have obtained in human carotid artery concerning the organization of an extended local renin angiotensin aldosterone system and its variations at different stages of atheroma. In a system view, we propose a model where concomitant increase in angiotensin and glucocorticoid signaling is induced and amplified in VSMC while vascular smooth muscle cells transdifferentiate toward a lipid storing phenotype.

Characterization of Ca2+ channels involved in ET-1-induced transactivation of EGF receptors

2002 ◽  
Vol 283 (6) ◽  
pp. H2671-H2675 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Nobuo Hashimoto ◽  
Tomoh Masaki
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Internal Carotid ◽  
Specific Inhibitor ◽  
Muscle Cells ◽  
Receptor Protein

The purpose of this study was to demonstrate the involvement of Ca2+ influx through voltage-independent Ca2+ channels (VICCs) in endothelin-1 (ET-1)-induced transactivation of epidermal growth factor receptor protein tyrosine kinase (EGFR PTK) using the Ca2+ channel blockers LOE-908 and SK&F-96365 in rabbit internal carotid artery vascular smooth muscle cells. ET-1-induced EGFR PTK transactivation was completely inhibited by AG-1478, which is a specific inhibitor of EGFR PTK. In the absence of extracellular Ca2+, the magnitude of EGFR PTK transactivation was near the basal level. Based on sensitivity to nifedipine, which is a specific blocker of voltage-operated Ca2+ channels (VOCCs), VOCCs have minor roles in EGFR PTK transactivation. In contrast, Ca2+ influx through VICCs plays an important role in EGFR PTK transactivation. Moreover, based on the sensitivity of VICCs to SK&F-96365 and LOE-908, VICCs were shown to consist of two types of Ca2+-permeable nonselective cation channels (NSCCs), which are designated NSCC-1 and NSCC-2, and a store-operated Ca2+ channel. In summary, Ca2+influx through VICCs plays an essential role in ET-1-induced EGFR PTK transactivation in rabbit internal carotid artery vascular smooth muscle cells.

A palm oil-enriched diet induces dyslipidemia and ultrastructural alterations of endothelium with vascular smooth muscle cells migration in carotid artery

2017 ◽  
Vol 280 ◽  
pp. S125
Author(s):  
Mohamed el Fadel Ousmaal ◽  
Maria del Carmen Martínez ◽  
Ramaroson Andriantsitohaina ◽  
Abderahim Gaceb ◽  
Lokman Kechekoul ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Palm Oil ◽  
Muscle Cells ◽  
Ultrastructural Alterations

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

2015 ◽  
Vol 308 (10) ◽  
pp. H1265-H1274 ◽  
Author(s):  
Kim Tardif ◽  
Vanessa Hertig ◽  
Natacha Duquette ◽  
Louis Villeneuve ◽  
Ismail El-Hamamsy ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Protein Levels ◽  
Vessel Remodeling ◽  
Peptide Growth Factor

Proliferation and hypertrophy of vascular smooth muscle cells represent hallmark features of vessel remodeling secondary to hypertension. The intermediate filament protein nestin was recently identified in vascular smooth muscle cells and in other cell types directly participated in proliferation. The present study tested the hypothesis that vessel remodeling secondary to hypertension was characterized by nestin upregulation in vascular smooth muscle cells. Two weeks after suprarenal abdominal aorta constriction of adult male Sprague-Dawley rats, elevated mean arterial pressure increased the media area and thickness of the carotid artery and aorta and concomitantly upregulated nestin protein levels. In the normal adult rat carotid artery, nestin immunoreactivity was observed in a subpopulation of vascular smooth muscle cells, and the density significantly increased following suprarenal abdominal aorta constriction. Filamentous nestin was detected in cultured rat carotid artery- and aorta-derived vascular smooth muscle cells and an analogous paradigm observed in human aorta-derived vascular smooth muscle cells. ANG II and EGF treatment of vascular smooth muscle cells stimulated DNA and protein synthesis and increased nestin protein levels. Lentiviral short-hairpin RNA-mediated nestin depletion of carotid artery-derived vascular smooth muscle cells inhibited peptide growth factor-stimulated DNA synthesis, whereas protein synthesis remained intact. These data have demonstrated that vessel remodeling secondary to hypertension was characterized in part by nestin upregulation in vascular smooth muscle cells. The selective role of nestin in peptide growth factor-stimulated DNA synthesis has revealed that the proliferative and hypertrophic responses of vascular smooth muscle cells were mediated by divergent signaling events.

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