The relationship between pre-existing subendothelial smooth muscle cell accumulations and foam cell lesions in cholesterol-fed rabbits

1994 ◽  
Vol 425 (1) ◽  
pp. 41-47 ◽  
Author(s):  
M. M. Kockx ◽  
N. Buyssens ◽  
R. Van den Bossche ◽  
G. R. Y. De Meyer ◽  
H. Bult ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Foam Cell ◽  
The Relationship

Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation

2021 ◽  
Author(s):  
Jiao-Hui Wu ◽  
Lisheng Zhang ◽  
Igor Nepliouev ◽  
Leigh Brian ◽  
Taiqin Huang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Foam Cell ◽  
Atherosclerotic Lesion ◽  
Foam Cells ◽  
Actin Binding ◽  
Cross Sectional ◽  
Cell Transdifferentiation

Abstract Aims The F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation and pro-inflammatory signaling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis. Methods and results SM22-Cre+/Dbnflox/flox/Ldlr-/- (SMC-Dbn-/-/Ldlr-/-) and control mice (SM22-Cre+/Ldlr-/-, Dbnflox/flox/Ldlr-/-, and Ldlr-/-) were fed a Western diet for 14-20 weeks. Brachiocephalic arteries of SMC-Dbn-/-/Ldlr-/- mice exhibited 1.5- or 1.8-fold greater cross-sectional lesion area than control mice at 14 or 20 wk, respectively. Aortic atherosclerotic lesion surface area was 1.2-fold greater in SMC-Dbn-/-/Ldlr-/- mice. SMC-Dbn-/-/Ldlr-/- lesions comprised necrotic cores that were two-fold greater in size than those of control mice. Consistent with their bigger necrotic core size, lesions in SMC-Dbn-/- arteries also showed more transdifferentiation of SMCs to macrophage-like cells: 1.5- to 2.5-fold greater, assessed with BODIPY or with CD68, respectively. In vitro data were concordant: Dbn-/- SMCs had 1.7-fold higher levels of KLF4 and transdifferentiated to macrophage-like cells more readily than Dbnflox/flox SMCs upon cholesterol loading, as evidenced by greater up-regulation of CD68 and galectin-3. Adenovirally mediated Drebrin rescue produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs. During early atherogenesis, SMC-Dbn-/-/Ldlr-/- aortas demonstrated 1.6-fold higher levels of reactive oxygen species than control mouse aortas. The 1.8-fold higher levels of Nox1 in Dbn-/- SMCs was reduced to WT levels with KLF4 silencing. Inhibition of Nox1 chemically or with siRNA produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs. Conclusions We conclude that SMC Drebrin limits atherosclerosis by constraining SMC Nox1 activity and SMC transdifferentiation to macrophage-like cells. Translational perspective Drebrin is abundantly expressed in vascular smooth muscle cells (SMCs) and is up-regulated in human atherosclerosis. A hallmark of atherosclerosis is the accumulation of foam cells that secrete pro-inflammatory cytokines and contribute to plaque instability. A large proportion of these foam cells in humans derive from SMCs. We found that SMC Drebrin limits atherosclerosis by reducing SMC transdifferentiation to macrophage-like foam cells in a manner dependent on Nox1 and KLF4. For this reason, strategies aimed at augmenting SMC Drebrin expression in atherosclerotic plaques may limit atherosclerosis progression and enhance plaque stability by bridling SMC-to-foam-cell transdifferentiation.

scholarly journals Associations between Vaspin Levels and Coronary Artery Disease

2020 ◽  
Vol 4 (3) ◽  
pp. 211-216
Author(s):  
Lutfu Askin ◽  
Okan Tanriverdi ◽  
Hakan Tibilli ◽  
Serdar Turkmen
Keyword(s):  
Coronary Artery Disease ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Foam Cell ◽  
Foam Cell Formation ◽  
Artery Disease

The relationship between serum vaspin levels and metabolic or coronary artery disease is currently of interest for researchers. Although adipokine concentrations have been shown to be increased significantly in atherosclerotic lesions, the role adipokines in the atherosclerotic process remains to be elucidated. Vaspin is a new biological marker associated with obesity and impaired insulin sensitivity. Plasma vaspin concentration has been shown to correlate with the severity of coronary artery disease. Vascular inflammation triggered by vaspin inhibits atherogenesis by suppressing macrophage foam cell formation and vascular smooth muscle cell migration and proliferation. Vaspin also contributes to plaque stabilization by increasing collagen content and reducing the intraplaque macrophage to vascular smooth muscle cell ratio. The therapeutic goal concerning vaspin is to fight atherosclerosis and related diseases, as well as to maintain vascular health.

scholarly journals Histopathological analysis of the coronary atheroma extracted during coronary artery bypass graft surgery

2018 ◽  
Vol 11 (3) ◽  
pp. 226
Author(s):  
Redoy Ranjan ◽  
Dipannita Adhikary ◽  
Mayank Acharya ◽  
Saumitra Chakravarty ◽  
Sanjoy Kumar Saha ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cell ◽  
Unstable Angina ◽  
Muscle Cell ◽  
Foam Cell ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Histopathological Analysis ◽  
Artery Bypass Graft

<p class="Abstract">This study aims to evaluate the histopathological analysis as well as the effect of coronary endarterectomy with severe calcified coronary artery disease. During the year of 2015 to 2017, a total of 135 patients (56 patients of stable angina and 79 patients of unstable angina) underwent atherectomy in adjunct to off-pump coronary artery bypass graft surgery. Histopathological study of atheroma specimen demonstrates the presence of calcification, foam cell, cholesterol clefts, thrombus, smooth muscle cell, and also necrotic tissue using standard hematoxylin and eosin stain techniques. However, smooth muscle cells and foam cell were identified with plaque using the monoclonal antibodies. Thrombus was more common in unstable angina group of patients (64.4%) in comparison to the patients with stable angina (23.2%). An accelerated progression pattern of smooth muscle cell proliferation and calcification were observed which was also common and significantly higher in unstable angina group of patients. The presence of thrombus and accelerated progressive pattern of smooth muscle cell proliferation in unstable angina patients imply the episodic disruption of atheromatous plaque followed by subsequent healing and may play a vital role in the pathophysiology of underlying angina pectoris.</p>

Sign in / Sign up

Export Citation Format

Share Document