Decreased caveolin-1 in atheroma: Loss of antiproliferative control of vascular smooth muscle cells in atherosclerosis

Schwencke, Carsten; Schmeißer, Alexander; Walter, Christina; Wachter, Rolf; Pannach, Sven; Weck, B; Braun-Dullaeus, Ruediger C.; Kasper, Michael; Strasser, Ruth H.

doi:10.1016/j.cardiores.2005.05.004

Cited by 43 publications

(37 citation statements)

References 34 publications

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“…It has been demonstrated that deletion of caveolin-1 promotes VSMCs proliferation increasing intimal hyperplasia upon carotid injury [34,35]. Additionally, reduced caveolin-1 levels have been reported for plaques from hypercholesterolemic rabbits and humans [22,36]. Lower caveolin-1 levels were also associated with features of plaque instability [37].…”

Section: Discussionmentioning

confidence: 99%

“…Caveolin-1 plays pivotal roles in physiological and pathophysiological conditions [17,18,19,20,21,22]. It has been demonstrated that deletion of caveolin-1 promotes VSMCs proliferation increasing intimal hyperplasia upon carotid injury [34,35].…”

Section: Discussionmentioning

confidence: 99%

“…Changes of caveolin-1 expression are associated with pathophysiological conditions [20,21]. For example, decreased caveolin-1 expression was correlated with increased cell cycle entry in VSMCs from wild type mice and over-expression of caveolin-1 inhibited proliferation of VSMCs [22]. Therefore, caveolin-1 may play a role in the development of VSMCs phenotypic changes.…”

Section: Introductionmentioning

confidence: 99%

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Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Carrillo-Sepúlveda

Matsumoto

2014

Cell Physiol Biochem

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Aims: Diabetes-induced vascular complications are associated with vascular smooth muscle cell (VSMC) phenotypic modulation, switching from a contractile to a synthetic-proliferative phenotype. Loss of caveolin-1 is involved with proliferation of VSMCs. We tested the hypothesis that mesenteric VSMCs from type 2 diabetic Goto-Kakizaki (GK) rat undergo phenotypic modulation and it is linked to decreased caveolin-1 expression. Methods: VSMCs were isolated from mesenteric arteries from GK rats and age-matched control Wistar rats. Western blotting was used to determine expression of target proteins such as caveolin-1, calponin (marker of differentiation), and proliferating cell nuclear antigen (PCNA, marker of proliferation). In addition, we measured intracellular reactive oxygen species (ROS) production using H2DCF-DA and activation of extracellular signal-regulated kinase (ERK1/2) by western blotting in VSMCs from GK stimulated with lipopolysaccharide (LPS), an endotoxin upregulated in diabetes. Results: Mesenteric VSMCs from diabetic GK rats exhibited decreased caveolin-1 and calponin expression and increased PCNA expression compared to control. Increased levels of ROS and phospho-ERK1/2 expression were also found in GK VSMCs. LPS augmented ROS and phosphorylated ERK1/2 levels to a greater extent in GK VSMCs than in control. Likewise, high glucose decreased caveolin-1 and calponin expression, increased PCNA expression and augmented ROS production in control mesenteric VSMCs. Conclusion: These results suggest that mesenteric VSMCs from diabetic GK rats undergo phenotypic modulation and it is associated with decreased caveolin-1 expression. These alterations may be due to enhanced inflammatory stimuli and glucose levels present in diabetic milieu.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Carrillo-Sepúlveda

Matsumoto

2014

Cell Physiol Biochem

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“…15 Consistent with these findings, previous investigations have shown that caveolin-1 expression is decreased in neointimal smooth muscle cells present in atherosclerotic lesions. 16 Taken together, these data suggest that while endothelial caveolin-1 may be proatherogenic, macrophage and smooth muscle cell caveolin-1 may play an inhibitory role in the development of atherosclerosis (Figure 1). …”

mentioning

confidence: 89%

Endothelial Caveolae and Caveolin-1 as Key Regulators of Atherosclerosis

Frank¹

2010

The American Journal of Pathology

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“…Serum and growth factors (e.g., TGF, EGF, and PDGF) can downregulate caveolin-1 expression (177,178). In addition, lung tissue and pulmonary fibroblasts isolated from patients with idiopathic pulmonary fibrosis or scleroderma show decreased caveolin-1 expression, which may contribute to increased kinase signaling, Smad phosphorylation and translocation, and collagen accumulation (178).…”

Section: Caveolins In the Lung: General Principles And A Role In Pulmmentioning

confidence: 99%

Caveolae as Organizers of Pharmacologically Relevant Signal Transduction Molecules

Patel¹,

Murray²,

Insel

2008

Annu. Rev. Pharmacol. Toxicol.

405

363

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Caveolae, a subset of membrane (lipid) rafts, are flask-like invaginations of the plasma membrane that contain caveolin proteins, which serve as organizing centers for cellular signal transduction. Caveolins (-1, -2, and -3) have cytoplasmic N and C termini, palmitolylation sites, and a scaffolding domain that facilitates interaction and organization of signaling molecules so as to help provide coordinated and efficient signal transduction. Such signaling components include upstream entities (e.g., G protein-coupled receptors (GPCRs), receptor tyrosine kinases, and steroid hormone receptors) and downstream components (e.g., heterotrimeric and low-molecularweight G proteins, effector enzymes, and ion channels). Diseases associated with aberrant signaling may result in altered localization or expression of signaling proteins in caveolae. Caveolin-knockout mice have numerous abnormalities, some of which may reflect the impact of total body knockout throughout the life span. This review provides a general overview of caveolins and caveolae, signaling molecules that localize to caveolae, the role of caveolae/caveolin in cardiac and pulmonary pathophysiology, pharmacologic implications of caveolar localization of signaling molecules, and the possibility that caveolae might serve as a therapeutic target.

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Decreased caveolin-1 in atheroma: Loss of antiproliferative control of vascular smooth muscle cells in atherosclerosis

Abstract: The proliferation of VSMC in vitro and in human atheroma is associated with a decrease of caveolin-1 expression. These data suggest that the loss of antiproliferative control by caveolin-1 plays a pivotal role in VSMC proliferation in atherosclerosis.

Cited by 43 publications

References 34 publications

Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Phenotypic Modulation of Mesenteric Vascular Smooth Muscle Cells from Type 2 Diabetic Rats is Associated with Decreased Caveolin-1 Expression

Endothelial Caveolae and Caveolin-1 as Key Regulators of Atherosclerosis

Caveolae as Organizers of Pharmacologically Relevant Signal Transduction Molecules

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