Static pressure drives proliferation of vascular smooth muscle cells via caveolin-1/ERK1/2 pathway

Luo, Dixian; Cheng, Jiming; Xiong, Yan; Li, Junmo; Xia, Chenglai; Xu, Chenghai; Wang, Chun; Zhu, Bing-Yang; Hu, Zhuowei; Liao, Duan‐Fang

doi:10.1016/j.bbrc.2009.12.132

Cited by 23 publications

(20 citation statements)

References 26 publications

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“…Previous studies revealed that Caveolin-1 blocked extracellular signal-regulated kinases (ERK) 1/2 and c-jun N-terminal kinase (JNK). 18,[35][36][37] Phospho-ERK1/2 induces Smad2/3 phosphorylation, which is the main pathway of TGF-b-dependent EMT. 38 Indeed, ERK activation leads to increased collagen expression in lung fibroblasts.…”

Section: Caveolin-1 Knockout Rpe Cells Increased Migrationmentioning

confidence: 99%

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

Nagasaka

Kaneko

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Proliferative vitreoretinopathy (PVR) is one of the most severe ocular diseases. Fibrotic changes in retinal cells are considered to be involved in the pathogenesis of PVR. Epithelial-mesenchymal transition (EMT) of RPE cells is one of the main concepts in the pathogenesis of fibrovascular membranes (FVMs) in PVR. In this study, we examined the expression of Caveolin-1 in human FVMs from patients with PVR. We also examined the role of Caveolin-1 in the pathogenesis of PVR.METHODS. Western blotting, real-time PCR, and immunohistochemistry were performed with human FVMs and mouse eyes with PVR. Cell migration assays were performed to evaluate the involvement of Caveolin-1 in EMT using primary human and mouse RPE cells. RESULTS.Caveolin-1 was expressed in human FVMs and upregulated in the mouse eyes with PVR. The alpha-smooth muscle actin (aSMA) expression and migration ability were increased in RPE cells with knockout or knockdown of Caveolin-1, whereas zonula occludens-1 (ZO-1) immunohistochemistry showed reduced morphology and expression of ZO-1. In addition, migration assays showed that Caveolin-1 reduction increased RPE cell migration abilities.CONCLUSIONS. These results indicated that Caveolin-1 in RPE cells prevents PVR by blocking EMT.

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Section: Caveolin-1 Knockout Rpe Cells Increased Migrationmentioning

confidence: 99%

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

Nagasaka

Kaneko

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…[14] . Recently, we found that static pressure significantly decreased caveolin-1 expression in VMSCs cultured in vitro, in pressure-and time-dependent manners [19] , and that cholesterol accumulation significantly increased in VSMCs [forthcoming data].…”

Section: Four Trafficking Systemsmentioning

confidence: 99%

A novel model of cholesterol efflux from lipid-loaded cells

et al. 2010

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Cholesterol efflux from lipid-loaded cells is a key athero-protective event that counteracts cholesterol uptake. The imbalance between cholesterol efflux and uptake determines the prevention or development of atherosclerosis. Many proteins and factors participate in the cholesterol efflux event. However, there are currently no systematic models of reverse cholesterol transport (RCT) that include most RCT-related factors and events. On the basis of recent research findings from other and our laboratories, we propose a novel model of one center and four systems with coupling transportation and networking regulation. This model represents a common way of cholesterol efflux; however, the systems in the model consist of different proteins/factors in different cells. In this review, we evaluate the novel model in vascular smooth muscle cells (VSMCs) and macrophages, which are the most important original cells of foam cells. This novel model consists of 1) a caveolae transport center, 2) an intracellular trafficking system of the caveolin-1 complex, 3) a transmembrane transport system of the ABC-A1 complex, 4) a transmembrane transport system of the SR-B1 complex, and 5) an extracelluar trafficking system of HDL/Apo-A1. In brief, the caveolin-1 system transports cholesterol from intracellular compartments to caveolae. Subsequently, both ABC-A1 and SR-B1 complex systems transfer cholesterol from caveolae to extracellular HDL/Apo-A1. The four systems are linked by a regulatory network. This model provides a simple and concise way to understand the dynamic process of atherosclerosis.

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“…Hu and Wu demonstrated the correlation between caveolin-1 and cellular cholesterol level [15,16] . Our previous studies demonstrated that caveolin-1 is involved in cellular cholesterol accumulation, vascular smooth muscle cell foam formation, intercellular cholesterol efflux, and vascular remodeling [17][18][19] . These findings indicate that caveolae and caveolin-1 may play an important role in cellular cholesterol homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Caveolae and caveolin-1 mediate endocytosis and transcytosis of oxidized low density lipoprotein in endothelial cells

Sun

Tuo

et al. 2010

Acta Pharmacol Sin

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Aim: To explore the mechanisms involved in ox-LDL transcytosis across endothelial cells and the role of caveolae in this process. Methods: An in vitro model was established to investigate the passage of oxidized low density lipoprotein (ox-LDL) through a tight monolayer of human umbilical vein endothelial cells (HUVEC) cultured on a collagen-coated filter. Passage of DiI-labeled ox-LDL through the monolayer was measured using a fluorescence spectrophotometer. The uptake and efflux of ox-LDL by HUVEC were determined using fluorescence microscopy and HPLC. Results: Caveolae inhibitors -carrageenan (250 μg/mL), filipin (5 μg/mL), and nocodazole (33 μmol/L)-decreased the transport of ox-LDL across the monolayer by 48.9%, 72.4%, and 79.8% as compared to the control group. In addition, they effectively decreased ox-LDL uptake and inhibited the efflux of ox-LDL. Caveolin-1 and LOX-1 were up-regulated by ox-LDL in a time-dependent manner and decreased gradually after depletion of ox-LDL (P<0.05). After treatment HUVEC with ox-LDL and silencing caveolin-1, NF-κB translocation to the nucleus was blocked and LOX-1 expression decreased (P<0.05). Conclusion: Caveolae can be a carrier for ox-LDL and may be involved in the uptake and transcytosis of ox-LDL by HUVEC.Keywords: caveolae; caveolin-1; oxidized low density lipoprotein; atherosclerosis; transcytosis; human umbilical vein endothelial cells Acta Pharmacologica Sinica (2010Sinica ( ) 31: 1336Sinica ( -1342 doi: 10.1038/aps.2010 published online 13 Sep 2010 Original Article * To whom correspondence should be addressed. E-mail dfliao66@yahoo.com.cn (Duan-fang LIAO); tchaoke@yahoo.com.cn (Chao-ke TANG) Received 2010-03-09 Accepted 2010-06-03 the vessel lumen and the arterial wall, and the control may be disturbed in arteriosclerotic blood vessels. Understanding the mechanisms of lipoprotein translocation, especially from arterial wall to vessel lumen, will be beneficial to the therapy of cardiovascular disorders. Caveolae are distinctive, flaskshaped invaginations of the plasma membrane generated in the Golgi complex. These organelles have a characteristic lipid composition and are associated with a 22 kDa protein called caveolin-1. Zhang reported that two ox-LDL receptors, CD36 and the related receptor SR-B1, localize to caveolae [4,5] . Several human studies have indicated transcytosis of macromolecules by means of caveolae in endothelial cells [6][7][8][9][10][11] . We hypothesized that ox-LDL may internalize and transcytose in this way. Bruneau described a model to study the passage of macromolecules through a monolayer of INT-407 cells [12] . We used this model to investigate the characteristics and mechanism of ox-LDL passage. LOX-1 is the major receptor for ox-LDL in endothelial cells [13] . [14] . Caveolin-1 is the main structural protein of caveolae, and it plays a crucial role in the formation of these invaginations of the plasma membrane. Caveolin-1 is a cholesterolbinding protein. Hu and Wu demonstrated the correlation between caveolin-1 and cellular choles...

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Static pressure drives proliferation of vascular smooth muscle cells via caveolin-1/ERK1/2 pathway

Cited by 23 publications

References 26 publications

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

Role of Caveolin-1 for Blocking the Epithelial-Mesenchymal Transition in Proliferative Vitreoretinopathy

A novel model of cholesterol efflux from lipid-loaded cells

Caveolae and caveolin-1 mediate endocytosis and transcytosis of oxidized low density lipoprotein in endothelial cells

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