Proteomic analysis of homocysteine induced proliferation of cultured neonatal rat vascular smooth muscle cells

Liu, Xiaohua; Shen, Jing; Zhan, Rui; Wang, Xingxing; Wang, Xiaoming; Zhang, Zhiqing; Xue, Lixiang; Yang, Zhihua; Lei, Qian

doi:10.1016/j.bbapap.2008.10.001

Cited by 32 publications

(21 citation statements)

References 56 publications

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“…1). VSMCs were not activated until Hcy reached 500 μM, which agrees with previous reports [5,8,10]. In contrast, in the presence of HUVECs, Hcy at 100 μM significantly increased VSMCs growth (Fig.…”

Section: Hcy Promotes Proliferation and Migration Of Vsmcs Via Huvecpsupporting

confidence: 90%

“…The underlying mechanism accounting for HHcyaccelerated atherosclerosis involves a complex series of events, including dysfunction of endothelial cells (ECs) and accelerated proliferation or migration of vascular smooth muscle cells (VSMCs) [3][4][5]. A number of studies have suggested that homocysteine (Hcy) triggers oxidative or ER stress in ECs but activates VSMCs via aberrant regulation of cyclin supplementation, which affects Hcy metabolism and alleviates HHcy formation, limits the aggressiveness of glioma by remethylation of PDGF-B [15].…”

Section: Introductionmentioning

confidence: 99%

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Homocysteine activates vascular smooth muscle cells by DNA demethylation of platelet-derived growth factor in endothelial cells

Zhang

Chen

Xie

et al. 2012

Journal of Molecular and Cellular Cardiology

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Section: Hcy Promotes Proliferation and Migration Of Vsmcs Via Huvecpsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Homocysteine activates vascular smooth muscle cells by DNA demethylation of platelet-derived growth factor in endothelial cells

Zhang

Chen

Xie

et al. 2012

Journal of Molecular and Cellular Cardiology

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“…Pyruvate kinase is a rate-controlling enzyme of the glycolytic cascade, which catalyses the formation of pyruvate and ATP from phosphoenol pyruvate and ADP. 37 In addition, enolase, which is composed of three distinct subunits (a, b, and g), is an abundant glycolytic enzyme present in vascular tissues. 38 Based on these studies, we speculate that upregulation of these proteins would accelerate glucose metabolism and the energy production, resulting in an increased number of metabolic active SMCs.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Tissue-Engineered Blood Vessel Walls Constructed by Adipose-Derived Stem Cells

Wang

Guo

Zhou

et al. 2013

Tissue Engineering Part A

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Adipose-derived stem cells (ASCs) can differentiate into smooth muscle cells and have been engineered into elastic small diameter blood vessel walls in vitro. However, the mechanisms involved in the development of three-dimensional (3D) vascular tissue remain poorly understood. The present study analyzed protein expression profiles of engineered blood vessel walls constructed by human ASCs using methods of two-dimensional gel electrophoresis (2DE) and mass spectrometry (MS). These results were compared to normal arterial walls. A total of 1701 -15 and 1265 -26 protein spots from normal and engineered blood vessel wall extractions were detected by 2DE, respectively. A total of 20 spots with at least 2.0-fold changes in expression were identified, and 38 differently expressed proteins were identified by 2D electrophoresis and ion trap MS. These proteins were classified into seven functional categories: cellular organization, energy, signaling pathway, enzyme, anchored protein, cell apoptosis/defense, and others. These results demonstrated that 2DE, followed by ion trap MS, could be successfully utilized to characterize the proteome of vascular tissue, including tissue-engineered vessels. The method could also be employed to achieve a better understanding of differentiated smooth muscle protein expression in vitro. These results provide a basis for comparative studies of protein expression in vascular smooth muscles of different origin and could provide a better understanding of the mechanisms of action needed for constructing blood vessels that exhibit properties consistent with normal blood vessels.

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“…Several mechanisms have been proposed to explain cardiovascular pathological changes associated with HHcy. These include endothelial dysfunction and damage 3, 4 , dysregulation of cholesterol and triglyceride (TG) biosynthesis 5, 6 , thrombosis activation 7, 8 , and stimulation of vascular smooth muscle cell (SMC) proliferation 9, 10 . Although these studies established that Hcy has profound atherogenic effects, the mechanisms by which HHcy contributes to arteriosclerosis remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Hyperhomocysteinemia promotes vascular remodeling in vein graph in mice

et al. 2014

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Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease. However, the mechanisms of HHcy-induced arteriosclerosis are largely unknown. In this study, we investigated the role and mechanism of HHcy on vascular remodeling in a carotid arterial vein patch model. We assessed the effect of HHcy on vascular remodeling using a carotid arterial vein patch model in mice with the gene deletion of cystathionine-β-synthase (Cbs, plasma Hcy 310 μM). Vein grafts were harvested 4 weeks after surgery. Cross sections of the transplanted vessel segment were analyzed using Verhoeff-van Gieson staining and Masson’s Trichrome staining for morphological analysis and total collagen protein level assessment. Further, the vessel sections were immunostained with antibodies against α-smooth muscle actin (α-SMA), type 1 collagen, CD45 (leukocyte marker), and Proliferating Cell Nuclear Antigen (PCNA). The effect of Hcy on collagen secretion was examined in cultured rat aortic smooth muscle cells (RASMC) by Western blot analysis. We found that Cbs−/− mice with severe HHcy exhibited thicker neointima and a higher percentage of luminal narrowing in the vein graft. In addition, severe HHcy increased elastin, total collagen, and type 1 collagen deposition in the neointima. Further, severe HHcy increases CD45 positive cells and proliferative cells in the lesions of vein grafts in Cbs−/− mice. Finally, Hcy increases collagen secretion in cultured rat aortic smooth muscle cells (RASMC). These results demonstrate that HHcy increases neointima formation, elastin and collagen deposition following a carotid arterial vein patch. The capacity of Hcy to promote vascular fibrosis and inflammation may contribute to the development of vascular remodeling.

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Proteomic analysis of homocysteine induced proliferation of cultured neonatal rat vascular smooth muscle cells

Cited by 32 publications

References 56 publications

Homocysteine activates vascular smooth muscle cells by DNA demethylation of platelet-derived growth factor in endothelial cells

Homocysteine activates vascular smooth muscle cells by DNA demethylation of platelet-derived growth factor in endothelial cells

Proteomic Profiling of Tissue-Engineered Blood Vessel Walls Constructed by Adipose-Derived Stem Cells

Hyperhomocysteinemia promotes vascular remodeling in vein graph in mice

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