neointima/برولين

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مقالاتالتجارب السريريةبراءات الاختراع

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13 النتائج

Protein kinase CK2 inhibition suppresses neointima formation via a proline-rich homeodomain-dependent mechanism.

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Neointimal hyperplasia is a product of VSMC replication and consequent accumulation within the blood vessel wall. In this study, we determined whether inhibition of protein kinase CK2 and the resultant stabilisation of proline-rich homeodomain (PRH) could suppress VSMC proliferation. Both silencing

Novel role of proline-rich nonreceptor tyrosine kinase 2 in vascular wall remodeling after balloon injury.

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OBJECTIVE To investigate the role of Pyk2, a proline-rich nonreceptor tyrosine kinase, in G protein-coupled receptor agonist, thrombin-induced human aortic smooth muscle cell growth and migration, and injury-induced vascular wall remodeling. RESULTS Thrombin, a G protein-coupled receptor agonist,

Curcumin inhibits platelet-derived growth factor-stimulated vascular smooth muscle cell function and injury-induced neointima formation.

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OBJECTIVE Vascular smooth muscle cell (VSMC) migration, proliferation, and collagen synthesis are key events involved in the pathogenesis of cardiovascular disease. Growth factors, such as platelet-derived growth factor (PDGF) and fibroblast growth factor, released during vascular injury plays a

Phytoestrogens inhibit growth and MAP kinase activity in human aortic smooth muscle cells.

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-Estrogens are known to induce cardioprotective effects by inhibiting smooth muscle cell (SMC) growth and neointima formation. However, the use of estrogens as cardioprotective agents is limited by carcinogenic effects in women and feminizing effects in men. If noncarcinogenic and nonfeminizing

Angiogenesis-dependent and independent phases of intimal hyperplasia.

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BACKGROUND Neointimal vascular smooth muscle cell (VSMC) proliferation is a primary cause of occlusive vascular disease, including atherosclerosis, restenosis after percutaneous interventions, and bypass graft stenosis. Angiogenesis is implicated in the progression of early atheromatous lesions in

BMP promotes motility and represses growth of smooth muscle cells by activation of tandem Wnt pathways.

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We present a novel cell-signaling paradigm in which bone morphogenetic protein 2 (BMP-2) consecutively and interdependently activates the wingless (Wnt)-β-catenin (βC) and Wnt-planar cell polarity (PCP) signaling pathways to facilitate vascular smooth muscle motility while simultaneously suppressing

Collagen biosynthesis by neointimal smooth muscle cells cultured from rabbit aortic explants 15 weeks after de-endothelialization.

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Extracellular matrix (ECM) accumulation in arterial neointima, developed in response to de-endothelialization, is a prolonged process. In this study, we examined the relationship between increased collagen accumulation and synthetic activity of neointimal smooth muscle cells (SMCs) derived from

Increase of PTP levels in vascular injury and in cultured aortic smooth muscle cells treated with specific growth factors.

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Migration and proliferation of vascular smooth muscle cells are key events in injury-induced neointima formation. Several growth factors and ANG II are thought to be involved in neointima formation. A recent report indicated that vascular injury is associated with increased mRNA levels of protein

Mechanisms of hepatocyte growth factor-mediated vascular smooth muscle cell migration.

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The migration of vascular smooth muscle cells (SMCs) from the media into the neointima and their subsequent proliferation is important in the pathogenesis of atherosclerosis. This process is regulated by multiple factors, including growth factors, and involves changes in the interaction of SMCs with

Endothelial AIP1 Regulates Vascular Remodeling by Suppressing NADPH Oxidase-2.

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Objective: AIP1 expression is downregulated in human atherosclerotic plaques and global deletion of AIP1 in mice exacerbates atherosclerosis in ApoE-KO mouse models. However, the direct role of AIP1 in endothelium, vascular remodeling and associated vascular diseases has not been determined.

Angiotensin II, focal adhesion kinase, and PRX1 enhance smooth muscle expression of lipoma preferred partner and its newly identified binding partner palladin to promote cell migration.

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Lipoma preferred partner (LPP) is a proline rich LIM domain family protein highly expressed at plasma membrane dense bodies and focal adhesions in smooth muscle cells.(1) Using the C-terminus of LPP as bait in a yeast two hybrid system, palladin, an actin-associated protein was identified. The

TGF-beta1 generates a specific multicomponent extracellular matrix in human coronary SMC.

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BACKGROUND Transforming growth factor (TGF-beta(1)) is postulated to play an important role in maintaining the structure and function of arterial tissue and protection against development of arteriosclerosis. The TGF-beta(1)-induced production of a stable extra-cellular matrix-rich plaque phenotype

Arginase: a critical regulator of nitric oxide synthesis and vascular function.

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1. Arginase is the focal enzyme of the urea cycle hydrolysing L-arginine to urea and L-ornithine. Emerging studies have identified arginase in the vasculature and have implicated this enzyme in the regulation of nitric oxide (NO) synthesis and the development of vascular disease. 2. Arginase

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