نتایج جستجو برای: vascular smooth muscle cell

تعداد نتایج: 2156167  

Journal: :Biochemical Society transactions 1993
J Loscalzo

Interactions between vascular cells and blood cells are central to the development of the atherosclerotic process. Under normal circumstances, blood cells do not associate with the blood vessel; however, in response to atherogenic stimuli, platelets, lymphocytes and mononuclear leukocytes interact with the vessel wall and induce changes in the vascular micro-environment that support atheroma fo...

Journal: :Development 1998
Q Lin J Lu H Yanagisawa R Webb G E Lyons J A Richardson E N Olson

The embryonic vasculature develops from endothelial cells that form a primitive vascular plexus which recruits smooth muscle cells to form the arterial and venous systems. The MADS-box transcription factor MEF2C is expressed in developing endothelial cells and smooth muscle cells (SMCs), as well as in surrounding mesenchyme, during embryogenesis. Targeted deletion of the mouse MEF2C gene result...

2018
Urmas Roostalu Bashar Aldeiri Alessandra Albertini Neil Humphreys Maj Simonsen-Jackson Jason K.F. Wong Giulio Cossu

RATIONALE Vascular smooth muscle turnover has important implications for blood vessel repair and for the development of cardiovascular diseases, yet lack of specific transgenic animal models has prevented it's in vivo analysis. OBJECTIVE The objective of this study was to characterize the dynamics and mechanisms of vascular smooth muscle turnover from the earliest stages of embryonic developm...

2004
Jennifer A. McCann Thomas J. Webster Karen M. Haberstroh

Introduction. The two most important cell types in the arteries are endothelial and smooth muscle cells; the behavior of these cells is determined by both hemodynamic and biochemical factors. In particular, shear stress and pressure forces have a direct impact on vascular endothelial and smooth muscle cell morphology and phenotype. In addition to direct hemodynamic effects, the communication sy...

Journal: :Hypertension 1994
F Zhang J R Sowers J L Ram P R Standley J D Peuler

Pioglitazone, an insulin-sensitizing, antidiabetic agent, has blood pressure-lowering effects in insulin-resistant hypertensive rats and attenuates growth factor-induced increases of intracellular Ca2+ in rat aortic vascular smooth muscle cells. To determine whether modulation of voltage-dependent Ca2+ channels plays a role in this association, we investigated the effects of pioglitazone on vol...

2014
Feng Shi Xiaochun Long Allison Hendershot Joseph M. Miano Jane Sottile

Smooth muscle cells are maintained in a differentiated state in the vessel wall, but can be modulated to a synthetic phenotype following injury. Smooth muscle phenotypic modulation is thought to play an important role in the pathology of vascular occlusive diseases. Phenotypically modulated smooth muscle cells exhibit increased proliferative and migratory properties that accompany the downregul...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2013
Kirsten A Turlo Jason Scapa Pooneh Bagher Allan W Jones Robert Feil Ronald J Korthuis Steven S Segal M Luisa Iruela-Arispe

OBJECTIVE Integrins contribute to vascular morphogenesis through regulation of adhesion and assembly of the extracellular matrix. However, the role of β1-integrin in the mature vascular wall is less clear. APPROACH AND RESULTS We sought to determine the function of β1-integrin in mature smooth muscle cells in vivo using a loss of function approach by crossing a tamoxifen-inducible sm22αCre li...

Journal: :Hypertension 1994
M G Davis S Ali G D Leikauf G W Dorn

The goal of this study was to determine the role of tyrosine phosphorylation in transducing deformation-stimulated vascular smooth muscle growth. Rat aorta-derived vascular smooth muscle cells were cultured on flexible silicone elastomer membranes and subjected to cyclic deformation (15 cycles per minute, deformed 2 seconds, relaxed 2 seconds). Deformation significantly increased proto-oncogene...

2017
Melissa A. Lyle Jonathan P. Davis Frank V. Brozovich

There are two primary components that produce pulmonary arterial hypertension (PAH); aberrant structural changes (smooth muscle cell proliferation, smooth muscle cell hypertrophy, and the deposition of matrix proteins within the media of pulmonary arterial vessels), and excess vasoconstriction. However, in PAH, the target and aim of all current therapeutic agents is to reduce the contractility ...

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