Cyclic strain causes heterogeneous induction of transcription factors, AP-1, CRE binding protein and NF-kB, in endothelial cells: Species and vascular bed diversity

Du, Wei; Mills, Ira; Sumpio, Bauer E.

doi:10.1016/0021-9290(95)00096-8

Cited by 105 publications

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Du et al (13) showed that cyclically strained HUVEC and HAEC (10% deformation average, 1 Hz) both induced AP-1 and NF-B in a monophasic manner, consistent with our findings that 10% cyclic strain upregulated VCAM-1 in both cell types. Interestingly, as noted by Dagia et al (9), redox-sensitive GATA is involved in VCAM-1 expression in tumor necrosis factor (TNF)-␣-stimulated HUVEC (41) but not TNF-␣-stimulated HAEC.…”

Section: Discussionsupporting

confidence: 93%

Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types

Sung

Yee²,

Eskin³

et al. 2007

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Buy / Rent full text

Sung H-J, Yee A, Eskin SG, McIntire LV. Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types. Am J Physiol Cell Physiol 293: C87-C94, 2007. First published February 21, 2007 doi:10.1152/ajpcell.00585.2006.-The phenotype of endothelial cells (ECs) is specific to the vascular bed from which they originate. To examine how mechanical forces alter the phenotype of different ECs, we compared the effects of cyclic strain and motion control on reactive oxygen species (ROS) production and metabolism and cell adhesion molecule expression in human umbilical vein endothelial cells (HUVEC) vs. human aortic endothelial cells (HAEC). HUVEC and HAEC were subjected to cyclic strain (10% or 20%, 1 Hz), to a motion control that simulated fluid agitation over the cells without strain, or to static conditions for 24 h. We measured H2O2 production with dichlorodihydrofluorescein acetate and superoxide with dihydroethidium fluorescence changes; superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities spectrophotometrically; and vascular cell adhesion molecule (VCAM)-1 and intercellular adhesion molecule (ICAM)-1 protein expression with Western blot analyses. HUVEC under cyclic strain showed 1) higher intracellular H2O2 levels, 2) increased SOD, catalase, and GPx activities, and 3) greater VCAM-1 and ICAM-1 protein expression, compared with motion control or static conditions. However, in HAEC, motion control induced higher levels of ROS, enzyme activities associated with ROS defense, and VCAM-1 and ICAM-1 expression than cyclic strain. The opposite responses obtained with these two human EC types may reflect their vessels of origin, in that HAEC are subjected to higher cyclic strain deformations in vivo than HUVEC.

show abstract

Section: Discussionsupporting

confidence: 93%

Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types

Sung

Yee²,

Eskin³

et al. 2007

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Buy / Rent full text

show abstract

“…41 Nonetheless, cyclic strain-mediated signaling pathways have been directly linked to specific trans-acting factors, such as nuclear factor-B and activator protein-2. 42,43 As noted, both factors have corresponding cis-acting elements in the syndecan-4 promoter region.…”

Section: Discussionmentioning

confidence: 87%

Mechanical Stress Regulates Syndecan-4 Expression and Redistribution in Vascular Smooth Muscle Cells

Chaikof

2002

ATVB

View full text Add to dashboard Buy / Rent full text

Abstract-Syndecan-4 is a unique membrane-associated heparan sulfate proteoglycan that colocalizes with integrin heterodimers in focal adhesion complexes. Because focal adhesions serve as a putative mechanotransduction system, we postulated that physical forces that are sensed by focal adhesions may regulate the expression and intracellular distribution of syndecan-4 and thereby modulate cell movement and orientation. In this report, syndecan-4 was identified as a transcriptionally regulated, immediate-early gene in response to the application of oscillatory stress. This fluctuation was associated with coordinate changes in the concentration and compartmentalization of syndecan-4 proteins. Specifically, syndecan-4 was lost from the dorsal aspect of the cell membrane and translocated from its intracellular pool to the ventral cell surface. Dissociation of syndecan-4 and vinculin from focal adhesions may contribute to promoting cell motility, because overexpression of syndecan-4, in part, blocked this dissociation and also retarded mechanical stretch-induced cell migration. These studies suggest that mechanical stress induces cell locomotion, in part, by the dynamic regulation of syndecan-4 expression and relocation. Key Words: restenosis Ⅲ hypertension Ⅲ atherosclerosis Ⅲ heparan sulfate Ⅲ syndecan V ascular smooth muscle cells (SMCs) are subjected to a dynamic, mechanical environment modulated by pulsatile pressure and oscillatory shear forces. Although these forces are important regulators of normal cell function, under certain conditions they may contribute to the development of a pathological state. For example, hypertension, which increases transmural stresses due to mechanical distension of the arterial wall, leads to vascular wall hypertrophy and is an independent risk factor for the development of atherosclerosis. 1 Strong correlations have also been noted between regions of elevated wall stresses and the propensity for rupture of either an atherosclerotic plaque or an aortic aneurysm. 2,3 Likewise, the restenosis response that often follows balloon angioplasty may be due, in part, to the extreme vessel wall strains that are associated with this mechanical intervention. 4 Although these observations support the notion that wall stress is a potent stimulus for pathophysiological adaptations of the vessel wall, the underlying molecular and cellular mechanisms that eventually lead to a pathological end point remain largely undefined.Syndecan-4 is a cell surface heparan sulfate proteoglycan (HSPG) widely expressed in tissues derived from ectoderm, mesenchyme, and endoderm in a position-, time-, and development-dependent manner. 5 The ectodomain of syndecan-4 bears 3 distinct heparan sulfate (HS) chains that are capable of binding a variety of ligands that modulate events relevant to acute tissue repair and chronic injury responses, including cell migration and proliferation, cellsubstrate interactions, and matrix remodeling. 6,7 In this regard, syndecan-4 serves as a coreceptor for a variety of soluble ligands...

show abstract

“…Mechanical force is classified into shear stress, compressive stress and stretch stress, and are thought to play roles as tissue-specific regulators of extracellular matrix (ECM) homeostasis. For example, bloodstream affects several vascular components as fluid shear stress, whereas blood pressure will act as stretch stress (Du et al, 1995). Also, in the bone, differentiation, growth and several phenotype expression in the osteoblasts were regulated by several mechanical forces (Singh et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Mechanical Strain Increases Expression of Type XII Collagen in Murine Osteoblastic MC3T3-E1 Cells

Arai

Nagashima

Takemoto

et al. 2008

Cell Struct. Funct.

View full text Add to dashboard Buy / Rent full text

ABSTRACT. In adult mouse, the mRNA corresponding to the alpha1 chain of type XII collagen (alpha 1(XII)) is predominantly detected in the bone. Additionally, murine osteoblastic cells, MC3T3-E1, increased the mRNA level of alpha 1(XII) response to the mechanical strain in the stretch culture system. Cyclic stretch stress resulted in a threefold increase in mRNA level of alpha 1(XII) as compared to the control experiment in MC3T3-E1. Transient transfection assays employing a reporter construct, together with site-directed mutagenesis studies, suggested that the AP-1 binding site in the first exon of mouse alpha 1(XII) gene is important for stretch stressmediated upregulation of alpha 1(XII) expression. Electrophoretic mobility shift assay and associated antibody supershift experiments showed that stretch stress promotes the binding of c-Jun and JunD. Further chromatin immunoprecipitation experiments confirmed the participation of these transcription factors in the region. Also, the exogenous induction of the dominant negative form of c-Jun canceled the effect of stretch stress on the stimulation of the alpha 1(XII) gene. Here, we reported a potential responsive element to the stretch stress in mouse alpha 1(XII) gene. These data will provide new information on the mechanical strain-mediated transcriptional control of alpha 1(XII)-mediated fibrillogenesis in the bone.

show abstract

Cyclic strain causes heterogeneous induction of transcription factors, AP-1, CRE binding protein and NF-kB, in endothelial cells: Species and vascular bed diversity

Cited by 105 publications

References 30 publications

Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types

Cyclic strain and motion control produce opposite oxidative responses in two human endothelial cell types

Mechanical Stress Regulates Syndecan-4 Expression and Redistribution in Vascular Smooth Muscle Cells

Mechanical Strain Increases Expression of Type XII Collagen in Murine Osteoblastic MC3T3-E1 Cells

Contact Info

Product

Resources

About