Endothelial Cell Modulation of Smooth Muscle Cell Morphology and Organizational Growth Pattern

Powell, Richard J.; Cronenwett, Jack L.; Fillinger, Mark F.; Wagner, Robert J.; Sampson, Lawrence N.

doi:10.1007/bf02002334

Cited by 53 publications

(38 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This result is consistent with that found by Powell et al 38 After 24 hours of shear stress (12 dyne/cm 2 ) application to the EC side, the SMCs in coculture tended to orient perpendicularly to the flow direction. This result is comparable to the in vivo orientation of SMCs in blood vessels 39 and to observations on homogeneous SMC culture directly exposed to flow.…”

Section: Morphological Findingssupporting

confidence: 93%

See 1 more Smart Citation

Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells

Chiu

Chen

Lee

et al. 2003

Blood

151

132

View full text Add to dashboard Cite

Vascular endothelial cells (ECs), which exist in close proximity to vascular smooth muscle cells (SMCs), are constantly subjected to blood flow-induced shear stress. Although the effect of shear stress on endothelial biology has been extensively studied, the influence of SMCs on endothelial response to shear stress remains largely unexplored. We examined the potential role of SMCs in regulating the shear stress-induced gene expression in ECs, using a parallel-plate coculture flow system in which these 2 types of cells were separated by a porous membrane. In this coculture system, SMCs tended to orient perpendicularly to the flow direction, whereas the ECs were elongated and aligned IntroductionVascular endothelial cells (ECs), which provide an interface between the blood and the vessel wall, are constantly subjected to hemodynamic forces, including the shear stress imposed by blood flow. Shear stress affects leukocyte-EC interaction and the subsequent leukocyte extravasation into inflamed tissues. 1,2 The effects of fluid shear stress on endothelial biology and gene expression have been extensively studied. [3][4][5][6][7] In addition to its physical influence on leukocyte-EC adhesion, 8,9 shear stress can alter the adhesive properties of ECs by modulating the surface expression of adhesive proteins, for example, intercellular adhesion molecule-1 (ICAM-1), 10-15 vascular cell adhesion molecule-1 (VCAM-1), 10,11,13,14,16,17 and E-selectin. 13,18 Exposure of ECs to laminar flow increases the gene and protein expression of ICAM-1. [10][11][12][13][14][15] Our recent study demonstrated that this shear flow-induced increase in ICAM-1 expression is partially due to an elevation of the levels of intracellular reactive oxygen species (ROS) in ECs. 15 In contrast to ICAM-1, shear stress treatment of ECs has only a minor effect on the surface expression of VCAM-1, or may even cause a reduction. 10,11,13,14,16,17 E-selectin has been reported to be less responsive to laminar shear stress 13 and more responsive to oscillatory flow condition. 18 Most studies on how shear stress affects ECs have been performed by using a cultured EC monolayer as an experimental model. The vessel wall is composed of several types of cells, including ECs, smooth muscle cells (SMCs), and fibroblasts. There is increasing evidence that cell-to-cell interactions can control cellular growth, migration, differentiation, and function. 19 Physical contact between ECs and SMCs via myoendothelial bridges has been demonstrated in vivo 20,21 and may play an important role in cellular communication. Hence, in vitro models for studying ECs need to simulate the in vivo environment by coculturing ECs in close proximity to SMCs. Several coculture models have recently been developed. [22][23][24][25][26] Ziegler et al 22 designed a coculture model that includes SMCs, ECs, and a matrix of collagen gel. They demonstrated that ECs cocultured with SMCs aligned with the flow direction more rapidly than ECs grown on plastic. Redmond et al 23 developed a system in whic...

show abstract

Section: Morphological Findingssupporting

confidence: 93%

“…† P Ͻ .05 vs control EC/SMC. 30,31,38,[42][43][44] Several growth factors (eg, activated transforming growth factor-␤1 [TGF-␤1]) have been shown to be produced by the ECs and SMCs in coculture and may be involved in some of the effects exerted by SMCs on ECs. 43 TGF-␤1 activation of ICAM-1, VCAM-1, and E-selectin in ECs has been reported.…”

mentioning

confidence: 99%

Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells

Chiu

Chen

Lee

et al. 2003

Blood

151

132

View full text Add to dashboard Cite

show abstract

“…58,59 ECs can modulate phenotypic change, regulate proliferation, and induce migration of SMCs. 60,61 These processes are regulated by growth factors such as PDGF and TGF-␤. PDGF derived from EC acts as a mitogen for mesenchymal cells, 62 whereas TGF-␤ induces differentiation of neural crest cells into SMCs.…”

Section: Discussionmentioning

confidence: 99%

Stromal cells expressing ephrin-B2 promote the growth and sprouting of ephrin-B2+ endothelial cells

Zhang

Takakura

Oike

et al. 2001

Blood

View full text Add to dashboard Cite

Ephrin-B2 is a transmembrane ligand that is specifically expressed on arterial endothelial cells (ECs) and surrounding cells and interacts with multiple EphB class receptors. Conversely, EphB4, a specific receptor for ephrin-B2, is expressed on venous ECs, and both ephrin-B2 and EphB4 play essential roles in vascular development. The bidirectional signals between EphB4 and ephrin-B2 are thought to be specific for the interaction between arteries and veins and to regulate cell mixing and the making of particular boundaries. However, the molecular mechanism during vasculogenesis and angiogenesis remains unclear. Manipulative functional studies were performed on these proteins in an endothelial cell system. Using in vitro stromal cells (OP9 cells) and a paraaortic splanchnopleura (P-Sp) coculture system, these studies found that the stromal cells expressing ephrin-B2 promoted vascular network formation and ephrin-B2 ؉ EC proliferation and that they also induced the recruitment and proliferation of ␣-smooth muscle IntroductionDuring embryogenesis, vascular development consists of 2 processes: vasculogenesis, whereby endothelial cell (EC) precursors differentiate and proliferate to form the initial vascular plexus, [1][2][3] and angiogenesis, in which the initial vascular plexus forms mature vessels by sprouting, branching, pruning, differential growth of ECs, and recruitment of supporting cells, such as pericytes and smooth muscle cells (SMCs). 1,3,4 To date, 3 growth factor systemsvascular endothelial growth factors (VEGFs), angiopoietins, and ephrins-have been identified as critical factors for angiogenesis. [2][3][4][5][6] VEGFs and their receptors VEGFR-2/Flk-1, VEGFR-1/Flt-1, and VEGFR-3/Flt-4 are key regulators of vasculogenesis and angiogenesis. VEGF and Flk-1 are required to grow and establish an endothelial lineage, 7-10 whereas VEGF and Flt-1 are involved in the organization of ECs into tubelike structures. 11 Flt-4 also contributes to angiogenesis and lymphangiogenesis. 12 Angiopoietins and their EC-specific receptors, TIEs, have been suggested to be important for vascular remodeling and cardiac development. [13][14][15] Platelet-derived growth factor (PDGF) and tumor growth factor (TGF)-␤ have been reported to be associated with pericyte proliferation and movement. [16][17][18][19] One of the most important events in vascularization is the development of arteries and veins. Generally, the differences between arteries and veins have been defined by function, anatomy, pressure, and blood flow direction. Recent studies have shown that the arterial and venous ECs are molecularly distinct from the earliest types of blood vessels. This distinction is revealed by a tyrosine kinase receptor, EphB4, that is dominantly expressed on venous ECs and whose cognate ligand, ephrin-B2, is expressed on arterial ECs. 20,21 The Eph receptor and ephrin ligand families play important roles in embryonic development. 22 They can be grouped into 2 subclasses based on structural homology and binding specificity: ephrin-A ligands...

show abstract

“…The endothelial dysfunction that takes place in PH may also contribute to the dediferentiation and proliferation of VSMCs [22]. Speciically, dysregulated endothelial cells can cause alterations in AKT signalling in VSMCs, which in turn triggers their phenotypic switch [23].…”

Section: Phenotypic Switching Of Vascular Smooth Muscle Cellsmentioning

confidence: 99%

Hypoxia and Pulmonary Hypertension

Charolidi¹,

Carroll²

2017

Hypoxia and Human Diseases

View full text Add to dashboard Cite

Vasoconstriction in response to low oxygen tension (hypoxia) in pulmonary arteries is an important physiological adaptation to reroute blood low to areas of higher oxygenation for efective gaseous exchange. However, chronic hypoxia is a common feature of lung disease, such as chronic obstructive pulmonary disease (COPD). Hypoxic stress triggers cellular phenotypic alterations including increased proliferation and migration of vascular smooth muscle cells (VSMCs), as well as synthesis of extracellular matrix (ECM) proteins that remodel lung vasculature. Remodelling of vessels increases the risk of pulmonary hypertension (PH)-elevated pulmonary arterial pressure-and eventually right heart failure. This chapter will summarise the major pathways and mechanisms involved in hypoxia-driven pulmonary hypertension (PH).

show abstract

Endothelial Cell Modulation of Smooth Muscle Cell Morphology and Organizational Growth Pattern

Cited by 53 publications

References 16 publications

Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells

Shear stress inhibits adhesion molecule expression in vascular endothelial cells induced by coculture with smooth muscle cells

Stromal cells expressing ephrin-B2 promote the growth and sprouting of ephrin-B2+ endothelial cells

Hypoxia and Pulmonary Hypertension

Contact Info

Product

Resources

About