Regulation of Foxo‐1 and the angiopoietin‐2/Tie2 system by shear stress

Chlench, Sven; Disassa, Nigussie Mecha; Hohberg, Margret; Hoffmann, Christian J.; Pohlkamp, Theresa; Beyer, G.; Bongrazio, Mauro; Silva-Azevedo, Luis Da; Baum, Oliver; Pries, Axel R.; Zakrzewicz, Andreas

doi:10.1016/j.febslet.2007.01.028

Cited by 63 publications

(52 citation statements)

References 25 publications

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“…Importantly, these changes in angiogenesis were associated with a decreased Ang-2 expression. Interestingly, although MCGs increased Ang-1 mRNA expression, the Ang-1 protein was not detected in this co-culture system, which was also observed by another group (24). This could be related to the different species or different tissue that we used (25,26).…”

Section: Discussionsupporting

confidence: 85%

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

Wang

Zhu

Jiang

et al. 2013

Braz J Med Biol Res

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Angiopoietin (Ang)-1 and Ang-2 interact in angiogenesis to activate the Tie-2 receptor, which may be involved in new vessel maturation and regression. Mast cells (MCs) are also involved in formation of new blood vessels and angiogenesis. The present study was designed to test whether MCs can mediate angiogenesis in myocardial microvascular endothelial cells (MMVECs). Using a rat MMVEC and MC co-culture system, we observed that Ang-1 protein levels were very low even though its mRNA levels were increased by MCs. Interestingly, MCs were able to enhance migration, proliferation, and capillary-like tube formation, which were associated with suppressed Ang-2 protein expression, but not Tie-2 expression levels. These MCs induced effects that could be reversed by either tryptase inhibitor [N-tosyl-L-lysine chloromethyl ketone (TLCK)] or chymase inhibitor (N-tosyl-L-phenylalanyl chloromethyl ketone), with TLCK showing greater effects. In conclusion, our data indicated that MCs can interrupt neovessel maturation via suppression of the Ang-2/Tie-2 signaling pathway.

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Section: Discussionsupporting

confidence: 85%

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

Wang

Zhu

Jiang

et al. 2013

Braz J Med Biol Res

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“…This could be related to the flow patterns around the developing valve that may be involved in establishing its gene expression profile and structure. Exposure of cultured cells to shear stress in vitro leads to upregulation and phosphorylation of Tie2 (22,23). In addition, expression of angiopoietin-2, an antagonistic Tie2 ligand, is downregulated under shear stress (23), which suggests that Tie2-mediated signaling may be involved in regulating endothelial cell responses to flow.…”

Section: Discussionmentioning

confidence: 91%

Genes regulating lymphangiogenesis control venous valve formation and maintenance in mice

et al. 2011

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Chronic venous disease and venous hypertension are common consequences of valve insufficiency, yet the molecular mechanisms regulating the formation and maintenance of venous valves have not been studied. Here, we provide what we believe to be the first description of venous valve morphogenesis and identify signaling pathways required for the process. The initial stages of valve development were found to involve induction of ephrin-B2, a key marker of arterial identity, by venous endothelial cells. Intriguingly, developing and mature venous valves also expressed a repertoire of proteins, including prospero-related homeobox 1 (Prox1), Vegfr3, and integrin-α9, previously characterized as specific and critical regulators of lymphangiogenesis. Using global and venous valve-selective knockout mice, we further demonstrate the requirement of ephrin-B2 and integrin-α9 signaling for the development and maintenance of venous valves. Our findings therefore identified molecular regulators of venous valve development and maintenance and highlighted the involvement of common morphogenetic processes and signaling pathways in controlling valve formation in veins and lymphatic vessels. Unexpectedly, we found that venous valve endothelial cells closely resemble lymphatic (valve) endothelia at the molecular level, suggesting plasticity in the ability of a terminally differentiated endothelial cell to take on a different phenotypic identity.

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“…Akt has several downstream targets implicated in angiogenesis, including endothelial nitric oxide synthase (eNOS) (16), hypoxiainducible factor (23), and the transcription factor forkhead box transcription factor (FOXO) (6). Of note, both eNOS activity and FOXO expression are regulated by WSS in ECs (6,16). Whether these signals are affected by the S1P signaling pathway in either 2-D or 3-D settings remains to be investigated.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, EC migration and tubulogenesis following preshearing are also attenuated by pertussis toxin (10). Akt has several downstream targets implicated in angiogenesis, including endothelial nitric oxide synthase (eNOS) (16), hypoxiainducible factor (23), and the transcription factor forkhead box transcription factor (FOXO) (6). Of note, both eNOS activity and FOXO expression are regulated by WSS in ECs (6,16).…”

Section: Discussionmentioning

confidence: 99%

Fluid shear stress modulates endothelial cell invasion into three-dimensional collagen matrices

Kang

Bayless²,

Kaunas³

2008

American Journal of Physiology-Heart and Circulatory Physiology

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Kang H, Bayless KJ, Kaunas R. Fluid shear stress modulates endothelial cell invasion into three-dimensional collagen matrices. Am J Physiol Heart Circ Physiol 295: H2087-H2097, 2008. First published September 19, 2008 doi:10.1152/ajpheart.00281.2008.-Endothelial cells are subjected to biochemical and mechanical stimuli, which regulate their angiogenic potential. We determined the synergistic effects of sphingosine-1-phosphate (S1P) and fluid wall shear stress (WSS) on a previously established model of human umbilical vein endothelial cell invasion into three-dimensional collagen matrices. Collagen matrices were incorporated into a parallel-plate flow chamber to apply controlled WSS to the surface of endothelial monolayers over a period of 24 h. Cell invasion required the presence of S1P, with the effects of S1P being enhanced by shear stress to an extent comparable with S1P combined with angiogenic growth factor stimulation. The number of invading cells depended on the magnitude of shear stress, with a maximal induction at a shear stress of ϳ5 dyn/cm 2 , whereas the invasion distance was proportional to the magnitude of shear stress. The enhancement of invasion by 5.3 dyn/cm 2 shear stress coincided with elevated phosphorylation of Akt and matrix metalloproteinase (MMP)-2 activation. Furthermore, invasion induced by the combined application of WSS and S1P was attenuated by inhibitors of MMPs (GM6001) and the phosphatidylinositol 3-kinase/Akt signaling pathway (wortmannin). These results provide evidence that shear stress is a positive modulator of S1P-induced endothelial cell invasion into collagen matrices through enhanced Akt and MMP-2 activation. endothelium; angiogenesis; sphingosine-1-phosphate; three dimensions; sprout formation ANGIOGENESIS, THE DEVELOPMENT of new blood vessels from preexisting vessels, is a critical step in physiological and pathological events such as wound healing and tumor vascularization (18). Sprouting angiogenesis in vivo involves endothelial cell (EC) degradation of the basement membrane, proliferation, and migration toward angiogenic stimuli. These events are coordinated with eventual formation of a lumen within the endothelial sprout and the joining of sprouts to form a capillary bed (4, 19). Importantly, both biochemical and mechanical forces influence these newly developing structures.Several biochemical factors are recognized to enhance angiogenesis. Basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) are the best characterized inducers. In vitro, FGF-2 and VEGF induce EC proliferation, matrix proteolytic activity, invasion into three-dimensional (3-D) collagen matrices, and formation of tubular structures (12,20). More recently, sphingosine-1-phosphate (S1P) has been identified as a potent proangiogenic factor (25). S1P can act as an intracellular signaling molecule and is also deposited by activated platelets during wound healing (5, 24). Exogenous S1P administration or endogenous S1P production by sphingosine kinase overexpression promotes...

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Regulation of Foxo‐1 and the angiopoietin‐2/Tie2 system by shear stress

Cited by 63 publications

References 25 publications

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway

Genes regulating lymphangiogenesis control venous valve formation and maintenance in mice

Fluid shear stress modulates endothelial cell invasion into three-dimensional collagen matrices

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