Electrospun polycaprolactone (PCL) scaffolds embedded with europium hydroxide nanorods (EHNs) with enhanced vascularization and cell proliferation for tissue engineering applications

2017 ◽  
Vol 5 (24) ◽  
pp. 4660-4672 ◽  
Author(s):  
Robin Augustine ◽  
Susheel Kumar Nethi ◽  
Nandakumar Kalarikkal ◽  
Sabu Thomas ◽  
Chitta Ranjan Patra
Keyword(s):  
Tissue Engineering ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Endothelial Cell Proliferation ◽  
Signaling Cascade ◽  
Engineering Applications ◽  
Blood Vessel Formation ◽  
Vessel Formation

PCL-EHNs scaffolds enhance endothelial cell proliferation, adhesion and blood vessel formation in a VEGFR2/Akt dependent signaling cascade.

scholarly journals Cdc42 is required for cytoskeletal support of endothelial cell adhesion during blood vessel formation in mice

Development ◽  
2015 ◽  
Vol 142 (17) ◽  
pp. 3058-3070 ◽  
Author(s):  
D. M. Barry ◽  
K. Xu ◽  
S. M. Meadows ◽  
Y. Zheng ◽  
P. R. Norden ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Endothelial Cell Adhesion

scholarly journals ANGPTL3 Stimulates Endothelial Cell Adhesion and Migration via Integrin αvβ3 and Induces Blood Vessel Formation in Vivo

2002 ◽  
Vol 277 (19) ◽  
pp. 17281-17290 ◽  
Author(s):  
Gieri Camenisch ◽  
Maria Teresa Pisabarro ◽  
Daniel Sherman ◽  
Joe Kowalski ◽  
Mark Nagel ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Integrin Αvβ3 ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Endothelial Cell Adhesion

scholarly journals Orientation of endothelial cell division is regulated by VEGF signaling during blood vessel formation

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1345-1352 ◽  
Author(s):  
Gefei Zeng ◽  
Sarah M. Taylor ◽  
Janet R. McColm ◽  
Nicholas C. Kappas ◽  
Joseph B. Kearney ◽  
...  
Keyword(s):  
Cell Division ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Embryonic Stem ◽  
Es Cell ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Vegf Signaling ◽  
Vascular Beds

Abstract New blood vessel formation requires the coordination of endothelial cell division and the morphogenetic movements of vessel expansion, but it is not known how this integration occurs. Here, we show that endothelial cells regulate division orientation during the earliest stages of blood vessel formation, in response to morphogenetic cues. In embryonic stem (ES) cell–derived vessels that do not experience flow, the plane of endothelial cytokinesis was oriented perpendicular to the vessel long axis. We also demonstrated regulated cleavage orientation in vivo, in flow-exposed forming retinal vessels. Daughter nuclei moved away from the cleavage plane after division, suggesting that regulation of endothelial division orientation effectively extends vessel length in these developing vascular beds. A gain-of-function mutation in VEGF signaling increased randomization of endothelial division orientation, and this effect was rescued by a transgene, indicating that regulation of division orientation is a novel mechanism whereby VEGF signaling affects vessel morphogenesis. Thus, our findings show that endothelial cell division and morphogenesis are integrated in developing vessels by flow-independent mechanisms that involve VEGF signaling, and this cross talk is likely to be critical to proper vessel morphogenesis.

Abstract 554: Multimerin2 Influences Vascularization Through Modulation of Perlecan

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Petra E Burgisser ◽  
Dennie Tempel ◽  
Dorien Hermkens ◽  
Stefan Schulte-Merker ◽  
Caroline Cheng ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Blood Vessel ◽  
Angiogenic Factor ◽  
Endothelial Cell Proliferation ◽  
G1 Arrest ◽  
Blood Vessel Formation ◽  
Binding Partner ◽  
Vessel Formation

Vascular development is crucial in normal physiology and pathophysiology, and is in part orchestrated by a dynamic balance between extracellular matrix (ECM) and endothelial cells. The molecular mechanisms that govern this balance and as such play a role in the formation of new blood vessels remain largely unknown. In order to identify new genes involved in blood vessel formation, we performed a genome-wide gene expression array analysis in Flk1+ angioblasts during mouse development using a commercial platform (Affymetrix). Multimerin2 (Mmrn2) expression was found to be upregulated in angioblasts and in the developing vasculature of zebrafish and mice. In vitro , using immunofluorescence, Mmrn2 was detected outside of human aortic endothelial cells (HAECs), were it co-localized with the extracellular matrix components perlecan, laminin and fibronectin. Direct interaction with these proteins was confirmed using a combination of co-immunoprecipitation followed by proteomics (LC-MS), and western blot to identify possible binding partners. Mmrn2 gain-of-function and loss-of-function in vitro studies, using Mmrn2 siRNA and adenoviral constructs likewise decreased and increased the expression of its binding partner perlecan. Perlecan is a well known modulator of the pro-angiogenic factor, FGF2, and is required for further signaling through the FGF receptor. Therefore, Mmrn2 may influence FGF2 signaling through perlecan expression and complex formation. Subsequent in vitro studies using an adenoviral construct to induce Mmrn2 overexpression resulted in a G1-arrest in HAECs (P<0.001, N=8). In FGF2 depleted medium a G1 arrest was also observed (P<0.05, N=3), Mmrn2 overexpression combined with FGF2 depleted medium did not enhance the G1 arrest, suggesting a role of Mmrn2 in FGF2 signaling. In addition, Mmrn2 silencing or overexpression in HAECs led to a loss of ECM organization or improved organization, respectively. In line, the binding partner of Mmrn2, perlecan, has been shown to be involved in stabilization of the ECM. These findings suggest that Mmrn2 plays a role during blood vessel formation by binding to perlecan and the ECM, thereby modulating FGF2 signaling and ECM organization and subsequently, regulating endothelial cell proliferation.

Abstract 528: Nogo-B Receptor is Essential for Primitive Blood Vessel Formation and Vasculature Development in Mouse Embryo

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Zhong Liu ◽  
Ujala Rana ◽  
Baofeng Zhao ◽  
Qing R Miao
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Mouse Embryo ◽  
Knockout Mice ◽  
Embryoid Body ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Body Culture ◽  
Embryonic Lethal

Nogo-B was previously identified as a protein that is expressed in endothelial cells and vascular smooth muscle cells. Nogo-A/B deficient mice show exaggerated neointimal proliferation and abnormal remodeling. Nogo-B receptor (NgBR) is a type I receptor, which was identified as a receptor specific for Nogo-B. Our previous work has shown that Nogo-B and its receptor (NgBR) are essential for chemotaxis and morphogenesis of endothelial cells in vitro and intersomitic vessel formation via Akt pathway in zebrafish. Our recent work reveals that NgBR is a critic membrane scaffold protein required for Ras translocation and activation, which is essential for VEGF-stimulated Ras-PI3K-Akt signaling pathway. Here, we further demonstrate the roles of NgBR in regulating primitive blood vessel formation in embryoid body culture systems and vasculature development in mouse embryo. Murine NgBR gene-targeting embryonic stem cells (ESC) were generated by homologous recombination approaches. Homozygous knockout of NgBR in ESC results in cell apoptosis. Heterozygous knockout of NgBR does not affect ESC cell survival, but reduces the formation and branching of primitive blood vessels in embryoid body culture systems. In addition, our preliminary results show that NgBR homozygous knockout mice are embryonic lethal happened at E6.5 or earlier, and endothelial cell specific NgBR knockout mice are embryonic lethal happened at E11.5 and have severe blood vessel formation defects in embryo. Mechanistically, NgBR has two potential regulatory roles during embryonic vasculature development. NgBR knockdown not only decreases both Nogo-B and VEGF-stimulated endothelial cell migration by abolishing Akt phosphorylation, but also impairs endothelial cell lineage commitment by delaying BMP4 production during the period of mesoderm formation. These results suggest that NgBR may be one of important genes coordinating the vasculature development.

Cdc42 is required for cytoskeletal support of endothelial cell adhesion during blood vessel formation in mice

2015 ◽  
Vol 128 (18) ◽  
pp. e1.2-e1.2
Author(s):  
D. M. Barry ◽  
K. Xu ◽  
S. M. Meadows ◽  
Y. Zheng ◽  
P. R. Norden ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Blood Vessel ◽  
Blood Vessel Formation ◽  
Vessel Formation ◽  
Endothelial Cell Adhesion
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