University of Wisconsin solution for the xeno-free storage of adipose tissue-derived microvascular fragments

2019 ◽  
Vol 14 (7) ◽  
pp. 681-691 ◽  
Author(s):  
Matthias W Laschke ◽  
Alexander Heß ◽  
Claudia Scheuer ◽  
Philipp Karschnia ◽  
Elena Kontaxi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Regenerative Medicine ◽  
Intravital Fluorescence Microscopy ◽  
Microvascular Networks ◽  
Uw Solution ◽  
University Of Wisconsin ◽  
Endothelial Cell Growth ◽  
Wisconsin Solution

Aim: Adipose tissue-derived microvascular fragments (ad-MVF) are vascularization units for regenerative medicine. We investigated whether University of Wisconsin (UW) solution is suitable for their xeno-free storage. Materials & methods: Murine ad-MVF were cultivated for 24 h in 4°C or 20°C UW solution and 20°C endothelial cell growth medium (control). The ad-MVF were seeded onto collagen–glycosaminoglycan scaffolds, which were analyzed in dorsal skinfold chambers by intravital fluorescence microscopy and histology. Results: All implants exhibited microvascular networks on day 14 with the highest functional microvessel density in controls. Ad-MVF cultivation in UW solution at 4°C resulted in an improved scaffold vascularization compared with cultivation at 20°C. Conclusion: UW solution is suitable for the hypothermic storage of ad-MVF.

scholarly journals Enhanced angiogenesis in obesity and in response to PPARγ activators through adipocyte VEGF and ANGPTL4 production

2008 ◽  
Vol 295 (5) ◽  
pp. E1056-E1064 ◽  
Author(s):  
Olga Gealekman ◽  
Alison Burkart ◽  
My Chouinard ◽  
Sarah M. Nicoloro ◽  
Juerg Straubhaar ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
Cell Growth And Differentiation ◽  
Endothelial Cell Growth ◽  
Sprout Formation

PPARγ activators such as rosiglitazone (RSG) stimulate adipocyte differentiation and increase subcutaneous adipose tissue mass. However, in addition to preadipocyte differentiation, adipose tissue expansion requires neovascularization to support increased adipocyte numbers. Paradoxically, endothelial cell growth and differentiation is potently inhibited by RSG in vitro, raising the question of how this drug can induce an increase in adipose tissue mass while inhibiting angiogenesis. We find that adipose tissue from mice treated with RSG have increased capillary density. To determine whether adipose tissue angiogenesis was stimulated by RSG, we developed a novel assay to study angiogenic sprout formation ex vivo. Angiogenic sprout formation from equally sized adipose tissue fragments, but not from aorta rings, was greatly increased by obesity and by TZD treatment in vivo. To define the mechanism involved in RSG-stimulated angiogenesis in adipose tissue, the expression of proangiogenic factors by adipocytes was examined. Expression of VEGFA and VEGFB, as well as of the angiopoietin-like factor-4 (ANGPTL4), was stimulated by in vivo treatment with RSG. To define the potential role of these factors, we analyzed their effects on endothelial cell growth and differentiation in vitro. We found that ANGPTL4 stimulates endothelial cell growth and tubule formation, albeit more weakly than VEGF. However, ANGPTL4 mitigates the growth inhibitory actions of RSG on endothelial cells in the presence or absence of VEGF. Thus, the interplay between VEGF and ANGPTL4 could lead to a net expansion of the adipose tissue capillary network, required for adipose tissue growth, in response to PPARγ activators.

NOR-1 is involved in VEGF-induced endothelial cell growth

2006 ◽  
Vol 184 (2) ◽  
pp. 276-282 ◽  
Author(s):  
Jordi Rius ◽  
José Martínez-González ◽  
Javier Crespo ◽  
Lina Badimon
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Endothelial Cell Growth

Endothelial Cell Growth and Protein Adsorption on Terminally Functionalized, Self-Assembled Monolayers of Alkanethiolates on Gold

Langmuir ◽  
1997 ◽  
Vol 13 (13) ◽  
pp. 3404-3413 ◽  
Author(s):  
Caren D. Tidwell ◽  
Sylvie I. Ertel ◽  
Buddy D. Ratner ◽  
Barbara J. Tarasevich ◽  
Sundar Atre ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Protein Adsorption ◽  
Self Assembled Monolayers ◽  
Assembled Monolayers ◽  
Endothelial Cell Growth ◽  
Self Assembled

Dose-dependent endothelial cell growth and stiffening by aldosterone: endothelial protection by eplerenone

2007 ◽  
Vol 25 (3) ◽  
pp. 639-647 ◽  
Author(s):  
Uta Hillebrand ◽  
Hermann Schillers ◽  
Christoph Riethmüller ◽  
Christian Stock ◽  
Marianne Wilhelmi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Endothelial Cell Growth ◽  
Dose Dependent

Abstract 3640: Mitochondrial Uncoupling Protein 2 Facilitates Endothelial Cell Growth and Angiogenesis via Reduction of Mitochondrial Superoxide

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yukio Shimasaki ◽  
Kai Chen ◽  
John F Keaney
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Mitochondrial Function ◽  
Endothelial Cell Proliferation ◽  
Wild Type ◽  
Sprouting Angiogenesis ◽  
Mitochondrial Superoxide ◽  
Endothelial Cell Growth ◽  
Aortic Explants

Background: Growing evidence suggests that mitochondrial function contributes to cell phenotype. One important component of mitochondrial function is the membrane potential that is controlled, in part, by uncoupling proteins (UCPs). Based on our previous data, the UCP2 is predominantly expressed in cultured endothelial cells. Therefore, we sought to examine the role of UCP2 in endothelial cell growth and angiogenesis. Methods and Results: Murine lung endothelial cells (MLECs) were isolated from UCP2-null and wild-type mice. UCP2-null cells were found less proliferative than wild-type cells (P<0.02, UCP2-null cells vs. wild-type cells, n=4). This defect of UCP2-null cells was rescued by UCP2 adenovirus transfection (19% increase, p<0.02 vs. LacZ adenovirus treated cells, n=3), and also rescued by transfection with manganese superoxide dismutase (MnSOD) adenovirus (53% increase, P<0.002 vs. LacZ adenovirus treated cells, n=3). We found a reciprocal relation such as no UCP2 expression and higher mitochondrial superoxide level in the MLECs (P<0.005, UCP2-null cells vs. wild-type cells, n=3), suggesting that mitochondrial superoxide may regulate endothelial cell growth. Then, we prepared murine aortic rings from UCP2-null and wild-type mice and embedded in rat tail collagen gel. The sprouting angiogenesis of UCP2-null explants was significantly less than wild-type explants (P<0.02, UCP2-null explants vs. wild-type explants, n=3– 4). Furthermore, MLECs from MnSOD-heterozygous mice showed less proliferation with lower expression of UCP2 protein and higher mitochondrial superoxide level compared to the MLECs from wild-type littermates (P<0.02, MnSOD-heterozygous cells vs. wild-type cells, n=4 – 8). We also observed less sprouting angiogenesis in MnSOD-heterozygous aortic explants than wild-type aortic explants (P<0.05, MnSOD-heterozygous explants vs. wild-type explants, n=3– 6). Conclusions: These data indicate that mitochondrial superoxide controls endothelial cell proliferation and angiogenesis, suggesting that mitochondrial metabolism modulates the endothelial cell growth and angiogenesis.

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