Generation of Cell-Derived Three Dimensional Extracellular Matrix Substrates from Two Dimensional Endothelial Cell Cultures

2011 ◽  
Vol 17 (5) ◽  
pp. 589-595 ◽  
Author(s):  
Christopher M. Zwolinski ◽  
Karen S. Ellison ◽  
Natacha DePaola ◽  
Deanna M. Thompson
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cell ◽  
Cell Cultures ◽  
Three Dimensional ◽  
Two Dimensional ◽  
Endothelial Cell Cultures

scholarly journals Metabolic response of blood vessels to TNFα

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Abidemi Junaid ◽  
Johannes Schoeman ◽  
Wei Yang ◽  
Wendy Stam ◽  
Alireza Mashaghi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Inflammatory Responses ◽  
Metabolic Response ◽  
Three Dimensional ◽  
Two Dimensional ◽  
Bioactive Lipids ◽  
Liquid Chromatography Tandem Mass ◽  
Endothelial Cell Cultures

TNFα signaling in the vascular endothelium elicits multiple inflammatory responses that drive vascular destabilization and leakage. Bioactive lipids are main drivers of these processes. In vitro mechanistic studies of bioactive lipids have been largely based on two-dimensional endothelial cell cultures that, due to lack of laminar flow and the growth of the cells on non-compliant stiff substrates, often display a pro-inflammatory phenotype. This complicates the assessment of inflammatory processes. Three-dimensional microvessels-on-a-chip models provide a unique opportunity to generate endothelial microvessels in a more physiological environment. Using an optimized targeted liquid chromatography–tandem mass spectrometry measurements of a panel of pro- and anti-inflammatory bioactive lipids, we measure the profile changes upon administration of TNFα. We demonstrate that bioactive lipid profiles can be readily detected from three-dimensional microvessels-on-a-chip and display a more dynamic, less inflammatory response to TNFα, that resembles more the human situation, compared to classical two-dimensional endothelial cell cultures.

Comparative Effects of Aβ(1-42)-Al Complex from Rat and Human Amyloid on Rat Endothelial Cell Cultures

2007 ◽  
Vol 11 (1) ◽  
pp. 33-44 ◽  
Author(s):  
Denise Drago ◽  
Marcella Folin ◽  
Silvia Baiguera ◽  
Giuseppe Tognon ◽  
Fernanda Ricchelli ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Endothelial Cell Cultures

Endothelial cell cultures derived from isolated cerenrbal microvessels

1980 ◽  
Vol 191 (2) ◽  
pp. 577-582 ◽  
Author(s):  
M. Spatz ◽  
J. Bembry ◽  
R.F. Dodson ◽  
H. Hervonen ◽  
M.R. Murray
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Endothelial Cell Cultures

scholarly journals Matrix metalloproteinase-1 and -9 activation by plasmin regulates a novel endothelial cell-mediated mechanism of collagen gel contraction and capillary tube regression in three-dimensional collagen matrices

2001 ◽  
Vol 114 (5) ◽  
pp. 917-930 ◽  
Author(s):  
G.E. Davis ◽  
K.A. Pintar ◽  
Allen, R. Salazar ◽  
S.A. Maxwell
Keyword(s):  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Plasminogen Activators ◽  
Collagen Matrices ◽  
Collagen Gel Contraction ◽  
Blocking Antibodies ◽  
Pai 1

Here, we describe a new function for plasmin and matrix metalloproteinases (MMPs), which is to regulate the regression of capillary tubes in three-dimensional extracellular matrix environments. Using a well-described capillary morphogenesis system in three-dimensional collagen matrices, a new model of capillary regression has been established by adding plasminogen to the culture medium. Plasminogen is converted to plasmin by endothelial cell plasminogen activators which then induces matrix metalloproteinase-dependent collagen gel contraction and capillary regression. Plasminogen addition results in activation of MMP-1 and MMP-9, which then results in collagen proteolysis followed by capillary regression. The endothelial cells undergo apoptosis following gel contraction as detected by flow cytometric analysis as well as by detectable caspase-3 cleavage and caspase-dependent cleavage of the actin cytoskeletal regulatory protein, gelsolin. In addition, directly correlating with the contraction response, tyrosine phosphorylation of p130cas, an adapter protein in the focal adhesion complex, is observed followed by disappearance of the protein. Proteinase inhibitors that block MMPs (TIMP-1 or TIMP-2), plasminogen activators (PAI-1) or plasmin (aprotinin) completely block the gel contraction and regression process. In addition, chemical inhibitors of MMPs that block capillary regression also block MMP-1 and MMP-9 activation suggesting that a key element in this regression response is the molecular control of MMP activation by endothelial cells. Blocking antibodies directed to MMP-1 or MMP-9 interfere with capillary regression while blocking antibodies directed to PAI-1 accelerate capillary regression suggesting that endogenous synthesis of PAI-1 negatively regulates this process. These data present a novel system to study a new mechanism that may regulate regression of capillary tubes, namely, plasmin and MMP-mediated degradation of extracellular matrix.

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