Dendritic cell immune potency on 2D and in 3D collagen matrices

2020 ◽  
Vol 8 (18) ◽  
pp. 5106-5120 ◽  
Author(s):  
Jiranuwat Sapudom ◽  
Aseel Alatoom ◽  
Walaa K. E. Mohamed ◽  
Anna Garcia-Sabaté ◽  
Ian McBain ◽  
...  
Keyword(s):  
Cell Culture ◽  
Dendritic Cell ◽  
Collagen Matrix ◽  
Collagen Matrices ◽  
Matrix Density ◽  
3D Collagen

Dendritic cell immune potency from two immunologically relevant perspectives is modulated by cell culture dimensionality and collagen matrix density.

scholarly journals Cell–Matrix Entanglement and Mechanical Anchorage of Fibroblasts in Three-dimensional Collagen Matrices

2005 ◽  
Vol 16 (11) ◽  
pp. 5070-5076 ◽  
Author(s):  
Hongmei Jiang ◽  
Frederick Grinnell
Keyword(s):  
Tight Binding ◽  
Three Dimensional ◽  
Collagen Matrix ◽  
Phagocytic Cells ◽  
Collagen Matrices ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
The Matrix ◽  
3D Collagen ◽  
Cell Matrix Interactions

Fibroblast-3D collagen matrix culture provides a physiologically relevant model to study cell–matrix interactions. In tissues, fibroblasts are phagocytic cells, and in culture, they have been shown to ingest both fibronectin and collagen-coated latex particles. Compared with cells on collagen-coated coverslips, phagocytosis of fibronectin-coated beads by fibroblasts in collagen matrices was found to be reduced. This decrease could not be explained by integrin reorganization, tight binding of fibronectin beads to the collagen matrix, or differences in overall bead binding to the cells. Rather, entanglement of cellular dendritic extensions with collagen fibrils seemed to interfere with the ability of the extensions to interact with the beads. Moreover, once these extensions became entangled in the matrix, cells developed an integrin-independent component of adhesion. We suggest that cell–matrix entanglement represents a novel mechanism of cell anchorage that uniquely depends on the three-dimensional character of the matrix.

scholarly journals Migration of Cytotoxic T Lymphocytes in 3D Collagen Matrices

2020 ◽  
Author(s):  
Z. Sadjadi ◽  
R. Zhao ◽  
M. Hoth ◽  
B. Qu ◽  
H. Rieger
Keyword(s):  
T Lymphocytes ◽  
Cytotoxic T Lymphocytes ◽  
Slow Motion ◽  
Collagen Matrix ◽  
Target Cells ◽  
Channel Network ◽  
Killer Cells ◽  
Collagen Matrices ◽  
Migration Patterns ◽  
3D Collagen

CD8+ cytotoxic T lymphocytes (CTL) and natural killer (NK) cells are the main cytotoxic killer cells of the human body to eliminate pathogen-infected or tumorigenic cells (= target cells). To find their targets they have to navigate and migrate through a complex biological microenvironments, a key component of which is the extracellular matrix (ECM). The mechanisms underlying killer cell’s navigation are not well understood. To mimic an ECM we use a matrix formed by different collagen concentrations, and analyze migration trajectories of primary human CTLs. Different migration patterns are observed and can be grouped into three motility types: slow, fast and mixed. The dynamics are well described by a two-state persistent random walk model which allows cells to switch between slow motion with low persistence, and fast motion with high persistence. We hypothesize that the slow motility mode describes CTLs creating channels through the collagen matrix by deforming and tearing apart collagen fibers, and that the fast motility mode describes CTLs moving within these channels. Experimental evidence supporting this scenario is presented by visualizing migrating T cells following each other on exactly the same track and showing cells moving quickly in channel-like cavities within the surrounding collagen matrix. Consequently, the efficiency of the stochastic search process of CTLs in the ECM should strongly be influenced by a dynamically changing channel network produced by the killer cells themselves.

Oriented Collagen Matrices: the Control of Biomineralizaton in Bone

1990 ◽  
Vol 218 ◽  
Author(s):  
Osamu Nakamura ◽  
David J. Fink ◽  
Arnold I. Caplan
Keyword(s):  
Cell Culture ◽  
Collagen Matrix ◽  
Collagen Matrices ◽  
Culture Systems ◽  
Osteogenic Cells ◽  
Cell Culture Systems ◽  
Mineralized Matrix

AbstractBone-forming cells fabricate a highly ordered collagen matrix (osteoid) which subsequently mineralizes. A variety of cell culture systems exist for osteogenic cells, yet none of these is optimal for the organized formation of a mineralized matrix. We have generated collagen substrates which have different degrees of fibrillar orientation, and have cultured osteogenic cells on these matrices. In this format, von Kossa-stained sections show that highly oriented collagen matrix starts to calcify in 6–7 days, while a random fibrillar matrix does not mineralize even after 21 days. Mineral has been detected only within the collagen matrix with a narrow, unmineralized region between the cells and the mineral.

scholarly journals Endothelial lumen signaling complexes control 3D matrix–specific tubulogenesis through interdependent Cdc42- and MT1-MMP–mediated events

Blood ◽  
2010 ◽  
Vol 115 (25) ◽  
pp. 5259-5269 ◽  
Author(s):  
Anastasia Sacharidou ◽  
Wonshill Koh ◽  
Amber N. Stratman ◽  
Anne M. Mayo ◽  
Kevin E. Fisher ◽  
...  
Keyword(s):  
Tube Formation ◽  
Dominant Negative ◽  
Collagen Matrices ◽  
Signaling Complex ◽  
Vascular Morphogenesis ◽  
Cytoplasmic Tails ◽  
3D Matrix ◽  
Dependent Signal ◽  
3D Collagen ◽  
Membrane Type

Abstract Here, we define an endothelial cell (EC) lumen signaling complex involving Cdc42, Par6b, Par3, junction adhesion molecule (Jam)–B and Jam-C, membrane type 1–matrix metalloproteinase (MT1-MMP), and integrin α2β1, which coassociate to control human EC tubulogenesis in 3D collagen matrices. Blockade of both Jam-B and Jam-C using antibodies, siRNA, or dominant-negative mutants completely interferes with lumen and tube formation resulting from a lack of Cdc42 activation, inhibition of Cdc42-GTP–dependent signal transduction, and blockade of MT1-MMP–dependent proteolysis. This process requires interdependent Cdc42 and MT1-MMP signaling, which involves Par3 binding to the Jam-B and Jam-C cytoplasmic tails, an interaction that is necessary to physically couple the components of the lumen signaling complex. MT1-MMP proteolytic activity is necessary for Cdc42 activation during EC tube formation in 3D collagen matrices but not on 2D collagen surfaces, whereas Cdc42 activation is necessary for MT1-MMP to create vascular guidance tunnels and tube networks in 3D matrices through proteolytic events. This work reveals a novel interdependent role for Cdc42-dependent signaling and MT1-MMP–dependent proteolysis, a process that occurs selectively in 3D collagen matrices and that requires EC lumen signaling complexes, to control human EC tubulogenesis during vascular morphogenesis.

scholarly journals Human platelet lysate improves human cord blood derived ECFC survival and vasculogenesis in three dimensional (3D) collagen matrices

2015 ◽  
Vol 101 ◽  
pp. 72-81 ◽  
Author(s):  
Hyojin Kim ◽  
Nutan Prasain ◽  
Sasidhar Vemula ◽  
Michael J. Ferkowicz ◽  
Momoko Yoshimoto ◽  
...  
Keyword(s):  
Cord Blood ◽  
Human Platelet ◽  
Three Dimensional ◽  
Platelet Lysate ◽  
Human Cord Blood ◽  
Collagen Matrices ◽  
Human Platelet Lysate ◽  
3D Collagen

Abstract P383: 3D-collagen Matrix Enhanced Integrins And Matrix Metalloproteinases Expression In Cardiac Mesenchymal Cells

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Senthilkumar Muthusamy ◽  
Asha V Nath ◽  
Shilpa Ajit ◽  
Anil K PR
Keyword(s):  
Matrix Metalloproteinases ◽  
Adhesion Molecules ◽  
Type I Collagen ◽  
Collagen Matrix ◽  
Mesenchymal Cells ◽  
Pcr Analysis ◽  
Type I ◽  
Culture Dish ◽  
Tissue Culture Dish ◽  
3D Collagen

Introduction: Use of cardiac mesenchymal cells (CMCs) has been shown to improve cardiac function following myocardial infarction. Main drawback in cardiac cell therapy is the major loss of injected cells within few hours. Increase the retention of these injected cells could increase their efficacy, where cardiac patches with various cell types showed better outcome. Among, collagen patch plays lead role as a cell-laden matrix in cardiac tissue engineering. Creating a detailed understanding of how collagen matrix changes the cellular phenotype could provide seminal insights to regeneration therapy. Hypothesis: Growing CMCs in three dimensional (3D) collagen matrix could alter the expression of extracellular matrix (ECM) and adhesion molecules, which may enhance their efficacy. Methods: The bovine type I collagen was chemically modified and solubilized in culture medium with photo-initiator. The mouse CMCs were isolated and resuspended in collagen solution, printed using 3D bioprinter and UV-crosslinked to form 3D-CMC construct. The 3D-CMC construct was submerged in growth medium and cultured for 48h and analyzed for the expression of ECM and adhesion molecules (n=5/group). CMCs cultured in regular plastic tissue culture dish was used as control. Results: RT profiler array showed changes in the ECM and adhesion molecules expression, specifically certain integrins and matrix metalloproteinases (MMPs) in CMCs cultured 3D collagen construct compared to 2D monolayer. Subsequent qRT-PCR analysis revealed significant (p<0.01) upregulation of integrins such as Itga2 (2.96±0.13), Itgb1 (3.18±0.2) and Itgb3 (2.4±0.27) and MMPs such as MMP13 (37.2±3.36), MMP9 (5.23±1.06) and MMP3 (7.14±2.07). Western blot analysis further confirmed significant elevation of these integrins and matrix metalloproteinases at protein level. Collagen encapsulation did not alter the expression of N-cadherin in CMCs, which is a potential mesenchymal cadherin adhesion molecule. Conclusion: Integrin αβ heterodimers transduce signals that facilitate cell homing, migration, survival and differentiation. Similarly, MMPs plays vital role in cell migration and proliferation. Our results demonstrate that the 3D-collagen Niche enhances the expression of certain integrins and MMPs in CMCs. This suggest that the efficacy of CMCs could be magnified by providing 3D architecture with collagen matrix and further in vivo experiments would reveal functional benefits from CMCs for clinical use.

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