A three dimensional environment containing epithelial cells and cell/matrix interactions is necessary for intestinal macrophage differentiation

2001 ◽  
Vol 120 (5) ◽  
pp. A190
Author(s):  
Tanja N. Spoetti ◽  
Martin Hausmann ◽  
Hans Herfarth ◽  
Marina Kreutz ◽  
Werner Falk ◽  
...  
Author(s):  
Jonas F. Eichinger ◽  
Maximilian J. Grill ◽  
Iman Davoodi Kermani ◽  
Roland C. Aydin ◽  
Wolfgang A. Wall ◽  
...  

AbstractLiving soft tissues appear to promote the development and maintenance of a preferred mechanical state within a defined tolerance around a so-called set point. This phenomenon is often referred to as mechanical homeostasis. In contradiction to the prominent role of mechanical homeostasis in various (patho)physiological processes, its underlying micromechanical mechanisms acting on the level of individual cells and fibers remain poorly understood, especially how these mechanisms on the microscale lead to what we macroscopically call mechanical homeostasis. Here, we present a novel computational framework based on the finite element method that is constructed bottom up, that is, it models key mechanobiological mechanisms such as actin cytoskeleton contraction and molecular clutch behavior of individual cells interacting with a reconstructed three-dimensional extracellular fiber matrix. The framework reproduces many experimental observations regarding mechanical homeostasis on short time scales (hours), in which the deposition and degradation of extracellular matrix can largely be neglected. This model can serve as a systematic tool for future in silico studies of the origin of the numerous still unexplained experimental observations about mechanical homeostasis.


2019 ◽  
Vol 25 (3) ◽  
pp. 753-761 ◽  
Author(s):  
Warren Colomb ◽  
Matthew Osmond ◽  
Charles Durfee ◽  
Melissa D. Krebs ◽  
Susanta K. Sarkar

AbstractThe absence of quantitative in vitro cell–extracellular matrix models represents an important bottleneck for basic research and human health. Randomness of cellular distributions provides an opportunity for the development of a quantitative in vitro model. However, quantification of the randomness of random cell distributions is still lacking. In this paper, we have imaged cellular distributions in an alginate matrix using a multiview light sheet microscope and developed quantification metrics of randomness by modeling it as a Poisson process, a process that has constant probability of occurring in space or time. We imaged fluorescently labeled human mesenchymal stem cells embedded in an alginate matrix of thickness greater than 5 mm with $\sim\! {\rm 2}{\rm. 9} \pm {\rm 0}{\rm. 4}\,\mu {\rm m}$ axial resolution, the mean full width at half maximum of the axial intensity profiles of fluorescent particles. Simulated randomness agrees well with the experiments. Quantification of distributions and validation by simulations will enable quantitative study of cell–matrix interactions in tissue models.


PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17833 ◽  
Author(s):  
Christian Franck ◽  
Stacey A. Maskarinec ◽  
David A. Tirrell ◽  
Guruswami Ravichandran

2005 ◽  
Vol 16 (11) ◽  
pp. 5070-5076 ◽  
Author(s):  
Hongmei Jiang ◽  
Frederick Grinnell

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.


2014 ◽  
Vol 35 (8) ◽  
pp. 1671-1679 ◽  
Author(s):  
D. Herrmann ◽  
J. R. W. Conway ◽  
C. Vennin ◽  
A. Magenau ◽  
W. E. Hughes ◽  
...  

2002 ◽  
Vol 13 (11) ◽  
pp. 3915-3929 ◽  
Author(s):  
Elisa Tamariz ◽  
Frederick Grinnell

When fibroblasts are placed within a three-dimensional collagen matrix, cell locomotion results in translocation of the flexible collagen fibrils of the matrix, a remodeling process that has been implicated in matrix morphogenesis during development and wound repair. In the current experiments, we studied formation and maturation of cell–matrix interactions under conditions in which we could distinguish local from global matrix remodeling. Local remodeling was measured by the movement of collagen-embedded beads towards the cells. Global remodeling was measured by matrix contraction. Our observations show that no direct relationship occurs between protrusion and retraction of cell extensions and collagen matrix remodeling. As fibroblasts globally remodel the collagen matrix, however, their overall morphology changes from dendritic to stellate/bipolar, and cell–matrix interactions mature from punctate to focal adhesion organization. The less well organized sites of cell–matrix interaction are sufficient for translocating collagen fibrils, and focal adhesions only form after a high degree of global remodeling occurs in the presence of growth factors. Rho kinase activity is required for maturation of fibroblast morphology and formation of focal adhesions but not for translocation of collagen fibrils.


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