scholarly journals A New Candidate Substrate for Cell-Matrix Adhesion Study: The Acellular Human Amniotic Matrix

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Qianchen Guo ◽  
Xuya Lu ◽  
Yuan Xue ◽  
Hong Zheng ◽  
Xiaotao Zhao ◽  
...  

In vivoadhesions between cells and the extracellular matrix play a crucial role in cell differentiation, proliferation, and migration as well as tissue remodeling. Natural three-dimensional (3D) matrices, such as self-assembling matrices and Matrigel, have limitations in terms of their biomechanical properties. Here, we present a simple method to produce an acellular human amniotic matrix (AHAM) with preserved biomechanical properties and a favorable adhesion potential. On the stromal side of the AHAM, human foreskin fibroblasts (HFFs) attached and extended with bipolar spindle-shaped morphology proliferated to multilayer networks, invaded into the AHAM, and migrated in a straight line. Moreover,αV integrin, paxillin, and fibronectin were observed to colocalize after 24 h of HFF culture on the stromal side of the AHAM. Our results indicate that the AHAM may be an ideal candidate as a cell-matrix adhesion substrate to study cell adhesion and invasion as well as other functionsin vitrounder a tensile force that mimics thein vivoenvironment.

2018 ◽  
Author(s):  
Fernanda Bajanca ◽  
Nadège Gouignard ◽  
Charlotte Colle ◽  
Maddy Parsons ◽  
Roberto Mayor ◽  
...  

AbstractWhen migratingin vivo, cells are exposed to numerous, and somewhat conflicting, signals: chemokines, repellents, extracellular matrix, growth factors. The roles of several of these molecules have been studied individuallyin vitroorin vivobut we have yet to understand how cells integrate them. To start addressing this question, we used the cephalic neural crest as a model system and looked at the roles of its best examples of positive and negative signals: stromal-cell derived factor 1 (Sdf1/Cxcl12) and class3-Semaphorins. Our results indicate that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac1 activity at the single cell level. Directional migration at the population level emerges as a result of global Semaphorin-dependent confinement and broad activation of adhesion by Sdf1 in the context of a biased Fibronectin distribution. These results indicate that unevenin vivotopology renders the need for precise distribution of secreted signals mostly dispensable.


2013 ◽  
Vol 63 (6) ◽  
pp. 561-569 ◽  
Author(s):  
Takuya Magome ◽  
Tsuyoshi Hattori ◽  
Manabu Taniguchi ◽  
Toshiko Ishikawa ◽  
Shingo Miyata ◽  
...  

2021 ◽  
Author(s):  
Yelena Y. Bernadskaya ◽  
Haicen Yue ◽  
Calina Copos ◽  
Lionel Christiaen ◽  
Alex Mogilner

AbstractPhysiological and pathological morphogenetic events involve a wide array of collective movements, suggesting that these multicellular arrangements confer biochemical and biomechanical properties that contribute to tissue scale organization. The cardiopharyngeal progenitors of the tunicate Ciona provide the simplest possible model of collective cell migration. They form cohesive bilateral cell pairs, leader-trailer polarized along the migration path as they migrate between the ventral epidermis and trunk endoderm. Here, circumventing difficulties in quantifying cellular mechanics in live embryos, we use the Cellular Potts Model to computationally probe the distributions of forces consistent with the shapes and collective polarity of migrating cell pairs. Combining computational modeling, confocal microscopy, and molecular perturbations, we first determine that cardiopharyngeal progenitors display hallmarks of supracellular organization, with differential distributions of protrusive forces, cell-matrix adhesion, and myosin-based retraction forces along the leader-trailer axis. Combined 4D simulations and experimental observations suggest that cell-cell communication helps establish a hierarchy that contributes to aligning collective polarity with the direction of migration, as observed with three or more cells both in silico and in vivo. Our approach reveals emerging properties of the migrating collective. Specifically, cell pairs are more persistent, thus migrating over longer distances, and presumably with higher accuracy. Finally, simulations suggest that polarized cell pairs literally join forces to deform the trunk endoderm, as they migrate through the extracellular space. We thus propose that the polarized supracellular organization of cardiopharyngeal progenitors confers emergent physical properties that determine mechanical interactions with their environment during morphogenesis.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Fernanda Bajanca ◽  
Nadège Gouignard ◽  
Charlotte Colle ◽  
Maddy Parsons ◽  
Roberto Mayor ◽  
...  

2005 ◽  
Vol 48 (21) ◽  
pp. 6750-6755 ◽  
Author(s):  
Thilo Bartolmäs ◽  
Tabea Heyn ◽  
Michael Mickeleit ◽  
Annette Fischer ◽  
Werner Reutter ◽  
...  

2003 ◽  
Vol 4 (9) ◽  
pp. 700-711 ◽  
Author(s):  
Melinda Larsen ◽  
Michel L. Tremblay ◽  
Kenneth M. Yamada

1993 ◽  
Vol 120 (4) ◽  
pp. 981-993 ◽  
Author(s):  
P Boukamp ◽  
N E Fusenig

Cells of the human keratinocyte line HaCaT were shifted to a mesenchymal/myogenic phenotype (DTHMZ cells) by MyoD1 transfection, 5-aza-2' deoxycytidine treatment, and selection for reduced adhesion on plastic. Since this correlated with loss of stratification (inability to form a multilayered tissue), we determined the status of cell-cell and cell-matrix adhesion molecules involved in epidermal morphogenesis. Expression of desmosomal proteins (plakoglobin, desmoglein, desmoplakin) and uvomorulin was no longer detectable at the mRNA and protein level in the DTHMZ cells while both HaCaT cells and malignant variants (transfected with c-Ha-ras oncogene) expressed uvomorulin in vitro and in transplants in vivo, the latter even in invasively growing tumor nodules. Furthermore, HaCaT cells stained positive for the integrin subunits beta 1, alpha 2, alpha 3, and alpha 5, typical for cultured keratinocytes. In contrast, the putative fibronectin receptor alpha 5 beta 1, common also in fibroblasts, was the only integrin showing strong staining in DTHMZ cells. The integrin subunits alpha v and a6, clearly expressed at the mRNA level, weakly stained HaCaT cultures and led to a dotlike fluorescence in DTHMZ cells, possibly representing focal adhesion plaques. The respective integrin status correlated well with the growth behavior on different matrices. While HaCaT cells readily attached and proliferated on collagen (type I), fibronectin-coated, and laminin-coated collagen gels, DTHMZ cells formed monolayers only on fibronectin-coated collagen. This was, however, not sufficient to allow stratification in vivo. Altogether, the status of adhesion molecules in DTHMZ cells more likely reflects that seen in mesenchymal cells as compared to the pattern of keratinocytes displayed by HaCaT cells. Moreover, since the DTHMZ cells were clearly HaCaT descendants, the results support our hypothesis of a "trans-differentiation" process from an epidermal (HaCaT) to a mesenchymal/myogenic phenotype (DTHMZ).


eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Yelena Y Bernadskaya ◽  
Haicen Yue ◽  
Calina Copos ◽  
Lionel Christiaen ◽  
Alex Mogilner

Physiological and pathological morphogenetic events involve a wide array of collective movements, suggesting that multicellular arrangements confer biochemical and biomechanical properties contributing to tissue scale organization. The Ciona cardiopharyngeal progenitors provide the simplest model of collective cell migration, with cohesive bilateral cell pairs polarized along the leader-trailer migration path while moving between the ventral epidermis and trunk endoderm. We use the Cellular Potts Model to computationally probe the distributions of forces consistent with shapes and collective polarity of migrating cell pairs. Combining computational modeling, confocal microscopy, and molecular perturbations, we identify cardiopharyngeal progenitors as the simplest cell collective maintaining supracellular polarity with differential distributions of protrusive forces, cell-matrix adhesion, and myosin-based retraction forces along the leader-trailer axis. 4D simulations and experimental observations suggest that cell-cell communication helps establish a hierarchy to align collective polarity with the direction of migration, as observed with three or more cells in silico and in vivo. Our approach reveals emerging properties of the migrating collective: cell pairs are more persistent, migrating longer distances, and presumably with higher accuracy. Simulations suggest that cell pairs can overcome mechanical resistance of the trunk endoderm more effectively when they are polarized collectively. We propose that polarized supracellular organization of cardiopharyngeal progenitors confers emergent physical properties that determine mechanical interactions with their environment during morphogenesis.


2020 ◽  
Vol 99 (8) ◽  
pp. 959-968 ◽  
Author(s):  
M. Liu ◽  
R. Banerjee ◽  
C. Rossa ◽  
N.J. D’Silva

Cell-cell adhesion is a key mechanism to control tissue integrity and migration. In head and neck squamous cell carcinoma (HNSCC), cell migration facilitates distant metastases and is correlated with poor prognosis. RAP1, a ras-like protein, has an important role in the progression of HNSCC. RAC1 is an integrin-linked, ras-like protein that promotes cell migration. Here we show that loss of cell-cell adhesion is correlated with inactivation of RAP1 confirmed by 2 different biochemical approaches. RAP1 activation is required for cell-matrix adhesion confirmed by adhesion to fibronectin-coated plates with cells that have biochemically activated RAP1. This effect is reversed when RAP1 is inactivated. In addition, RAP1GTP-mediated adhesion is only facilitated through α5β1 integrin complex and is not a function of either α5 or β1 integrin alone. Moreover, the inside-out signaling of RAP1 activation is coordinated with RAC1 activation. These findings show that RAP1 has a prominent role in cell-matrix adhesion via extracellular matrix molecule fibronectin-induced α5β1 integrin and supports a critical role for the RAP1/RAC1 signaling axis in HNSCC cell migration.


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