scholarly journals A 3-D in vitro co-culture model of mammary gland involution

2014 ◽  
Vol 6 (6) ◽  
pp. 618-626 ◽  
Author(s):  
Jonathan J. Campbell ◽  
Laur-Alexandru Botos ◽  
Timothy J. Sargeant ◽  
Natalia Davidenko ◽  
Ruth E. Cameron ◽  
...  

An in vitro model of mammary gland supporting 3D cell–cell and cell–matrix interactions demonstrates complete in vivo-like neo-tissue formation and remodelling processes (involution) under hormonal control.

2002 ◽  
Vol 223 (4) ◽  
pp. 497-516 ◽  
Author(s):  
Janine M. Prince ◽  
Teresa C.M. Klinowska ◽  
Emma Marshman ◽  
Emma T. Lowe ◽  
Ulrike Mayer ◽  
...  

2020 ◽  
Author(s):  
Edi Meco ◽  
W. Sharon Zheng ◽  
Anahita H. Sharma ◽  
Kyle J. Lampe

AbstractDemyelinating injuries and diseases, like multiple sclerosis, affect millions of people worldwide. Oligodendrocyte precursor cells (OPCs) have the potential to repair demyelinated tissue because they can both self-renew and differentiate into oligodendrocytes (OLs), the myelin producing cells of the central nervous system (CNS). Cell-matrix interactions impact OPC differentiation into OLs, but the process is not fully understood. Biomaterial hydrogel systems help to elucidate cell-matrix interactions because they can mimic specific properties of native CNS tissue in an in vitro setting. We investigated whether OPC maturation into OLs is influenced by interacting with a urokinase plasminogen activator (uPA) degradable extracellular matrix (ECM). uPA is a proteolytic enzyme that is transiently upregulated in the developing rat brain, with peak uPA expression correlating with an increase in myelin production in vivo. OPC-like cells isolated through the Mosaic Analysis with Double Marker technique (MADM OPCs) produced low molecular weight uPA in culture. MADM OPCs were encapsulated into two otherwise similar elastin-like protein (ELP) hydrogel systems: one that was uPA degradable and one that was non-degradable. Encapsulated MADM OPCs had similar viability, proliferation, and metabolic activity in uPA degradable and non-degradable ELP hydrogels. Expression of OPC maturation-associated genes, however, indicated that uPA degradable ELP hydrogels promoted MADM OPC maturation although not sufficiently for these cells to differentiate into OLs.Graphical Abstract – For table of contents only


Oncogene ◽  
2003 ◽  
Vol 22 (24) ◽  
pp. 3680-3684 ◽  
Author(s):  
Vincenzo M Varallo ◽  
Bing Siang Gan ◽  
Shannon Seney ◽  
Douglas C Ross ◽  
James H Roth ◽  
...  

2017 ◽  
Vol 14 (127) ◽  
pp. 20160877 ◽  
Author(s):  
X. Cui ◽  
Y. Hartanto ◽  
H. Zhang

Three-dimensional multicellular spheroids (MCSs) have a complex architectural structure, dynamic cell–cell/cell–matrix interactions and bio-mimicking in vivo microenvironment. As a fundamental building block for tissue reconstruction, MCSs have emerged as a powerful tool to narrow down the gap between the in vitro and in vivo model. In this review paper, we discussed the structure and biology of MCSs and detailed fabricating methods. Among these methods, the approach in microfluidics with hydrogel support for MCS formation is promising because it allows essential cell–cell/cell–matrix interactions in a confined space.


1979 ◽  
Vol 38 (1) ◽  
pp. 267-281
Author(s):  
S.L. Schor ◽  
J. Court

The attachment of cells to collagen has been reported previously to require the presence of serum and the particular serum protein involved in this process, variously known as CIG, CAP or fibronectin, has been isolated. This conclusion that cell attachment to collagen requires serum (or more precisely, fibronectin) is based on experiments measuring the kinetics of cell attachment to films of collagen. We have measured the kinetics of attachment of HeLa and attachment to films of collagen-containing substrata under a variety of experimental conditions and present evidence that the serum-dependent mechanism of cell attachment described by others is actually only the case for films of denatured collagen, while cell attachment to native collagen fibres occurs by a different, serum-independent, mechanism. The possible relevance of these findings to cell-matrix interactions in vivo is discussed.


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.


2020 ◽  
Vol 85-86 ◽  
pp. 15-33 ◽  
Author(s):  
J.C. Ashworth ◽  
J.L. Thompson ◽  
J.R. James ◽  
C.E. Slater ◽  
S. Pijuan-Galitó ◽  
...  

2000 ◽  
Vol 20 (14) ◽  
pp. 5208-5215 ◽  
Author(s):  
X. Z. Huang ◽  
J. F. Wu ◽  
R. Ferrando ◽  
J. H. Lee ◽  
Y. L. Wang ◽  
...  

ABSTRACT Members of the integrin family of adhesion receptors mediate both cell-cell and cell-matrix interactions and have been shown to play vital roles in embryonic development, wound healing, metastasis, and other biological processes. The integrin α9β1 is a receptor for the extracellular matrix proteins osteopontin and tenacsin C and the cell surface immunoglobulin vascular cell adhesion molecule-1. This receptor is widely expressed in smooth muscle, hepatocytes, and some epithelia. To examine the in vivo function of α9β1, we have generated mice lacking expression of the α9 subunit. Mice homozygous for a null mutation in the α9 subunit gene appear normal at birth but develop respiratory failure and die between 6 and 12 days of age. The respiratory failure is caused by an accumulation of large volumes of pleural fluid which is rich in triglyceride, cholesterol, and lymphocytes. α9 −/− mice also develop edema and lymphocytic infiltration in the chest wall that appears to originate around lymphatics. α9 protein is transiently expressed in the developing thoracic duct at embryonic day 14, but expression is rapidly lost during later stages of development. Our results suggest that the α9 integrin is required for the normal development of the lymphatic system, including the thoracic duct, and that α9 deficiency could be one cause of congenital chylothorax.


2020 ◽  
Author(s):  
Austin G. Gouldin ◽  
Jennifer L. Puetzer

AbstractIn connective tissues there is a clear link between increasing age and degeneration. It is believed advanced glycation end-products (AGEs) play a central role in this degeneration. AGEs are sugar induced non-enzymatic crosslinks which accumulate in collagen with age and diabetes, altering tissue mechanics and cellular function. Despite ample correlative evidence linking collagen glycation to degeneration, little is known how AGEs impact cell-matrix interactions, limiting therapeutic options. One reason for this limited understanding is AGEs are typically induced in vitro using high concentrations of ribose which decrease cell viability and make it impossible to investigate cell-matrix interactions. The objective of this study was to develop a system to trigger AGE accumulation while maintaining cell viability. Using cell-seeded high density collagen gels, we investigated the effect of two different systems for AGE induction, ribose at low concentrations (30, 100, and 200 mM) over 15 days of culture and riboflavin (0.25 mM and 0.75mM) induced with blue light for 40 seconds. We found ribose and riboflavin with blue light are capable of producing a wide range of AGE crosslinks which match and/or exceed reported human AGE levels for various tissues, ages, and diseases, without affecting cell viability and metabolism. Interestingly, a single 40 second treatment of riboflavin and blue light produced similar levels of AGEs as 3 days of 100 mM ribose treatment and matched aged mouse tendon AGE levels. This riboflavin treatment option is an exciting means to trigger AGE crosslinks on demand in vivo or in vitro without impacting cell metabolism or viability and holds great promise for further unraveling the mechanism of AGEs in age and diabetes related tissue degeneration.


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