Bovine chondrocyte behaviour in three-dimensional type I collagen gel in terms of gel contraction, proliferation and gene expression

Biomaterials ◽  
2006 ◽  
Vol 27 (1) ◽  
pp. 79-90 ◽  
Author(s):  
Laurent Galois ◽  
Sandrine Hutasse ◽  
Delphine Cortial ◽  
Cécile F. Rousseau ◽  
Laurent Grossin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Type I Collagen ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Type I ◽  
Type I Collagen Gel

scholarly journals Differentiation of embryonic stem cells into fibroblast-like cells in three-dimensional type I collagen gel cultures

2010 ◽  
Vol 47 (2) ◽  
pp. 114-124 ◽  
Author(s):  
Shinsaku Togo ◽  
Tadashi Sato ◽  
Hisatoshi Sugiura ◽  
Xingqi Wang ◽  
Hesham Basma ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Type I Collagen ◽  
Three Dimensional ◽  
Embryonic Stem ◽  
Collagen Gel ◽  
Type I ◽  
Type I Collagen Gel

Apical beta 1 integrin in polarized MDCK cells mediates tubulocyst formation in response to type I collagen overlay

1996 ◽  
Vol 109 (7) ◽  
pp. 1875-1889 ◽  
Author(s):  
A. Zuk ◽  
K.S. Matlin
Keyword(s):  
Plasma Membranes ◽  
Type I Collagen ◽  
Mdck Cells ◽  
Basolateral Membrane ◽  
Collagen Gel ◽  
Type I ◽  
Membrane Markers ◽  
Polarized Epithelia ◽  
Beta 1 Integrin ◽  
Type I Collagen Gel

A number of epithelia form tubulocysts in vitro when overlaid with type I collagen gel. Because collagen receptors are generally believed to be expressed on the basolateral domain, the mechanism by which collagen elicits this morphogenetic response from the apical surface is unclear. To investigate the role of beta 1 integrins, the major receptor family for collagen, in this process, we overlaid polarized monolayers of MDCK II cells grown on permeable supports with type I collagen gel and correlated integrin polarity with the polarity of other apical and basolateral membrane markers during tubulocyst formation. Polarized monolayers of one clone of MDCK II cells, referred to as Heidelberg MDCK, initially respond to collagen overlay by stratifying; within 48 hours, lumena develop between the cell layers giving rise to tubulocysts. Tight junctions remain intact during tubulocyst formation because transepithelial electrical resistance does not significantly change. Major alterations are observed, however, in the expression and localization of apical and basolateral membrane markers. beta 1 integrins are necessary for tubulocyst morphogenesis because a function-blocking antibody administered to the apical pole of the cells completely inhibits the formation of these structures. To determine how apical-cell collagen interactions elicit tubulocyst formation, we examined whether beta 1 integrins are mobilized to apical plasma membranes in response to collagen overlay. We found that in the absence of collagen, polarized monolayers of Heidelberg MDCK cells endogenously express on apical plasma membranes a small pool of the beta 1 family, including alpha 2 beta 1 and alpha 3 beta 1. Collagen overlay does not mobilize additional beta 1 integrins to apical domains. If beta 1 integrins are not already apically expressed, as in the C6 MDCK cell line (Schoenenberger et al. (1994) J. Cell Biol. 107, 527–541), beta 1 integrins are not directed apically and tubulocysts do not develop in response to collagen. Thus, interaction of beta 1 integrin pre-existing on apical plasma membranes of polarized epithelia with type I collagen gel is the mechanism by which apical application of collagen elicits the formation of tubulocysts. Depolarized integrins on apical plasma membranes of polarized epithelia may be relevant to the pathogenesis of disease and injury.

A Continuous-Discrete Finite Element Model of Angiogenesis That Couples Vessel Growth With Matrix Deformation

2013 ◽  
Author(s):  
Lowell T. Edgar ◽  
Steve A. Maas ◽  
James E. Guilkey ◽  
Jeffrey A. Weiss
Keyword(s):  
Type I Collagen ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Element Model ◽  
Fibrillar Structure ◽  
Type I ◽  
Major Pathway ◽  
Vessel Growth ◽  
Discrete Finite Element

Recent developments in tissue engineering have created demand for the ability to create microvascular networks with specific topologies in vitro. During angiogenesis, sprouting endothelial cells apply traction forces and migrate along components of the extracellular matrix (ECM), resulting in neovessel elongation [1]. The fibrillar structure of the ECM serves as the major pathway for mechanotransduction between contact-dependent cells. Using a three-dimensional (3D) organ culture model of microvessel fragments within a type-I collagen gel, we have shown that subjecting the culture to different boundary conditions during angiogenesis can lead to drastically different vascular topologies [2]. Fragments cultured in a rectangular gel that were free to contract grew into a randomly oriented network [3, 4]. When the long-axis of the gel was constrained as to prevent contraction, microvessels and collagen fibers were found aligned along the constrained axis (Fig. 1) [4].

The Physicochemical Property of Shark Type I Collagen Gel and Membrane

2000 ◽  
Vol 48 (6) ◽  
pp. 2028-2032 ◽  
Author(s):  
Yoshihiro Nomura ◽  
Shinzi Toki ◽  
Yasuhiro Ishii ◽  
Kunio Shirai
Keyword(s):  
Physicochemical Property ◽  
Type I Collagen ◽  
Collagen Gel ◽  
Type I ◽  
Type I Collagen Gel

scholarly journals Thrombospondin gene expression by endothelial cells in culture is modulated by cell proliferation, cell shape and the substratum

1990 ◽  
Vol 268 (1) ◽  
pp. 225-230 ◽  
Author(s):  
A E Canfield ◽  
R P Boot-Handford ◽  
A M Schor
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Shape ◽  
Type I Collagen ◽  
Three Dimensional ◽  
Type I ◽  
Mrna Levels ◽  
Collagen Gels ◽  
Cells Cultured

Endothelial cells plated on the surface of a two-dimensional substratum (gelatin-coated dishes, dishes coated with native type I collagen or collagen gels) form a cobblestone monolayer at confluence, whereas cells plated within a three-dimensional gel matrix elongate into a sprouting morphology and self-associate into tube-like structures. In this study, we have compared the synthesis of thrombospondin by quiescent endothelial cells displaying (a) the same morphological phenotype (cobblestone) on different substrata (gelatin and collagen) and (b) different morphological phenotypes (cobblestone and sprouting) on the same substratum (collagen). We demonstrate that thrombospondin is a major biosynthetic product of confluent, quiescent cells cultured on dishes coated with either gelatin or collagen, and that the synthesis of this protein is markedly decreased when cells are plated on or in three-dimensional collagen gels. Moreover, we demonstrate that cells plated in gel (sprouting) secrete less thrombospondin than do cells plated on the gel surface (cobblestone). The regulation of thrombospondin synthesis is reversible and occurs at the level of transcription, as steady-state mRNA levels for thrombospondin decrease in a manner comparable with the levels of protein secreted by these cells. We also show that mRNA levels for laminin B2 chains are increased when cells are cultured on and in collagen gels compared with on gelatin-coated dishes, suggesting that the syntheses of thrombospondin and laminin are regulated by different mechanisms. When cells are cultured on gelatin- or collagen-coated dishes, thrombospondin gene expression is directly proportional to the proliferative state of the cultures. By contrast, the synthesis of thrombospondin by cells cultured on collagen gels remains at equally low levels whether they are labelled when they are sparse and rapidly proliferating or when they are confluent and quiescent. Fibronectin synthesis was found to increase with increasing confluency of the cells plated on all three substrata. These results demonstrate that thrombospondin gene expression is modulated by cell shape, cell proliferation and the nature of the substratum used for cell culture.

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