Contraction of Hydrated Collagen Gels by Fibroblasts: Evidence for Two Mechanisms by which Collagen Fibrils are Stabilized

Guidry, Clyde; Grinnell, Frederick

doi:10.1016/s0174-173x(87)80050-x

Cited by 142 publications

(79 citation statements)

References 13 publications

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“…Cells were removed by treating the matrices with 0.5% sodium deoxycholate as described (49). Precontracted matrices were collected by centrifugation onto coverslips at 22°C for 2 h at 693 ϫ g in a GLC-2B centrifuge (Sorvall, Newton, CT) using a modified HL-4 rotor (49).…”

Section: Methodsmentioning

confidence: 99%

Microtubule function in fibroblast spreading is modulated according to the tension state of cell–matrix interactions

Rhee

Jiang

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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144

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Mechanical and physical features of the extracellular environment dramatically impact cell shape. Fibroblasts interacting with 3D relaxed collagen matrices appear much different from cells on 2D collagen-coated surfaces and form dendritic cell extensions that contain microtubule cores and actin-rich tips. We found that interfering with cellular microtubules caused cells in relaxed matrices to remain round and unable to form dendritic extensions, whereas fibroblasts on coverslips formed lamellipodial extensions and were spread completely without microtubules but were unable to become polarized. Fibroblasts in relaxed collagen matrices lack stress fibers, focal adhesions, and focal adhesion signaling. Fibroblasts on collagen-coated coverslips that were unable to develop stress fibers and focal adhesions, because of either adding blebbistatin to the cells or use of soft coverslips, also formed microtubule-dependent dendritic extensions. Conversely, fibroblasts interacting with precontracted collagen matrices developed stress fibers and lamellipodial extensions and required microtubules for polarization but not spreading. Our findings demonstrate an unexpected relationship between the role of microtubules in cell spreading and the tension state of cell-matrix interactions. At a low tension state (absence of stress fibers and focal adhesions) typical of fibroblasts in relaxed collagen matrices, cells spread with dendritic extensions whose formation requires microtubules; at a high tension state (stress fibers and focal adhesions) typical of cells on coverslips, cells spread with lamellipodial extensions and microtubules are required for cell polarization but not for spreading.adhesion ͉ cell plasticity ͉ cytoskeleton ͉ extracellular matrix ͉ mechanosignaling M echanistic explanations for the functions of hierarchical systems such as tissue cells require an understanding of cell shape and cell composition (1). Since the early days of cell culture, it has been clear that mechanical and physical features of the extracellular environment have a dramatic impact on cell shape. More than 80 years ago, Lewis and Lewis (2) observed mesenchymal cells on glass coverslips and reported that the cells were highly flattened with ''tension striae'' or stress fibers. Around the same time, Weiss (3) cultured mesenchymal cells in blood plasma clots and showed that cell shape varied from stellate to bipolar depending on the orientation of the fibrous network of the clot.Subsequent work has confirmed differences in the shape of cells interacting with 2D rigid surfaces (glass or plastic) vs. 3D flexible matrices (e.g., collagen or fibrin) (4-6). Ironically, most research concerning regulation of cell shape has been carried out with 2D rigid surfaces although stress fibers can rarely be seen in fibroblasts in tissues except under conditions of wound repair and fibrosis (7,8). On the other hand, the diversity of fibroblast shapes observed by Weiss (3) resembles the plasticity of cells in tissues (9-11).Recently, it has become clear that dif...

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Section: Methodsmentioning

confidence: 99%

Microtubule function in fibroblast spreading is modulated according to the tension state of cell–matrix interactions

Rhee

Jiang

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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145

144

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“…Tractional forces generated by cells play critical roles in both embryogenesis (5,6) and wound healing (7,8). Fibroblasts grown on type I collagen gels extensively modify the collagen gels (7)(8)(9)(10)(11)(12)(13)(14)(15). This contraction of collagen gels composed of reconstituted collagen fibrils by fibroblasts in vitro is used by many Manuscript received August 16, 1991; revised manuscript received August 5, 1992; accepted August 10, 1992.…”

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confidence: 99%

Contraction of collagen gels by intestinal epithelial cells depends on microfilament function

Olson

1993

Digest Dis Sci

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“…The second approach to modulate intracellular tension was through addition of cytochalasin D. This inhibits fibroblast contractile properties by disrupting the actin microfilament network, [31][32][33] which clearly occurred within 30 min in our setup. Cells were thoroughly washed to ensure that cytochalasin D would not be transferred with the conditioned medium to the tibiotarsi in the organ cultures.…”

Section: Discussionmentioning

confidence: 99%

Intracellular tension in periosteum/perichondrium cells regulates long bone growth

Foolen

Donkelaar

Ito

2010

Journal Orthopaedic Research

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Perichondrium/periosteum is involved in regulating long bone growth. Long bones grow faster after removal or circumferential division of periosteum. This can be countered by culturing them in conditioned medium from perichondrium/periosteum cells. Because both complete removal and circumferential division are effective, we hypothesized that perichondrium/periosteum cells require an intact environment to release the appropriate soluble factors. More specifically, we propose that this release depends on their ability to generate intracellular tension. This hypothesis was explored by modulating the ability of perichondrium/periosteum cells to generate intracellular tension and monitoring the effect thereof on long bone growth. Perichondrium/periosteum cells were cultured on substrates with different stiffness. The medium produced by these cultures was added to embryonic chick tibiotarsi from which perichondrium/periosteum was either stripped or left intact. After 3 culture days, long bone growth was proportionally related to the stiffness of the substrate on which perichondrium/periosteum cells were grown while they produced conditioned medium. A second set of experiments demonstrated that the effect occurred through expression of a growth-inhibiting factor, rather than through the reduction of a stimulatory factor. Finally, evidence for the importance of intracellular tension was obtained by showing that the inhibitory effect was abolished when perichondrium/periosteum cells were treated with cytochalasin D, which disrupts the actin microfilaments. Thus, we concluded that modulation of long bone growth occurs through release of soluble inhibitors by perichondrium/periosteum cells, and that the ability of cells to develop intracellular tension through their actin microfilaments is at the base of this mechano-regulated control pathway.

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Contraction of Hydrated Collagen Gels by Fibroblasts: Evidence for Two Mechanisms by which Collagen Fibrils are Stabilized

Cited by 142 publications

References 13 publications

Microtubule function in fibroblast spreading is modulated according to the tension state of cell–matrix interactions

Microtubule function in fibroblast spreading is modulated according to the tension state of cell–matrix interactions

Contraction of collagen gels by intestinal epithelial cells depends on microfilament function

Intracellular tension in periosteum/perichondrium cells regulates long bone growth

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