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PubMedDate not supplied

The effect of static in vivo bending on the murine intervertebral disc.

BACKGROUND CONTEXT: Intervertebral disc cell function in vitro has been linked to features of the local environment that can be related to deformation of the extracellular matrix. Epidemiologic data suggest that certain regimens of spinal loading accelerate disc degeneration in vivo. Yet, the direct association between disc cell function, spinal loading and ultimately tissue degeneration is poorly characterized. PURPOSE: To examine the relationships between tensile and compressive matrix strains, cell activity and annular degradation. STUDY DESIGN/SETTING: An in vivo study of the biologic, morphologic and biomechanical consequences of static bending applied to the murine intervertebral disc. SUBJECT SAMPLE: Twenty-five skeletally mature Swiss Webster mice (12-week-old males) were used in this study. OUTCOME MEASURES: Bending neutral zone, bending stiffness, yield point in bending, number of apoptotic cells, annular matrix organization, cell shape, aggrecan gene expression, and collagen II gene expression. METHODS: Mouse tail discs were loaded for 1 week in vivo with an external device that applied bending stresses. Mid-sagittal sections of the discs were analyzed for cell death, collagen II and aggrecan gene expression, and tissue organization. Biomechanical testing was also performed to measure the bending stiffness and strength. RESULTS: Forceful disc bending induced increased cell death, decreased aggrecan gene expression and decreased tissue organization preferentially on the concave side. By contrast, collagen II gene expression was symmetrically reduced. Asymmetric loading did not alter bending mechanical behavior of the discs. CONCLUSIONS: In this model, annular cell death was related to excessive matrix compression (as opposed to tension). Collagen II gene expression was most negatively influenced by the static nature of the loading (immobilization), rather than the specific state of stress (tension or compression).

Analysis of Variance↗
PubMed2000

Pressure-independent contribution of sodium to large artery structure and function in hypertension.

BACKGROUND: Sodium sensitivity is usually studied in terms of change of blood pressure (BP) but the specific effects on conduit arteries have not been addressed. EXPERIMENTAL STUDIES: In genetic models of hypertension, chronically increased sodium diet is associated with aortic hypertrophy and development of extracellular matrix independent of BP. These alterations, often associated with increased stiffness and secretory properties of vascular smooth muscle, are reversed by lowering sodium intake and/or giving diuretics, independently of BP changes. The arterial changes are chronically modulated by hormonal counterregulatory mechanisms since, when sodium intake is high, bradykinin blockade produces more carotid hypertrophy, and when sodium intake is normal, less aortic collagen accumulates because of AT(1)-receptor blockade. CLINICAL STUDIES: In longitudinal studies on hypertensive subjects, increased sodium intake not only increases BP but also decreases brachial artery diameter, implying pressure-independent mechanisms acting on the arterial wall. The antihypertensive effect of diuretics is associated with little change of arterial geometry and stiffness, probably resulting from marked angiotensin-induced increase of arterial stiffness. This latter effect is blocked by converting-enzyme inhibition. All these arterial changes may be genetically modulated since in salt-sensitive hypertensives, increased sodium intake is associated with decreased arterial distensibility, and in some hypertensive subjects, a polymorphism of the AT(1)-receptor gene has been described in association with increased aortic stiffness and is reversed by converting-enzyme inhibition independent of BP. CONCLUSION: In genetic models of human and rat hypertension, increased sodium intake is associated with specific alterations of the structure and function of conduit arteries involving extracellular matrix, but independent of BP and atherosclerosis.

Aged↗
PubMed2003

Stability of bipedal stance: the contribution of cocontraction and spindle feedback.

The aim of this study is to assess the contribution of cocontraction and spindle feedback to local stability during bipedal stance. To that aim, an existing nonlinear state space model of the human musculoskeletal system is linearized in a reference equilibrium state. The maximal real part of the eigenvalues of the linearized system matrix A and the low-frequency joint stiffness are used as a measure of local stability. Muscle properties, as represented in a Hill-type muscle model, are shown to improve the behavior, the improvement being larger at high cocontraction. However, even at maximal cocontraction the low-frequency joint stiffness generated by the muscle properties is insufficient to yield a locally stable system. It follows that feedback is necessary to ensure local stability. In this study, the potential contribution of spindle feedback is investigated by optimizing the feedback gains for contractile element length and velocity for each muscle. It is found that in the case of time-delayed negative feedback, it is impossible to stabilize the system on the basis of spindle feedback. When positive time-delayed feedback is allowed, a barely stable system is obtained. When the time delays are removed, the feedback gains can be chosen such that a locally stable system is obtained, indicating the limitations imposed by the presence of time delays. Finally, it is shown that for small perturbations the response of the linear system to an arbitrary perturbation is similar to that of the nonlinear system, indicating the validity of the approach used. It is concluded that the combination of muscle properties and time-delayed spindle feedback is insufficient to obtain a system with reasonable local stability.

Feedback↗
PubMed1988

Nodulous corpuscles and mitochondrial inclusions in Sertoli cells of deer hybrids.

Unusual transformations of endoplasmic reticulum and mitochondria were identified in the Sertoli cells of deer hybrids. A portion of the mitochondrial population was converted from the common, flexible mitochondrial form into stiff rods, with an increased volume of the matrix and relative paucity of cristae. The matrix displayed arrays of tubuloid elements or percursors at various stages of assembly. The second and more conspicuous adaptation concerned the agranular endoplasmic reticulum, which frequently transformed into oval or elongate, often interconnected bodies. These bodies consisted of a dozen or more concentrically arranged fenestrated cisternae and a variable amount of glycogen in between. An integral and distinctive feature of the cisternous bodies was nodes, together constituting the so-called nodulous corpuscles (NC). The nodes appeared as a dense meshwork or lattice, which has the potential to generate a new set of cisternae and NC that interconnect into a chain or tridimensional complex. The course of NC evolution from precursors to mature complexes is proposed. Both organelle adaptations occurred independently and in only Sertoli cells. They are believed to be a product of hybridization in deer.

Animals↗
PubMed2001

Polymer composites in 2000: structure, performance, cost and compromise.

Polymer matrix composites are based on the combination of stiff, strong reinforcing fibres with either thermosetting or thermoplastic polymer matrices. Since their introduction in the early 1940s, the world market has increased to some 5 million tonnes per annum, and some composites may now be considered commodity materials. The spectrum of fibre-reinforced plastics ranges from very high-performance speciality materials costing more than $1000/kg to these commodity composites, with more modest properties, at less than $10/kg. The performance of composites is determined by the properties of the fibre, the fraction of fibre in the composite and the structure, or fibre architecture. Processing technologies have been developed which maximise fibre content and precisely control the fibre architecture allowing for the manufacture of components with mechanical properties tailored to service requirements. Many composites offer significant advantages in specific stiffness and/or specific strength over metals. This makes them attractive for applications where high mechanical performance and minimum weight are important. However, the wider acceptance of composites is based on their ability to offer a more cost-effective alternative. In particular, composites also allow a dramatic reduction in the parts count in many applications, which leads to significant manufacturing advantages and greater economy.

Journal Article↗
PubMed2001

Effects of loading frequency on mechanically induced bone formation.

The anabolic effect of mechanical loading on bone tissue is modulated by loading frequency. The objective of this study was to characterize the new bone formation on the periosteal and endocortical surfaces of the ulnar diaphysis in adult, female rats in response to controlled dynamic loading and to examine the interactions between strain magnitude, loading frequency, and bone formation rate (BFR/BS) for frequencies ranging from 1 to 10 Hz. Cyclic, compressive loading was applied to the ulnas of 60 adult, female rats divided into 12 loading groups. Loading was applied for 360 cycles/day with peak loads ranging from 4.3 to 18N at frequencies of 1, 5, and 10 Hz. After 2 weeks of loading, bone formation on the periosteal and endocortical surfaces of the ulna was quantified using double-label histomorphometry on transverse sections obtained at the middiaphysis. Periosteal bone formation increased in a dose-response manner with peak load at each of the three loading frequencies tested. Loading frequency significantly affected the x intercepts and slopes of the peak strain versus BFR/BS (p < 0.001) and peak strain versus mineralizing surface (MS/BS; p < 0.001) curves. Periosteal osteogenesis was best predicted by a mathematical model that assumed: (1) bone cells are activated by fluid shear stresses and (2) that stiffness of the bone cells and the extracellular matrix near the cells increases at higher loading frequencies because of viscoelasticity. Consequently, mechanotransduction appears to involve a complex interaction between extracellular fluid forces and cellular mechanics.

Animals↗
PubMed1993

The role of ions and mineral-organic interfacial bonding on the compressive properties of cortical bone.

Bone tissue is a composite material composed of an inorganic stiff mineral phase embedded in a compliant organic matrix. Similar to other composites, the mechanical properties of bone depend upon the properties, volume fraction, and orientation of its constituents as well as the bonding interactions. Interfacial bonding between the mineral and organic constituents are based, in part, on electrostatic interactions between negatively charged organic domains and positively charged mineral surface. Phosphate and fluoride ions can alter mineral-organic interfacial causing a permutation in the mechanical properties. Partial debonding between the mineral and organic constituents of bone may play an important role in the mechanical properties of aged and diseased bone. The present study examines the effects of phosphate and fluoride ion treatment on the compression properties of cortical bone and the reversibility of the effect.

Animals↗
PubMed2005

Synergistic effect of angiotensin II and nitric oxide synthase inhibitor in increasing aortic stiffness in mice.

Although they are implicated on their own as risk factors for cardiovascular disease, the potential link between nitric oxide (NO) deficiency, ANG II, and vascular stiffening has not been tested before. We evaluated the role of chronic ANG II treatment and NO deficiency, alone and in combination, on aortic stiffness in mice and tested parameters contributing to increases in active or passive components of vascular stiffness, including blood pressure, vascular smooth muscle contractility, and extracellular matrix components. Untreated (control) mice and mice treated with a NO synthase (NOS) inhibitor [N(omega)-nitro-L-arginine methyl ester (L-NAME), 0.5 g/l] were implanted with osmotic minipumps delivering ANG II (500 ng.kg(-1).min(-1)) for 28 days. Aortic stiffness was then measured in vivo by pulse wave velocity (PWV) and ex vivo by load-strain analysis to obtain values of maximal passive stiffness (MPS). Blood pressure and aortic contractility ex vivo were measured. ANG II treatment or NOS inhibition with L-NAME did not independently increase vascular stiffness; however, the combined treatments worked synergistically to increase PWV and MPS. The combined treatments of ANG II + L-NAME also significantly increased aortic wall collagen content while decreasing elastin. These novel results suggest that NO deficiency and ANG II act synergistically to increase aortic stiffness in mice predominantly via changes in aortic wall collagen/elastin ratio.

Angiotensin II↗
PubMed2000

Cell mechanics studied by a reconstituted model tissue.

Tissue models reconstituted from cells and extracellular matrix (ECM) simulate natural tissues. Cytoskeletal and matrix proteins govern the force exerted by a tissue and its stiffness. Cells regulate cytoskeletal structure and remodel ECM to produce mechanical changes during tissue development and wound healing. Characterization and control of mechanical properties of reconstituted tissues are essential for tissue engineering applications. We have quantitatively characterized mechanical properties of connective tissue models, fibroblast-populated matrices (FPMs), via uniaxial stretch measurements. FPMs resemble natural tissues in their exponential dependence of stress on strain and linear dependence of stiffness on force at a given strain. Activating cellular contractile forces by calf serum and disrupting F-actin by cytochalasin D yield "active" and "passive" components, which respectively emphasize cellular and matrix mechanical contributions. The strain-dependent stress and elastic modulus of the active component were independent of cell density above a threshold density. The same quantities for the passive component increased with cell number due to compression and reorganization of the matrix by the cells.

Animals↗
PubMed2003

Cell organization in soft media due to active mechanosensing.

Adhering cells actively probe the mechanical properties of their environment and use the resulting information to position and orient themselves. We show that a large body of experimental observations can be consistently explained from one unifying principle, namely that cells strengthen contacts and cytoskeleton in the direction of large effective stiffness. Using linear elasticity theory to model the extracellular environment, we calculate optimal cell organization for several situations of interest and find excellent agreement with experiments for fibroblasts, both on elastic substrates and in collagen gels: cells orient in the direction of external tensile strain; they orient parallel and normal to free and clamped surfaces, respectively; and they interact elastically to form strings. Our method can be applied for rational design of tissue equivalents. Moreover, our results indicate that the concept of contact guidance has to be reevaluated. We also suggest that cell-matrix contacts are up-regulated by large effective stiffness in the environment because, in this way, build-up of force is more efficient.

Cell Adhesion↗
PubMed2000

Effects of antihypertensive therapy on hypertensive vascular disease.

Hypertension is associated with alterations in the structure, function, and mechanical properties of large and small arteries. Changes in the endothelium, smooth muscle cell, extracellular matrix, and possibly the adventitia, contribute to complications of hypertension. In large arteries, vascular hypertrophy is found, often with increased stiffness of media components. In small arteries, particularly in mild hypertension, rearrangement of smooth muscle cells around a smaller lumen without changes in media volume (eutrophic remodeling) occurs; in more severe hypertension, hypertrophic remodeling with increased vascular stiffness can be found. Vascular remodeling is accompanied by an increase in the extracellular matrix, particularly collagen deposition. Recent studies have demonstrated that vascular remodeling and endothelial dysfunction of small and large vessels may be normalized by treatment with some antihypertensive agents (angiotensin converting enzyme inhibitors, angiotensin AT(1) receptor antagonists, and long-acting calcium channel blockers). Angiotensin converting enzyme inhibitors have now been shown to improve outcomes in hypertensive patients, an effect that may in part be related to the vascular protective effects reviewed here.

Angiotensin I↗
PubMed2000

The deformation behavior and viscoelastic properties of chondrocytes in articular cartilage.

Chondrocytes in articular cartilage utilize mechanical signals in conjunction with other environmental factors to regulate their metabolic activity. However, the sequence of biomechanical and biochemical events involved in the process of mechanical signal transduction has not been fully deciphered. A fundamental step in determining the role of various factors in regulating chondrocyte activity is to characterize accurately the biophysical environment within the tissue under physiological conditions of mechanical loading. Microscopic imaging studies have revealed that chondrocytes as well as their nuclei undergo shape and volume changes in a coordinated manner with deformation of the tissue matrix. Through micromechanical experiments, it has been shown that the chondrocyte behaves as a viscoelastic solid material with a mechanical stiffness that is several orders of magnitude lower than that of the cartilage extracellular matrix. These properties seem to be due to the structure of the chondrocyte cytoskeleton, and in part, the viscoelastic properties of the cell nucleus. The mechanical properties of the pericellular matrix that immediately surrounds the chondrocyte significantly differ from those of the chondrocyte and the extracellular matrix, suggesting that the pericellular matrix plays an important role in defining the mechanical environment of the chondrocyte. These experimentally measured values for chondrocyte and cartilage mechanical properties have been used in combination with theoretical constitutive modeling of the chondrocyte within articular cartilage to predict the non-uniform and time-varying stress-strain and fluid flow environment of the cell. The ultimate goal of these studies has been to elucidate the sequence of biomechanical and biochemical events through which mechanical stress influences chondrocyte activity in both health and in disease.

Animals↗
PubMed1987

Bone structure and function.

Bone is a complex, living, constantly changing tissue. The architecture and composition of cancellous and cortical bone allow the skeleton to perform its essential mechanical functions. The stiffer cortical bone responds more slowly to changes in loads while cancellous bone has a much larger surface area per unit volume and a greater rate of metabolic activity. Periosteum covers the external surface of bone and consists of two layers: an outer fibrous layer and an inner more cellular and vascular layer. The inner osteogenic layer or cambium layer can form new bone while the outer layer forms part of the insertions of tendons, ligaments and muscles. The cortical bone of diaphyses and metaphyses has a dual blood supply that allows loss of one source of circulation without adversely affecting the viability of the tissue. Many epiphyses, even in adults, depend only on a single source of blood supply, the penetrating epiphyseal vessels. For this reason epiphyseal bone may infarct more easily than metaphyseal or diaphyseal bone. The bone matrix has an organic component, primarily type I collagen, which gives it tensile strength and an inorganic component, primarily hydroxyapatite, which gives it stiffness to compression. Specialized populations of bone cells form, maintain and remodel this matrix. We recognize four types of bone cells based on their locations, morphology and functions: osteoprogenitor cells, osteoblasts, osteocytes and osteoclasts. Osteoblasts develop from undifferentiated cells while osteocytes form from osteoblasts. Osteoclasts have a separate stem cell line, blood-borne monocytes. Bone matrix apparently attracts these monocytes and stimulates their differentiation into osteoclasts. The processes of bone modeling and remodeling require osteoclastic resorption of bone matrix and deposition of a new matrix by osteoblasts. Modeling shapes and reshapes bones during growth and stops at skeletal maturity. Physiologic remodeling does not change bone shape and consists of bone resorption followed by bone deposition in approximately the same location. Since it continues throughout life it appears to be important for maintenance of the skeleton, but its exact function remains obscure. Adaptive remodeling is the response of the bone to altered loads and may alter the strength, density and shape of bone. In recent years understanding of the control of bone cell function has increased significantly. The study of electrical effects on bone formation has lead to new treatments of nonunions and delayed unions. Physicians have applied understanding of matrix-induced bone formation to reconstruction of skeletal defects.(ABSTRACT TRUNCATED AT 400 WORDS)

Bone Development↗
PubMed1998

Use of a collagen-hydroxyapatite matrix in spinal fusion. A rabbit model.

STUDY DESIGN: The efficacy of a specially designed mineralized bovine collagen matrix as a carrier for bone marrow stem cells was studied in a rabbit posterolateral spinal fusion model. OBJECTIVES: To determine if bone marrow cells added to Healos matrix will lead to fusion rates, biomechanical properties, and histologic properties comparable with those of fusions using autologous iliac crest bone graft; and to determine if the addition of preservative-free heparin to anticoagulate the bone marrow during harvest will adversely affect the fusion rate. SUMMARY OF BACKGROUND DATA: Although the development of new preparations of osteoinductive agents has advanced rapidly in recent years, the carrier systems that have been used in their application have received less attention. The composition and structure of the matrix used are key components affecting the ability of the matrix to function as a scaffold on which cells can migrate, adhere, proliferate, and form bone. The composition and design of matrix components also determine the ability of osteoinductive agents to influence local and hematogenously derived osteogenic precursor cells, which migrate to or are brought into the fusion site. Thus, the properties of the carrier can affect the behavior and efficacy of the osteoinductive agent that is used. The authors studied the properties of a new mineralized collagen matrix called Healos, which has been engineered specifically for spinal fusion application. METHODS: Forty-four adult female New Zealand white rabbits were divided into five groups. Groups 1-4 underwent bilateral intertransverse fusion between L5 and L6. The fusions were augmented with either autologous iliac crest bone graft, Healos matrix alone, Healos matrix mixed with autologous bone marrow, or Healos matrix combined with heparinized autologous bone marrow. At 8 weeks after surgery, the fusions were characterized radiographically, histologically, and biomechanically. The rate of fusion was determined by radiographic analysis. The fifth group consisted of two animals whose bone marrow was aspirated from their tibias and femurs and then sent for determination of total nucleated cell count. RESULTS: At 8 weeks, the radiographically determined fusion rate for autologous bone graft was 75% (9/12 animals), compared with 100% (10/10 and 9/9 animals) for groups in which fusions were done by using Healos matrix augmented with bone marrow (P < or = 0.1). Matrix used alone yielded a fusion rate of 18% (2/11 animals, P < or = 0.006). Histologically, the most mature bone was seen in the group augmented with autologous iliac crest graft, followed in decreasing order by the groups augmented with Healos with heparinized bone marrow, Healos with unheparinized bone marrow, and Healos alone. Biomechanically, the group augmented with autologous graft had the highest mean stiffness, followed by the groups augmented with Healos with heparinized bone marrow, Healos with untreated bone marrow, and finally Healos matrix alone. However, the differences in stiffness between groups were not statistically significant with the number of spines tested. CONCLUSIONS: These results show that Healos is an osteoconductive matrix that can be a useful carrier in the biologic and mechanical environment of a posterolateral intertransverse fusion site. In combination with bone marrow, it produces fusion rates that are comparable with those of autologous bone graft. However, it must be combined with an osteoinductive or osteogenic agent to ensure reliable fusion rates and alone cannot produce reliable osteogenesis. The Healos matrix was not compared with other commercially available matrices currently in use. Therefore, the efficacy of Healos relative to these other materials could not be determined.

Animals↗
PubMed2003

Physiological genomics of human arteries: quantitative relationship between gene expression and arterial stiffness.

BACKGROUND: Previous genomic studies with human tissues have compared differential gene expression between 2 conditions (ie, normal versus diseased) to identify altered gene expression in a binary manner; however, a potentially more informative approach is to correlate the levels of gene expression with quantitative physiological parameters. METHODS AND RESULTS: In this study, we have used this approach to examine genes whose expression correlates with arterial stiffness in human aortic specimens. Our data identify 2 distinct groups of genes, those associated with cell signaling and those associated with the mechanical regulation of vascular structure (cytoskeletal-cell membrane-extracellular matrix). Although previous studies have concentrated on the contribution of the latter group toward arterial stiffness, our data suggest that changes in expression of signaling molecules play an equally important role. Alterations in the profiles of signaling molecules could be involved in the regulation of cell cytoskeletal organization, cell-matrix interactions, or the contractile state of the cell. CONCLUSIONS: Although the influence of smooth muscle contraction/relaxation on arterial stiffness could be controversial, our provocative data would suggest that further studies on this subject are indicated.

Aged↗
PubMed1994

Activation of the non-actomyosin component of aortic wall contraction by phorbol ester.

The mechanisms of smooth muscle tissue contractile system functioning are in many respects unexplained. According to the existing hypothesis, the mechanism of smooth muscle contraction is based on the interaction between myosin and actin. The change of muscle tissue stiffness during the contractive process is the important and obligatory feature of this actomyosin interaction. Earlier we have shown that, together with the smooth muscle cells, the connective tissue matrix can also produce the active mechanical strength. This process is not accompanied by changes of stiffness. We suggested that in some cases the induced contraction of smooth muscles is fulfilled, entirely or in part, by the connective tissue matrix. We report here that contractive reaction induced by the phorbol ester--activator of protein kinase C, which is one of the most important enzymes involved in the regulation of the smooth muscle contraction--occurs without any stiffness changes. The results obtained can not be explained in terms of the generally accepted hypothesis of actomyosin interaction. The conclusion is made that phorbol ester during the action on the smooth muscle tissue activates the mechanical strength generation by the connective tissue matrix.

Actomyosin↗
PubMed2004

Brittle IV mouse model for osteogenesis imperfecta IV demonstrates postpubertal adaptations to improve whole bone strength.

UNLABELLED: The Brtl mouse model for type IV osteogenesis imperfecta improves its whole bone strength and stiffness between 2 and 6 months of age. This adaptation is accomplished without a corresponding improvement in geometric resistance to bending, suggesting an improvement in matrix material properties. INTRODUCTION: The Brittle IV (Brtl) mouse was developed as a knock-in model for osteogenesis imperfecta (OI) type IV. A Gly349Cys substitution was introduced into one col1a1 allele, resulting in a phenotype representative of the disease. In this study, we investigate the effect of the Brtl mutation on whole bone architecture, strength, and composition across a range of age groups. MATERIALS AND METHODS: One-, 2-, 6-, and 12-month-old Brtl and wildtype (WT) mice were analyzed. Femurs were assessed at the central diaphysis for cortical geometric parameters using microCT and were subsequently mechanically tested to failure by four-point bending. Matrix material properties were predicted using microCT data to normalize data from mechanical tests. Raman spectroscopy and DXA were used to assess matrix composition. RESULTS: Our findings show a postpubertal adaptation in which Brtl femoral strength and stiffness increase through a mechanism independent of changes in whole bone geometry. These findings suggest an improvement in the material properties of the bone matrix itself, rather than improvements in whole bone geometry, as seen in previous mouse models of OI. Raman spectroscopic results suggest these findings may be caused by changes in mineral/matrix balance rather than improvements in mineral crystallinity. CONCLUSIONS: Our findings parallel the currently unexplained clinical observation of decreased fractures in human OI patients after puberty. The Brtl mouse remains an important tool for investigating therapeutic interventions for OI.

Adaptation, Physiological↗
PubMed1997

An in vitro force measurement assay to study the early mechanical interaction between corneal fibroblasts and collagen matrix.

An in vitro force measurement assay has been developed to quantify the forces exerted by single corneal fibroblasts during the early interaction with a collagen matrix. Corneal fibroblasts were sparsely seeded on top of collagen matrices whose stiffness was predetermined by micromanipulation with calibrated fine glass microneedles. The forces exerted by individual cells were calculated from time-lapse videomicroscopic recordings of the 2-D elastic distortion of the matrix. In additional experiments, the degree of permanent reorganization of the collagen matrices was assessed by lysing the cells with 1% Triton X-100 solution at the end of a 2-hour incubation and recording the subsequent relaxation. The data suggest that a cell can exert comparable centripetal force during either extension of a cell process or partial retraction of an extended pseudopodia. The rates of force associated with pseudopodial extension and partial retraction were 0.180 +/- 0.091 (x 10(-8)) N/min (n = 8 experiments) and 0.213 +/- 0.063 (x 10(-8)) N/min (n = 8 experiments), respectively. Rupture of pseudopodial adhesion associated with cell locomotion causes a release of force on the matrix and a complete recoil of the pseudopodia concerned; a simultaneous release of force on the matrix was also observed at the opposite end of the cell. Lysis of cells resulted in 84 +/- 18% relaxation of the matrix, suggesting that little permanent remodeling of matrix is produced by the actions of isolated migrating cells.

Animals↗