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PubMed2000

Quantifying the adherence of fibroblasts to titanium and its enhancement by substrate-attached material.

Normal human skin fibroblasts were cultured on tissue culture polystyrene and on commercially pure titanium. In addition, substrate-attached material that remained on the surfaces after detachment of fibroblasts with a chelating agent was examined. The force required to detach 50% of the fibroblasts from each substrate was assessed by centrifugation. The results showed a time-dependent decrease in the force required to detach fibroblasts from titanium not seen on tissue culture polystyrene. Nearly all cells detached from the titanium surfaces at 7.85 x 10(x3) dynes/cell after 3 or 5 days in culture, whereas few cells detached from tissue culture polystyrene. Cells freshly seeded onto titanium substrates that had been coated with substrate-attached material by prior culture of fibroblasts for 3 or 5 days showed an approximately sixfold increased adherence. The results of immunofluorescence staining for fibronectin and its receptor suggest that the nature of the interaction between this extracellular matrix ligand and the substrate may be important in determining cellular stiffness at the cell-extracellular matrix interface.

Biocompatible Materials↗
PubMed1988

Running exercise as a modulatory of proteoglycan matrix in the articular cartilage of young rabbits.

Proteoglycans (PGs) and collagen were quantified in the knee articular cartilages of femoral and tibial medial condyles following 1-8 weeks of moderate running exercise of 4- to 6-month-old rabbits. The total content of PGs extractable with 4 mol/l guanidium chloride was elevated in the weight-bearing cartilage of the tibial medial condyle, while their concentration, expressed as uronic acid per wet weight, and collagen remained unchanged. The content of glucosamine (GlcN) and its ratio to galactosamine (GalN) was elevated in femoral cartilage PGs purified by centrifugation in dissociative CsCl gradients, indicating an increase in keratan sulfate. After 8 weeks of running, the chondroitin sulfate chains of PGs from tibial medial condyle contained less unsulfated disaccharide units. The content of chondroitin sulfate was elevated in the nonextractable residue of the tibial medial condyle as indicated by uronic acid and GaN assays. The content of nonextractable GlcN was increased even more, both in tibial medial and femoral cartilages. Moderate running thus increased (1) keratan sulfate-rich PGs, (2) the degree of sulfation of the chondroitin sulfate chains, and (3) nonextractable PGs; these modulatory alterations probably enhance the stability and elastic stiffness of the PG matrix.

Animals↗
PubMed2005

The relationship of normal and abnormal microstructural proliferation to the mitral valve closure sound.

BACKGROUND: Many diseases that affect the mitral valve are accompanied by the proliferation or degradation of tissue microstructure. The early acoustic detection of these changes may lead to the better management of mitral valve disease. In this study, we examine the nonstationary acoustic effects of perturbing material parameters that characterize mitral valve tissue in terms of its microstructural components. Specifically, we examine the influence of the volume fraction, stiffness and splay of collagen fibers as well as the stiffness of the nonlinear matrix in which they are embedded. METHODS AND RESULTS: To model the transient vibrations of the mitral valve apparatus bathed in a blood medium, we have constructed a dynamic nonlinear fluid-coupled finite element model of the valve leaflets and chordae tendinae. The material behavior for the leaflets is based on an experimentally derived structural constitutive equation. The gross movement and small-scale acoustic vibrations of the valvular structures result from the application of physiologic pressure loads. Material changes that preserved the anisotropy of the valve leaflets were found to preserve valvular function. By contrast, material changes that altered the anisotropy of the valve were found to profoundly alter valvular function. These changes were manifest in the acoustic signatures of the valve closure sounds. Abnormally, stiffened valves closed more slowly and were accompanied by lower peak frequencies. CONCLUSION: The relationship between stiffness and frequency, though never documented in a native mitral valve, has been an axiom of heart sounds research. We find that the relationship is more subtle and that increases in stiffness may lead to either increases or decreases in peak frequency depending on their relationship to valvular function.

Animals↗
PubMed2001

Coordinated regulation of procollagens I and III and their post-translational enzymes by dissipation of mechanical tension in human dermal fibroblasts.

Mechanical tension governs fibroblast proliferation and survival and the homeostasis of the extracellular matrix to adapt its resistance to the mechanical requirements of the organs. To consolidate this view, we analysed the effect of tension release on the expression of molecules involved in the architecture and stabilisation of the collagen fibres, namely the procollagens type I and III, the amino- and carboxy-procollagen peptidases (N-pCP and C-pCP) and lysyl oxidase. Cells were cultured in conditions of high mechanical stress in monolayer on a collagen coat and under reduced tension by disruption of the cytoskeleton upon treatment with cytochalasin D in monolayer on a collagen coat or by integrin-mediated stress relaxation in a freely retracting collagen gel. The mRNAs were measured by quantitative RT-PCR monitored by simultaneous reverse-transcription and amplification of an original internal standard. Tension relaxation resulted in a decreased expression of the procollagens type I and III, of the two expressed forms of C-pCP, of the two forms of N-pCP and of lysyl oxidase. Type III collagen, known to control diameter of the fibres, was less down-regulated than type I collagen. Interestingly, the expression of the two alternatively spliced forms of the N-pCP was dissimilarly regulated. These data suggest that mechanical tension may modulate the stiffness of the extracellular matrix by controlling not only the level of expression of its fibrillar constituents but also that of the enzymes participating in their extracellular processing and mechanical stabilisation.

Adolescent↗
PubMed2002

Extracellular matrix- and cytoskeleton-dependent changes in cell shape and stiffness.

Cell spreading is correlated with changes in important cell functions including DNA synthesis, motility, and differentiation. Spreading is accompanied by a complex reorganization of the cytoskeleton that can be related to changes in cell stiffness. While cytoskeletal organization and the resulting cell stiffness have been studied in motile cells such as fibroblasts, less is known of these events in nonmigratory, epithelial cells. Hence, we examined the relationship between cell function, spreading, and stiffness, as measured by atomic force microscopy. Cell stiffness increased with spreading on a high density of fibronectin (1000 ng/cm(2)) but remained low in cells that stayed rounded on a low fibronectin density (1 ng/cm(2)). Disrupting actin or myosin had the same effect of inhibiting spreading, but had different effects on stiffness. Disrupting f-actin assembly lowered both stiffness and spreading, while inhibiting myosin light chain kinase inhibited spreading but increased cell stiffness. However, disrupting either actin or myosin inhibited DNA synthesis. These results demonstrate the relationship between cell stiffness and spreading in hepatocytes. They specifically show that normal actin and myosin function is required for hepatocyte spreading and DNA synthesis and demonstrate opposing effects on cell stiffness upon disruption of actin and myosin.

Actins↗
PubMed2004

Rigidity and spontaneous curvature of lipidic monolayers in the presence of trehalose: a measurement in the DOPE inverted hexagonal phase.

Trehalose is a sugar which plays an important protectant role in organisms against damage due to dehydration. To explore the basic molecular mechanism which governs the protective function exerted on lipid membranes, X-ray diffraction and osmotic stress experiments have been performed on L: -alpha-dioleoyl-phosphatidyl-ethanolamine (DOPE) in trehalose solutions of different concentrations. In pure water, DOPE forms an inverted hexagonal (H(II)) phase; in sugar solutions, a strong dehydration, which induces a large reduction of the H(II) lattice parameter, has been detected, but nevertheless no phase transitions occur. Structural data, directly obtained from reconstructed electron density maps, show that the bending of the lipid monolayer induced by the sugar is coupled to changes in the DOPE molecular shape. By osmotic stress, the work required to dehydrate the monolayer has been obtained and the overall free energy described as a function of trehalose concentration. Three results should be stressed: (1) dehydration experiments performed in the presence of sugar demonstrate that the protective effect cannot be purely osmotic; (2) the pivotal surface, that location on the molecule whose area is invariant upon isothermal bending, has been analyzed by two different methods: the approach by Rand and co-workers and the approach by Templer and co-workers; in both cases its presence along the DOPE molecule has been revealed and its position estimated; (3) the spontaneous radius of curvature and the rigidity constant of the lipid monolayer, measured at the pivotal plane, changes from 3.06 nm (in pure water) to 2.82 nm (in 1.4 M trehalose), and from 0.55 x 10(-19) to 0.74 x 10(-19) J, respectively. We assume that these modifications are related to direct interactions between trehalose and DOPE that alter the interface geometry, reducing the repulsion between the polar heads. However, the increased bending rigidity also accounts for the changes of the property of the aqueous compartment, reflecting the rigidity and stiffness of the sugar matrix around and inside the lipid phase.

Lipid Bilayers↗
PubMed2002

Aging, articular cartilage chondrocyte senescence and osteoarthritis.

The incidence of osteoarthritis (OA), the disease characterized by joint pain and loss of joint form and function due to articular cartilage degeneration, is directly correlated with age. The strong association between age and increasing incidence of osteoarthritis (OA) marks OA as an age related disease. Yet, like many other age related diseases, OA is not an inevitable consequence of aging; instead, aging increases the risk of OA. Articular cartilage aging changes that may lead to articular cartilage degeneration include fraying and softening of the articular surface, decreased size and aggregation of proteoglycan aggrecans and loss of matrix tensile strength and stiffness. These changes most likely are the result of an age related decrease in the ability of chondrocytes to maintain and repair the tissue manifested by decreased mitotic and synthetic activity, decreased responsiveness to anabolic growth factors and synthesis of smaller less uniform aggrecans and less functional link proteins. Our recent work suggests that progressive chondrocyte senescence marked by expression of the senescence associated enzyme beta-galactosidase, erosion of chondrocyte telomere length and mitochondrial degeneration due to oxidative damage causes the age related loss of chondrocyte function. New efforts to prevent the development and progression of OA might include strategies that slow the progression of chondrocyte senescence or replace senescent cells.

Aging↗
PubMed2004

Biomechanical responses of normal and delipidized articular cartilage subjected to varying rates of loading.

In alignment with the proposition that a lipid layer overlays the superficial zone of the articular cartilage, this study presents the consequence of the removal of lipids on the load-bearing characteristics of the tissue. Both normal unmodified and delipidized cartilage matrices were loaded at four different strain-rates of 1.3 x 10(-4)/s, 1.3 x 10(-3)/s, 1.3 x 10(-2)/s, and 1.3 x 10(-1)/s to strains of no more than 40%, to compare their stress-strain and stiffness-strain-rate characteristics. Our results demonstrate that at the lowest strain-rate of 1.3 x 10(-4)/s, the stiffness of the delipidized matrix was lower in comparison to that of the normal unmodified tissue. This response was reversed at higher strain-rates of 1.3 x 10(-2)/s and above. We conclude, therefore, that in general, at physiological rates of loading, the depletion of lipids from the articular cartilage reduces its compliance by at least 25%. We infer from the present study that this degenerative stiffening is an important contributing factor in impairing the tissue's load processing function in osteoarthritic joints.

Animals↗
PubMed2005

Comparative effects of dehydroepiandrosterone sulfate on ventricular diastolic function with young and aged female mice.

The adrenal steroid hormone dehydroepiandrosterone (DHEA) and its sulfated derivative [DHEA(S)] have been extensively studied for their potential anti-aging effects. Associated with aging, DHEA levels decline in humans, whereas other adrenal hormones remain unchanged, suggesting that DHEA may be important in the aging process. However, the effect of DHEA(S) supplementation on cardiac function in the aged has not been investigated. Therefore, we administered to young and old female mice a 60-day treatment with exogenous DHEA(S) at a dose of 0.1 mg/ml in the drinking water and compared the effects on left ventricular diastolic function and the myocardial extracellular matrix composition. The left ventricular stiffness (beta) was 0.30 +/- 0.06 mmHg/mul in the older control mice compared with 0.17 +/- 0.02 mmHg/mul in young control mice. Treatment with DHEA(S) decreased left ventricular stiffness to 0.12 +/- 0.03 mmHg/mul in the older mice and increased left ventricular stiffness to 0.27 +/- 0.04 mmHg/mul in young mice. The mechanism for the DHEA(S)-induced changes in diastolic function appeared to be associated with altered matrix metalloproteinase activity and the percentage of collagen cross-linking. We conclude that exogenous DHEA(S) supplementation is capable of reversing the left ventricular stiffness and fibrosis that accompanies aging, with a paradoxical increased ventricular stiffness in young mice.

Aging↗
PubMed1999

Micromechanics of the equine hoof wall: optimizing crack control and material stiffness through modulation of the properties of keratin.

Small-scale components of the equine hoof wall were tested to determine their mechanical roles in the morphological hierarchy. Macroscale tensile tests conducted on samples of the inner wall tubules and intertubular material showed a sixfold difference in mean initial stiffnesses (0.47 and 0.08 GPa, respectively), indicating that the inner wall tubules stiffen the wall along its longitudinal axis. The similarity in material properties of tubule and intertubular samples from the mid-wall suggests that tubules in this region offer only minor reinforcement along the longitudinal axis. Microscale tests conducted on rows of keratin strands from the inner wall tubules and intertubular material, and on intertubular keratin strands of the mid-wall, produced estimates of the stiffnesses of the hydrated matrix (0.03 GPa) and intermediate filament (IF; 3-4 GPa) components of the nanoscale ( &agr; -keratin) composite. The results from these tests also suggest that the properties of the keratin composite vary through the wall thickness. Birefringence measurements on inner wall and mid-wall regions agree with these observations and suggest that, although the keratin IF volume fraction is locally constant, the volume fraction changes through the thickness of the wall. These findings imply that modulation of the hoof wall properties has been achieved by varying the IF volume fraction, countering the effects of specific IF alignments which serve another function and would otherwise adversely affect the modulus of a particular region.

Animals↗
PubMed2003

Modeling of biomedical interfaces with nonlinear friction properties.

Proper isotropic and anisotropic friction constitutive equations are developed based on previous friction measurements at cancellous bone-porous coated implant interfaces exhibiting nonlinear load-displacement curves. The simulated friction response is dependent on relative tangential displacements in both orthogonal directions. The interface constitutive matrix contains cross-stiffness terms identical in isotropic friction but different in anisotropic friction. These terms are due mainly to nonlinearity in response and vanish in unidirectional friction along a principal direction and in cases with Coulomb or linear friction. The interface ultimate resistance is evaluated by an elliptic criterion which becomes circular in isotropic cases. These constitutive relations are implemented in a finite element program which is employed to analyze a bone cube sliding on top of a porous-surfaced metallic plate, an experimental model used in our earlier measurements. The results for both isotropic and anisotropic frictions demonstrate the coupling between two orthogonal directions. The direction of resultant displacement under a variable load coincides with that of the load only when the friction is isotropic with coupling terms considered. In anisotropic friction, the resultant displacement occurs in a direction different from that of loading. Our previous bi-directional measurements corroborate well the findings of this study.

Anisotropy↗
PubMed2004

Molecular design of the alpha-keratin composite: insights from a matrix-free model, hagfish slime threads.

We performed mechanical tests on a matrix-free keratin model-hagfish slime threads-to test the hypothesis that intermediate filaments (IFs) in hydrated hard alpha-keratins are maintained in a partly dehydrated state. This hypothesis predicts that dry IFs should possess mechanical properties similar to the properties of hydrated hard alpha-keratins, and should swell more than hard alpha-keratins in water. Mechanical and swelling measurements of hagfish threads were consistent with both of these predictions, suggesting that an elastomeric keratin matrix resists IF swelling and keeps IF stiffness and yield stress high. The elastomeric nature of the matrix is indirectly supported by the inability of matrix-free IFs (i.e. slime threads) to recover from post-yield deformation. We propose a general conceptual model of the structural mechanics of IF-based materials that predicts the effects of hydration and cross-linking on stiffness, yield stress and extensibility.

Animals↗
PubMed2003

Negative impact of DEP exposure on human airway epithelial cell adhesion, stiffness, and repair.

Epidemiological and experimental studies suggest that diesel exhaust particles (DEPs) may be associated with increased respiratory mortality and morbidity. Several recent studies have also shown that DEPs increase the production of inflammatory cytokines by human bronchial epithelium (HBE) cells in vitro. The present study investigates the effects of DEPs on the interaction of l-HBE cells (16HBE14o-) with the cell and matrix microenvironment based on evaluation of integrin-type cell/matrix ligand expression, cytoskeleton (CSK) stiffness, and matrix remodeling via matrix metalloproteinase (MMP)-1, MMP-2, and MMP-9 expression. The results showed that DEP exposure induced: 1) a net dose-dependent decrease in CSK stiffness through actin fibers, 2) a concomitant specific reduction of both alpha(3)- and beta(1)-integrin subunits extensively expressed on the HBE cell surface, 3) a decrease in the level of CD44, which is a major HBE cell-cell and HBE cell-matrix adhesion molecule; and 4) an isolated decrease in MMP-1 expression without any change in tissue inhibitor of matrix metalloproteinase (TIMP)-1 or TIMP-2 tissue inhibitors. Restrictive modulation of cell-matrix interaction, cell-cell connection, CSK stiffness, and fibrillary collagen remodeling results in a decreased wound closure capacity and an increased deadhesion capacity. In conclusion, on the basis of these results, we can propose that, in addition to their ability to increase the production of inflammatory cytokines, DEPs could also alter the links between actin CSK and the extracellular matrix, suggesting that they might facilitate HBE cell detachment in vivo.

Actins↗
PubMed2001

Glycation cross-links inhibit matrix metalloproteinase-2 activation in vascular smooth muscle cells cultured on collagen lattice.

AIMS/HYPOTHESIS: Extracellular matrix glycation has been proposed to contribute to the arterial stiffness observed in aging and diabetes. We examined whether matrix protein glycation regulates the proleolytic process through the manipulation of matrix metalloproteinases (MMPs) activation, using collagen fibrils model. METHODS: Vascular smooth muscle cells were cultured on control or glycated collagen fibrils. Matrix metalloproteinase-2 activation and the production of tissue inhibitors of metalloproteinase (TIMPs) were measured in the conditioned medium by using gelatin zymography and immunoblotting. Membrane type 1 matrix metalloproteinase (MT1-MMP) expression was also measured in cell lysates. RESULTS: When smooth muscle cells were cultured on collagen fibrils, pro-MMP-2 processing to active form was observed in the conditioned medium in coincidence with the increased MT1-MMP expression and the suppressed TIMP-2 production. Culturing smooth muscle cells on glycated collagen fibrils inhibited MMP-2 activation and attenuated MT1-MMP expression without the alteration of TIMP-2 production compared with control fibrils, indicating the possible mechanism of the suppression of MT1-MMP expression for the inhibition of MMP-2 activation on glycated collagen fibrils. Inclusion of aminoguanidine, an inhibitor of cross-linking formation, during collagen glycation restored the MMP-2 activation, suggesting the role of cross-links on the inhibition of MMP-2 activation. CONCLUSION/INTERPRETATION: These observations suggest that glycation-induced cross-linking formation in interstitial collagen contributes to arterial stiffness in aging and diabetes through the manipulation of matrix metalloproteinase activation along with the reduction of the susceptibility to proteolytic enzymes.

Cell Adhesion↗
PubMed1984

Fundamentals of fluid transport through cartilage in compression.

This paper describes the flow patterns and related viscoelastic behaviors of articular cartilage under four different loading configurations: 1) confined compression, 2) unconfined compression, 3) translating parabolic surface traction of constant loading span over a cartilage layer, and 4) spreading parabolic surface traction of periodically varying span on a cartilage layer. Brief summaries of formulations and solutions of these problems are given and discussed. For the first two cases, emphasis is given to the differences in the flow mechanisms giving rise to the observed compressive viscoelastic behavior of the tissue. These two fundamental solutions can provide a basis for interpreting the results of the deformation and flow patterns obtained from more complicated loading configurations. The last two cases simulate two main geometric features of joint articulations. Fluid efflux patterns at the articulating surface depend on the kinematics of loading as well as the intrinsic material properties of the tissue: the moduli and permeability of the solid matrix. The predominant mechanism controlling the viscoelastic behavior of the tissue in compression is determined by the relative magnitude of the fluid drag and the intrinsic stiffness of the organic solid matrix.

Biomechanical Phenomena↗
PubMed1992

Role of the extracellular matrix in age-related modifications of the rat aorta. Ultrastructural, morphometric, and enzymatic evaluations.

Connective tissues such as blood vessels are known to be greatly affected by age because of impaired functional properties and increased susceptibility to diseases. With the aim of providing further information on the role of the extracellular matrix in age-related modifications, we investigated the aorta in the rat model from birth to senescence by means of morphological and morphometric observations and by evaluation of lysyl oxidase activity. Results focused on the dramatic vascular rearrangements due to progressive fibrosis of the extracellular matrix and on prominent elastin modifications. The presence of lysyl oxidase activity, even in the oldest animals, might be at least partly responsible for the increased stiffness of the aging extracellular matrix. The striking age-related remodeling of the aortic architecture and the alterations of the interactions between cellular and extracellular compartments might greatly influence the functional properties of the arterial wall in senescence, at least contributing to the consequences of some apparently age-related vascular disorders.

Aging↗
PubMed2003

Percutaneous treatment of long bone nonunions: the use of autologous bone marrow and allograft bone matrix.

Sixty-six patients with 69 "stiff" nonunions (no gross motion) of long bones were entered into a prospective study. The only therapeutic intervention was the percutaneous administration of a mixture of autologous bone marrow and allograft demineralized bone matrix on an outpatient basis. Sixty-one of the percutaneous treatments (88%) resulted in union at an average of 8.1 months (range: 2 months to 3 years). This method of treating nonunions is as successful as standard iliac crest autologous bone grafting and offers the distinct advantages of decreased morbidity, reduced costs, and shorter hospital stay.

Adolescent↗
PubMed2000

Estrogen replacement reduces age-associated remodeling in rat mesenteric arteries.

Estrogen replacement therapy significantly decreases the incidence of cardiovascular disease in postmenopausal women. In aging, there is an increase in vascular stiffness along with a decrease in matrix metalloproteinase (MMP) activity. Our hypothesis was that estrogen replacement would increase MMPs and therefore reduce the vascular stiffness that is associated with aging. Female Sprague-Dawley rats were implanted with a placebo or 17ss-estradiol-containing pellet (0.5 mg/pellet, 60-day release) at 10 months of age (n=6, each). Six young rats (3 months old) were also studied. After a 2-month exposure to the pellet, mesenteric arteries were studied on a pressurized arteriograph system. Distensibility and wall thickness were measured in response to stepwise increases in intraluminal pressure in Ca(2+)-free physiological saline solution buffer with papaverine (10(-4) mol/L). In response to increasing pressure, aged placebo rats exhibited a significant decrease in distensibility compared with young rats (P<0.05) that was accompanied by an increase in wall thickness (P<0.05). Conversely, estrogen replacement increased distensibility and decreased wall thickness in aged rats (old estrogen-replaced versus old placebo, P<0.05). Zymography data indicated that MMP-2 activity decreased in aging but was increased by estrogen replacement. In summary, estrogen replacement in aging female rats reduces age-associated vascular remodeling.

Aging↗