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PubMed2004

Relaxin modifies systemic arterial resistance and compliance in conscious, nonpregnant rats.

Relaxin emanates from the corpus luteum of the ovary and circulates during pregnancy. Because the hormone is a potent renal vasodilator and mediates the renal vasodilation and hyperfiltration of pregnancy in conscious rats, we reasoned that it might also contribute to the broader cardiovascular changes of pregnancy. We began investigating this concept by testing whether relaxin can modify systemic arterial hemodynamics and load when chronically administered to nonpregnant rats. The major objectives of the present work were to determine whether relaxin administration to nonpregnant rats 1) modifies cardiac output (CO), systemic vascular resistance, and global arterial compliance (AC), and 2) regulates the passive mechanics of isolated arteries. To accomplish the first objective, we developed a conscious rat model for assessment of global AC. Passive mechanics of small renal arteries were assessed using a pressure arteriograph. Chronic administration of recombinant human relaxin by sc osmotic minipump to conscious, female, nonpregnant rats reduced the steady arterial load by decreasing systemic vascular resistance, increased CO, and reduced the pulsatile arterial load by increasing global AC as quantified by two indices-AC estimated from the diastolic decay of aortic pressure and CO and AC estimated by the ratio of stroke volume-to-pulse pressure. In another group of rats, relaxin administration also regulated the passive mechanics of small renal arteries, indicating that, in addition to reduction in vascular smooth muscle tone, modification of the vascular structure (e.g. extracellular matrix) contributes to the increase in global AC. These findings suggest a role for relaxin in the systemic hemodynamic changes of pregnancy, as well as novel therapeutic potential for relaxin in modifying arterial stiffness and cardiac afterload.

Animals↗

PubMed2001

Integration of engineered cartilage.

The structure and function of cartilaginous constructs, engineered in vitro using bovine articular chondrocytes, biodegradable scaffolds and bioreactors, can be modulated by the conditions and duration of tissue cultivation. We hypothesized that the integrative properties of engineered cartilage depend on developmental stage of the construct and the extracellular matrix content of adjacent cartilage, and that some aspects of integration can be studied under controlled in vitro conditions. Disc-shaped constructs (cultured for 5+/-1 days or 5+/-1 weeks) or explants (untreated or trypsin treated cartilage) were sutured into ring-shaped explants (untreated or trypsin treated cartilage) to form composites that were cultured for an additional 1-8 weeks in bioreactors and evaluated biochemically, histologically and mechanically (compressive stiffness of the central disk, adhesive strength of the integration interface). Immature constructs had poorer mechanical properties but integrated better than either more mature constructs or cartilage explants. Integration of immature constructs involved cell proliferation and the progressive formation of cartilaginous tissue, in contrast to the integration of more mature constructs or native cartilage which involved only the secretion of extracellular matrix components. Integration patterns correlated with the adhesive strength of the disc-ring interface, which was markedly higher for immature constructs than for either more mature constructs or cartilage explants. Trypsin treatment of the adjacent cartilage further enhanced the integration of immature constructs.

Animals↗

PubMed2003

Mechanical state of airway smooth muscle at very short lengths.

Although the shortening of smooth muscle at physiological lengths is dominated by an interaction between external forces (loads) and internal forces, at very short lengths, internal forces appear to dominate the mechanical behavior of the active tissue. We tested the hypothesis that, under conditions of extreme shortening and low external force, the mechanical behavior of isolated canine tracheal smooth muscle tissue can be understood as a structure in which the force borne and exerted by the cross bridge and myofilament array is opposed by radially disposed connective tissue in the presence of an incompressible fluid matrix (cellular and extracellular). Strips of electrically stimulated tracheal muscle were allowed to shorten maximally under very low afterload, and large longitudinal sinusoidal vibrations (34 Hz, 1 s in duration, and up to 50% of the muscle length before vibration) were applied to highly shortened (active) tissue strips to produce reversible cross-bridge detachment. During the vibration, peak muscle force fell exponentially with successive forced elongations. After the episode, the muscle either extended itself or exerted a force against the tension transducer, depending on external conditions. The magnitude of this effect was proportional to the prior muscle stiffness and the amplitude of the vibration, indicating a recoil of strained connective tissue elements no longer opposed by cross-bridge forces. This behavior suggests that mechanical behavior at short lengths is dominated by tissue forces within a tensegrity-like structure made up of connective tissue, other extracellular matrix components, and active contractile elements.

Animals↗

PubMed1998

Degeneration affects the anisotropic and nonlinear behaviors of human anulus fibrosus in compression.

Axial and radial specimens of non-degenerate and degenerate human anulus fibrosus (AF) were tested in confined compression to test the hypothesis that degeneration significantly affects the compressive properties of AF. Due to the highly oriented structure of AF, a secondary objective was to investigate anisotropic behaviors of AF in compression. Uniaxial swelling and stress relaxation experiments were performed on site-matched samples of anulus from the anterior outer region of L2-3 intervertebral discs. The experimental stress-relaxation behavior was modeled using the finite deformation biphasic theory and a finite-difference approximation scheme. Significant effects of degeneration but not orientation were detected for the reference stress offset, sigma(offset), and parameters describing the compressive stiffness (i.e. reference aggregate modulus, H(A0), and nonlinear stiffening coefficient, beta). Average values were 0.13+/-0.06 and 0.05+/-0.05 MPa for sigma(offset), 0.56+/-0.21 and 1.10+/-0.53 MPa for H(A0) and 2.13+/-1.48 and 0.44+/-0.61 for beta for all normal and degenerate specimens, respectively. No significant effect of degeneration or orientation were detected for either of the parameters describing the strain-dependent permeability (i.e. reference permeability, k0 and strain-dependent permeability coefficient, M) with average values for all specimens of 0.20+/-0.10 x 10(-15) m4/N-s and 1.18+/-1.30 for k0 and M, respectively. The loss of sigma(offset) was compensated with an elastic stiffening and change in the shape of the equilibrium stress-strain curve with H(A0) for degenerate tissues almost twice that of normal tissues and beta less than one sixth. The increase in reference elastic modulus with degeneration is likely related to an increase in tissue density resulting from the loss of water content. The significant effects of degeneration reported in this study suggested a shift in load carriage from fluid pressurization and swelling pressure to deformation of the solid matrix of the AF. The results also suggest that the highly organized and layered network of the anulus fibrosus, which gives rise to significant anisotropic effects in tension, does not play a major role in contributing to the magnitude of compressive stiffness or the mechanisms of fluid flow of the anulus in the confined compression configuration.

Adolescent↗

PubMed2004

Clinical and radiographic findings in multiple epiphyseal dysplasia caused by MATN3 mutations: description of 12 patients.

Multiple epiphyseal dysplasia (MED) is characterized by pain and stiffness in joints and delayed and irregular ossification of epiphyses. Causative mutations have been recognized in six different genes. We have identified disease-causing mutations in the gene encoding matrilin-3, an extracellular matrix protein, in seven families with autosomal dominant MED. Review of the clinical and radiographic features in 12 of the affected family members shows a uniform pattern of skeletal anomalies in all patients with considerable degree of variability in severity, both between and within families. The characteristic clinical findings are onset of symptoms in early childhood with predominance of knee and hip related complaints, normal stature, and early-onset osteoarthritis. Radiographs show small and irregular epiphyses and mild metaphyseal irregularities and striations, especially at the knees and hips and mild spinal changes. Despite overlap, both clinically and radiographically, with other forms of MED, the described features may help to differentiate this particular form from other entities within the MED spectrum.

Adolescent↗

PubMed2004

Tissue-engineered trachea from sheep marrow stromal cells with transforming growth factor beta2 released from biodegradable microspheres in a nude rat recipient.

OBJECTIVE: The purpose of this study was to evaluate the feasibility of using autologous sheep marrow stromal cells cultured onto polyglycolic acid mesh to develop helical engineered cartilage equivalents for a functional tracheal replacement. We also explored the potential benefit of local delivery of transforming growth factor beta 2 with biodegradable gelatin microspheres. METHODS: Bone marrow was obtained by iliac crest aspiration from 6-month-old sheep and cultured in monolayer for 2 weeks. At confluence, the cells were seeded onto nonwoven polyglycolic acid fiber mesh and cultured in vitro with transforming growth factor beta 2 and insulin-like growth factor 1 for 1 week. Cell-polymer constructs were wrapped around a silicone helical template. Constructs were then coated with microspheres incorporating 0.5 microg transforming growth factor beta 2. The cell-polymer-microsphere structures were then implanted into a nude rat. On removal, glycosaminoglycan content and hydroxyproline were analyzed in both native and tissue-engineered trachea. Histologic sections of both native and tissue-engineered trachea were stained with hematoxylin and eosin, safranin-O, and a monoclonal anti-type II collagen antibody. RESULTS: Cell-polymer constructs with transforming growth factor beta 2 microspheres formed stiff cartilage de novo in the shape of a helix after 6 weeks. Control constructs lacking transforming growth factor beta 2 microspheres appeared to be much stiffer than typical cartilage, with an apparently mineralized matrix. Tissue-engineered trachea was similar to normal trachea. Histologic data showed the presence of mature cartilage. Glycosaminoglycan and hydroxyproline contents were also similar to native cartilage levels. CONCLUSIONS: This study demonstrates the feasibility of engineering tracheas with sheep marrow stromal cells as a cell source. Engineering the tracheal equivalents with supplemental transforming growth factor beta 2 seemed to have a positive effect on retaining a cartilaginous phenotype in the newly forming tissue.

Absorbable Implants↗

PubMed1998

Behaviour of photopolymerized silicate glass fibre-reinforced dimethacrylate composites subjected to hydrothermal ageing: part II. Hydrolytic stability of mechanical properties.

The flexural properties and failure morphologies of dimethacrylate-copolymer composites reinforced with either S2-glass or quartz fibres ( approximately 33-66 vol%) were examined after hydrothermal ageing (0-3 mon at 37 degrees C). Initially the S2-glass composites were generally stiffer and stronger than comparably reinforced quartz composites, but within 1 wk the properties of S2-glass composites decreased by 12%-26%. The properties of quartz composites were relatively stable, except for those of composites with the least reinforcement (35 vol%), which decreased by roughly 15%. Scanning electron microscopy revealed that in all composites buckling had occurred at the site of load application. Evidence of good fibre-matrix adhesion was observed for both types of composites under all conditions. Modelling of degradation between 1 wk and 3 mon revealed that: (1) the only temporal change was a slight increase in the stiffness of S2-glass composites; and (2) higher reinforcement levels reduced the retention of strength in S2-glass composites but had the opposite effect (on both properties) for quartz composites (p<0.05). For the most highly reinforced S2-glass composites, susceptibility to degradation was offset by high initial properties; and after ageing (elastic modulus approximately 50 GPa, strength approximately 1.2 GPa), these composites were still, on average, approximately 25% stiffer and 50% stronger than the more hydrostable quartz counterparts.

Journal Article↗

PubMed1994

Regulation of the structural remodelling of the myocardium: from hypertrophy to heart failure.

The Framingham heart study has shown that arterial hypertension is the major aetiological factor for the development of heart failure. In the presence of heart failure, various regulatory systems may be operative. These include the Frank-Starling mechanism, the neurohormonal system, regulation of cardiac growth and peripheral oxygen delivery. Recently, the interrelationship of the neuroendocrine system and cardiac growth has been examined. In the pressure or volume overloaded heart, growth of the myocardium involves the enlargement of cardiac myocytes, an adaptation governed by ventricular loading. Non-myocyte cell growth, including cardiac fibroblasts, may also occur. However, the haemodynamic load does not appear to be its major physiological stimulus. Cardiac fibroblast activation is responsible for the accumulation of type I and III collagens, the major fibrillar proteins of the myocardial collagen matrix, while vascular smooth muscle cell growth accounts for medial thickening of coronary resistance vessels. This structural remodelling of the cardiac interstitium represents a major determinant of pathological hypertrophy: it accounts for abnormal myocardial stiffness and impaired coronary reserve, thereby leading to ventricular diastolic and systolic dysfunction and ultimately the appearance of symptomatic heart failure. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems are involved in the structural remodelling of the non-myocyte compartment, including the 'cardioprotective' effects of angiotensin converting enzyme (ACE) inhibition or the beneficial effects of anti-aldosterone treatment that were found to prevent myocardial fibrosis in renovascular hypertension due to unilateral renal ischaemia under experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Alcohol-induced bone loss and deficient bone repair.

BACKGROUND: Chronic consumption of excessive alcohol eventually results in an osteopenic skeleton and increased risk for osteoporosis. Alcoholics experience not only increased incidence of fractures from falls, but also delays in fracture healing compared with non-alcoholics. In this review the term "alcohol-induced bone disease" is used to refer to these skeletal abnormalities. Alcohol-induced osteopenia is distinct from osteoporoses such as postmenopausal osteoporosis and disuse osteoporosis. Gonadal insufficiency increases the rate of bone remodeling, whereas alcohol decreases this rate. Thus, histomorphometric studies show different characteristics for the bone loss that occurs in these two disease states. In particular, alcohol-induced osteopenia results mainly from decreased bone formation rather than increased bone resorption. Human, animal and cell culture studies of the effects of alcohol on bone strongly suggest alcohol has a dose-dependent toxic effect on osteoblast activity. The capacity of bone marrow stromal cells to differentiate into osteoblasts has a critical role in the cellular processes involved in the maintenance of the adult human skeleton by bone remodeling. Chronic alcohol consumption suppresses osteoblastic differentiation of bone marrow cells and promotes adipogenesis. In fracture healing, the effect of alcohol is to suppress synthesis of an ossifiable matrix, possibly due to inhibition of cell proliferation and maldifferentiation of mesenchymal cells in the repair tissue. This results in the deficient bone repair observed in animal studies, characterized by repair tissue of lower stiffness, strength and mineral content. Current knowledge of cellular effects and molecular mechanisms involved in alcohol-induced bone disease is insufficient to develop interventional strategies for its prevention and treatment. OBJECTIVES: The objectives of this review are 1) to identify the characteristics of alcohol-induced bone loss and deficient bone repair as revealed in human and animal studies, 2) to determine the current understanding of the cellular effects underlying both skeletal abnormalities, and 3) to suggest directions for future studies to resolve current ambiguities regarding the cellular basis of alcohol-induced bone disease.

Animals↗

PubMed1995

Urokinase receptor mediates mechanical force transfer across the cell surface.

The tripartite complex formed by the urokinase receptor, urokinase, and its inhibitor is an enzymatic system that controls plasmin formation involved in degradation of extracellular matrix proteins. With the use of magnetic twisting cytometry with urokinase-coated ferromagnetic beads, we applied mechanical stress directly to the urokinase receptor on the surface of human myogenic cells in culture. The stiffness and the stiffening response measured through the urokinase receptor resembled those of integrins, which are linked mechanically to the cytoskeleton. Furthermore, stiffness decreased with disruption of actin microfilaments. These results demonstrate that the urokinase receptor is coupled mechanically to the cytoskeleton. Inhibition of the tripartite complex formation with antibodies led to a twofold increase in cytoskeletal stiffness. A stiffened cytoskeleton might impede cytoskeletal remodeling and reorganization and thus impede cell motility. Our results demonstrate that the urokinase receptor mediates mechanical force transfer across the cell surface. As such, it is a novel pathway to regulate cytoskeletal stiffness and, thereby, possibly to modulate motility of normal and abnormal adherent cells.

Cell Membrane↗

PubMed1998

Effects of acid-etching on the tensile properties of demineralized dentin matrix.

OBJECTIVES: Little research has been done to evaluate the effects of acids commonly used in adhesive dentistry, on the tensile properties of the demineralized dentin matrix. The purpose of this study was to evaluate the effects of a number of acidic conditioners on the ultimate tensile strength (UTS) and modulus of elasticity (E) of human coronal dentin matrix. METHODS: Small hour-glass shaped (for UTS) or l-beam shaped (for determination of E) were prepared from mid-coronal dentin of extracted human third molars. After protecting the ends with varnish, the middle of the specimens was completely demineralized in 0.5 M EDTA (pH 7). UTS was determined by tensile stressing to failure. Modulus of elasticity was calculated from stress strain curves. The results were analyzed by ANOVA and Student-Neuman-Keuls test at the 95% confidence level. RESULTS: Brief (ca. 1-2 min) exposure of demineralized dentin matrix to acids had no measurable effects on its tensile properties. Ten-minute exposures to 2.5% and 17.5% nitric acid lowered (p < 0.05) the UTS compared to phosphate buffered saline (PBS)-exposed controls. Exposure of the decalcified dentin to 10% citric acid containing 3% ferric chloride, 10% citric acid, 37% phosphoric acid or 17.5% nitric acid containing 3% ferric chloride for 10 min had no effect on UTS. None of these acids consistently lowered stiffness. SIGNIFICANCE: The results indicate that relatively long exposures to acids are required to alter the tensile properties of demineralized dentin. It is unlikely that the brief exposures to acids that are used in adhesive dentistry would acutely weaken the physical properties of demineralized dentin. However, long-term studies should be done to determine if such treatment increases the susceptibility of the matrix to hydrolysis.

Acid Etching, Dental↗

PubMed2003

Thermal and mechanical characteristics of poly(L-lactic acid) nanocomposite scaffold.

Inorganic nanosized silicate nanoplatelets were incorporated into biodegradable poly(L-lactic acid) (PLLA) for the purpose of tailoring mechanical stiffness of PLLA porous scaffold systems. Increasing the nucleation density around the foreign body surfaces, the montmorillonite (MMT) nanoplatelets modified with dimethyl dihydrogenated tallow ammonium cations decreased the glass transition temperature and the degree of PLLA crystallinity, which seemingly caused the accelerated biodegradation rate of PLLA nanocomposites due to the enhanced segmental mobility of backbone chains and the expanded amorphous region of PLLA matrix. The tensile modulus was increased from 121.2MPa of pristine polymer scaffold to 170.1MPa of MMT/PLLA nanocomposite scaffold (ca. 40% increment) by the addition of small amount of MMT platelets (5.79 vol%) acting as a mechanical reinforcement of polymer chains in the nanoscale molecular level. Overall, the nanotechnology used in this study may be applied to various scaffold systems of biodegradable polymers and hard/soft scaffold structures requiring critical control and design characteristics of mechanical stiffness and biodegradation rate.

Culture Techniques↗

PubMed1997

Tissue remodeling with micro-structurally based material laws.

Cardiomyocytes and the extracellular collagen matrix which holds them together respond to changes in their mechanical environment by adapting their orientation, size and composition. We examine local mechanical feedback mechanisms affecting the fiber orientation, sheet orientation and passive fiber direction stiffness, using an axisymmetric finite element model of the left ventricle (LV), with material constitutive laws based on the fibrous-sheet microstructure of myocardium.

Animals↗

PubMed2002

Microstructural elasticity and regional heterogeneity in human femoral bone of various ages examined by nano-indentation.

The elastic modulus and hardness of secondary osteonal and interstitial bone was examined through the thickness of the cortex of human femora of various ages by nano-indentation. There was a clear difference between the stiffness and hardness of secondary osteonal and interstitial bone, the latter being stiffer (F(1,48)=56.0, P<0.001). There were some differences between the bones of different subjects; however, there were no differences that could be reliably associated with the chronological age of the subject, or with differences in location through the thickness of the cortex (F(2,48)=0.21, P=0.810). Previous studies have been equivocal in relating changes in the macroscopic 'composite' material stiffness of bone to the age of the individual. By combining the results of the nano-tests with histological measures, we were able to produce a good relationship of the microstructural properties at the matrix level with the bending modulus of whole bone (R(2)=0.88, P<0.001) and this improved further by taking into account the age of the individual (R(2)=0.94, P<0.001). Our results suggest that using differences in the volumetric proportions of secondary osteons versus interstitial bone, and the properties of these elements/structures in isolation may be a more accurate method of determining differences in elastic modulus of whole bone between individuals of various ages.

Adult↗

PubMed2002

Influence of surface morphology and chemistry on the enzyme catalyzed biodegradation of polycarbonate-urethanes.

Polycarbonate based polyurethanes were synthesized with varying hard segment content as well as hard segment chemistry based on three different diisocyanates,1,6-hexane diisocyanate (HDI), 4.4'-methylene bisphenyl diisocyanate (MDI) and 4,4-methylene biscyclohexyl diisocyanate (HMDI). The surface chemistry and morphology were characterized using X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The polymers were incubated with cholesterol esterase (CE) in a phosphate buffer solution at 37 degrees C over 10 weeks. XPS results showed that the surface chemistry changed as the size and chemistry of the hard segment varied within the materials. AFM images exhibited distinctive surface morphologies for all polymers, and this was particularly apparent with changes in the hard segment chemistry. The results showed that the surface of HDI polymers consisted of relatively stiff rod-like structures, which corresponded to the soft segment domains. Polymers with a higher HDI content exhibited a dense top layer containing a relatively higher hard segment component, covering the sub-surface matrix of rod like structures. The MDI based polyurethane had large aggregates on its top surface, which corresponded to the aggregation of harder components. The HMDI based polycarbonate-urethane presented a relatively homogeneous surface where no phase separation could be detected. The relative differences in hard and soft segment content in their surface structure was supported by XPS findings. The analysis of the biodegradation results, concluded that enzyme catalyzed biodegradation within these materials was initiated in amorphous soft segment regions located in the region of the interface between hard and soft segments. A higher hard segment content at the surface contributed significantly to an increase in biostability. The findings provided an enhanced understanding for the role of surface molecular structure in the enzyme catalyzed biodegradation of polyurethanes.

Biocompatible Materials↗

PubMed2006

Pifithrin-alpha, an inhibitor of p53 transactivation, alters the inflammatory process and delays tendon healing following acute injury.

Transcription factor p53, which was initially associated with cancer, has now emerged as an important regulator of inflammation and extracellular matrix homeostasis, two processes highly relevant to tendon repair. The goal of this study was to evaluate the effect of a p53 transactivation inhibitor, namely, pifithrin-alpha, on the pathophysiological sequence following collagenase-induced tendon injury. Administration of pifithrin-alpha during the inflammatory phase reduced the accumulation of neutrophils and macrophages by 30 and 40%, respectively, on day 3 postinjury. Pifithrin-alpha failed to reduce the percentage of apoptotic cells following collagenase injection but delayed functional recovery. In uninjured Achilles tendons, pifithrin-alpha increased metalloprotease activity 2.4-fold. Accordingly, pifithrin-alpha reduced the collagen content in intact tendons as well as in injured tendons 7 days posttrauma compared with placebo. The effect of pifithrin-alpha on load to failure and stiffness was also evaluated. The administration of pifithrin-alpha during the inflammatory phase did not significantly decrease the functional deficit 3 days posttrauma. More importantly, load to failure and stiffness were significantly decreased in the pifithrin-alpha group from day 7 to day 28 compared with placebo. Overall, our results suggest that administration of pifithrin-alpha alters the inflammatory process and delays tendon healing. The present findings also support the concept that p53 can regulate extracellular matrix homeostasis in vivo.

Achilles Tendon↗

PubMed2005

Extracellular matrix rigidity governs smooth muscle cell motility in a biphasic fashion.

Increasing evidence suggests that mechanical cues inherent to the extracellular matrix (ECM) may be equally as critical as its chemical identity in regulating cell behavior. We hypothesized that the mechanical properties of the ECM directly regulate the motility of vascular smooth muscle cells (SMCs) and tested this hypothesis using polyacrylamide substrates with tunable mechanical properties. Quantification of the migration speed on uniformly compliant hydrogels spanning a range of stiffnesses (Young's moduli values from 1.0 to 308 kPa for acrylamide/bisacrylamide ratios between 5/0.1% and 15/1.2%, respectively) revealed a biphasic dependence on substrate compliance, suggesting the existence of an optimal substrate stiffness capable of supporting maximal migration. The value of this optimal stiffness shifted depending on the concentration of ECM protein covalently attached to the substrate. Specifically, on substrates presenting a theoretical density of 0.8 microg/cm(2) fibronectin, the maximum speed of 0.74 +/- 0.09 microm/min was achieved on a 51.9 kPa gel; on substrates presenting a theoretical density of 8.0 microg/cm(2) fibronectin, the maximum speed of 0.72 +/- 0.06 microm/min occurred on a softer 21.6 kPa gel. Pre-treatment of cells with Y27632, an inhibitor of the Rho/Rho-kinase (ROCK) pathway, reduced these observed maxima to values comparable to those on non-optimal stiffnesses. In parallel, quantification of TritonX-insoluble vinculin via Western blotting, coupled with qualitative fluorescent microscopy, revealed that the formation of focal adhesions and actin stress fibers also depends on ECM stiffness. Combined, these data suggest that the mechanical properties of the underlying ECM regulate Rho-mediated contractility in SMCs by disrupting a presumptive cell-ECM force balance, which in turn regulates cytoskeletal assembly and ultimately, cell migration.

Acrylic Resins↗

PubMed2002

The contribution of the organic matrix to bone's material properties.

Bone is a two-phase porous composite material comprised primarily of collagen and mineral, which together provide its mechanical properties. The contribution of the mineral phase to bone's mechanical properties has dominated scientific thinking. Collagen's role has been underappreciated and not very well studied. However, there is evidence that changes in collagen content, or changes to inter- and intrafibrillar collagen cross-linking, can reduce the energy required to cause bone failure (toughness), and increase fracture risk. Although collagen may have less effect on bone's strength and stiffness than does mineral, it may have a profound effect on bone fragility. Collagen changes that occur with age and reduce bone's toughness may be an important factor in the risk of fracture in older women with low bone mass.

Animals↗