Tissue elasticity and the ageing elastic fibre

Sherratt, Michael J.

doi:10.1007/s11357-009-9103-6

Cited by 263 publications

(206 citation statements)

References 208 publications

(266 reference statements)

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“…We also found a relationship between the polymorphism studied in ELN (elastin) and the severity and recovery time of ligamentous injuries. The absence of elastin or poorly constituted protein distorts the presentation and stability of other components of the extracellular matrix and the interactions, making the ELN very important for elastogenesis and functioning of living in elastic fibers [20]. In this case, players with AA genotype are more prone to severe injuries and take much longer to recover from them than those with AG/GG genotypes.…”

Section: Genetics and Injury Occurrencementioning

confidence: 99%

Influence of Genetics on Sports Injuries

Pruna¹,

Clos²,

Bahdur³

et al. 2017

J Nov Physiother

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SummaryThe identification of risk factors and the assessment of athlete's predisposition to suffer an injury and the way in which it will occur is hard to predict due to the multifactorial origin of the lesions. In recent years, the importance of the genetic component of each individual as a possible cause of injury predisposition is being evaluated.The objective of this work was to write a review of the genetic studies carried out to date on connective tissue injuries and propose future research lines that would allow the development of more personalized training programs and specify preventive therapies in order to reduce the injury risk.The multifactorial origin of injuries complicates the identification of risk factors (extrinsic and intrinsic factors). Together, these factors and their interaction predisposes an athlete to injuries. In recent years, the genetic component of each individual as a possible cause of injury predisposition has become of importance.The aim of this article was to propose a review of published genetic studies related to connective tissue repair or regeneration and to pave the way for future Sports Medicine Research. This information could be very useful in order to individualize the preventive strategies to avoid injuries and to optimize the therapeutic and rehabilitation process after injuries.Applied biology is already contributing new knowledge by providing new biomarkers that will give information and increase understanding regarding the susceptibility of individuals to suffer certain types of injury. Genetic analysis can offer us reliable and objective predictive parameter that combined with the current methods of analysis will help improve the performance and management of athletes.

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Section: Genetics and Injury Occurrencementioning

confidence: 99%

Influence of Genetics on Sports Injuries

Pruna¹,

Clos²,

Bahdur³

et al. 2017

J Nov Physiother

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“…3A). However, old extracellular matrix is altered by protein modifications including AGEs that might affect correct analyses of matrix proteins (45). These age-related matrix changes are additionally indicated by the lower enzymatic solubility of old collagen without simultaneous effect of RAGE (Fig.…”

Section: Rage Trans Interaction In Alveolar Epithelial Cellsmentioning

confidence: 99%

The receptor for advanced glycation end-products supports lung tissue biomechanics

Al‐Robaiy

Weber

Simm

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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The receptor for advanced glycation end-products (RAGE) and its soluble forms are predominantly expressed in lung but its physiological importance in this organ is not yet fully understood. Since RAGE acts as a cell adhesion molecule, we postulated its physiological importance in the respiratory mechanics. Respiratory function in a buffer-perfused isolated lung system and biochemical parameters of the lung were studied in young, adult, and old RAGE knockout (RAGE-KO) mice and wild-type (WT) mice. Lungs from RAGE-KO mice showed a significant increase in the dynamic lung compliance and a decrease in the maximal expiratory air flow independent of age-related changes. We also determined lower mRNA and protein levels of elastin in lung tissue of RAGE-KO mice. RAGE deficiency did not influence the collagen protein level, lung capillary permeability, and inflammatory parameters (TNF-␣, high-mobility group box protein 1) in lung. Overexpressing RAGE as well as soluble RAGE in lung fibroblasts or cocultured lung epithelial cells increased the mRNA expression of elastin. Moreover, immunoprecipitation studies indicated a trans interaction of RAGE in lung epithelial cells. Our findings suggest the physiological importance of RAGE and its soluble forms in supporting the respiratory mechanics in which RAGE trans interactions and the influence on elastin expression might play an important role.receptor for advanced glycation end-products; aging; biomechanics; elastin; mouse THE RECEPTOR FOR ADVANCED glycation end-products (RAGE) is a pattern recognition receptor of the immunoglobulin superfamily (32). RAGE is predominantly expressed in lung, particularly in the type I alveolar epithelial (ATI) cells (12,15,46). This specific localization suggests its important physiological function in the alveolar epithelium. In other cell types and tissues, the expression of RAGE is activated in response to pathophysiological conditions, such as the accumulation of advanced glycation end-products (AGEs) and inflammation (1). RAGE expression is highly associated with lung development and increases during the alveolarization (29,40). High RAGE expression prior to the alveolarization period has adverse effects associated with a severe pulmonary dysplasia (16,41). A reduced alveolar expression of RAGE is related to pathophysiological changes of the lung tissue, such as carcinoma (3), fibrosis (34, 37), and chronic obstructive pulmonary disease (COPD) (34). In addition to the membrane-bound receptor, soluble RAGE (sRAGE) forms exist as the result of either alternative splicing (22) or protein shedding by metalloproteinases (39, 52). sRAGE normally exists in the bronchoalveolar lavage (BAL) at a high level (53), but it is deficient in neutrophilic asthma and COPD (47, 49).The physiological importance of RAGE in lung is not yet fully understood because mice lacking RAGE do not show obvious pulmonary alterations (5, 9). Only intervention studies indicated an adverse effect of RAGE in the development of lung fibrosis (14, 19) and acute lung injury (4...

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“…Disease and ageing, however, alter the respective compositions, leading to often undesirable changes in function. Ageing has been shown to cause a loss of medial elastin followed by an increase in the stiffer collagen fibres, further stiffened by additional cross-linking, to compensate [8,9,10,11]. This results in the elastin-collagen interaction altering and the stiffer collagen fibres being recruited at smaller deformations, leading to an observed stiffening of the arterial wall.…”

Section: Introductionmentioning

confidence: 99%

Creating a model of diseased artery damage and failure from healthy porcine aorta

Noble

Smulders

Green

et al. 2016

Journal of the Mechanical Behavior of Biomedical Materials

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Article available under the terms of the CC-BY-NC-ND licence (https://creativecommons.org/licenses/by-nc-nd/4.0/) eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request.Creating a model of diseased artery damage and failure from healthy porcine aorta AbstractLarge quantities of diseased tissue are required in the research and development of new generations of medical devices, for example for use in physical testing. However, these are difficult to obtain. In contrast, porcine arteries are readily available as they are regarded as waste. Therefore, reliable means of creating from porcine tissue physical models of diseased human tissue that emulate well the associated mechanical changes would be valuable. To this end, we studied the effect on mechanical response of treating porcine thoracic aorta with collagenase, elastase and glutaraldehyde. The alterations in mechanical and failure properties were assessed via uniaxial tension testing. A constitutive model composed of the Gasser-Ogden-Holzapfel model, for elastic response, and a continuum damage model, for the failure, was also employed to provide a further basis for comparison [1,2]. For the concentrations used here it was found that: collagenase treated samples showed decreased fracture stress in the axial direction only; elastase treated samples showed increased fracture stress in the circumferential direction only; and glutaraldehyde samples showed no change in either direction. With respect to the proposed constitutive model, both collagenase and elastase had a strong effect on the fibre-related terms. The model more closely captured the tissue response in the circumferential direction, due to the smoother and sharper transition from damage initiation to complete failure in this direction. Finally, comparison of the results with those of tensile tests on diseased tissues suggests these treatments indeed provide a basis for creation of physical models of diseased arteries.

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Tissue elasticity and the ageing elastic fibre

Cited by 263 publications

References 208 publications

Influence of Genetics on Sports Injuries

Influence of Genetics on Sports Injuries

The receptor for advanced glycation end-products supports lung tissue biomechanics

Creating a model of diseased artery damage and failure from healthy porcine aorta

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