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Skin Microstructure is a Key Contributor to Its Friction Behaviour.

ABSTRACT: Due to its multifactorial nature, skin friction remains a multiphysics and multiscale phenomenon poorly understood despite its relevance for many biomedical and engineering applications (from superficial pressure ulcers, through shaving and cosmetics, to automotive safety and sports equipment). For example, it is unclear whether, and in which measure, the skin microscopic surface topography, internal microstructure and associated nonlinear mechanics can condition and modulate skin friction. This study addressed this question through the development of a parametric finite element contact homogenisation procedure which was used to study and quantify the effect of the skin microstructure on the macroscopic skin frictional response. An anatomically realistic two-dimensional image-based multilayer finite element model of human skin was used to simulate the sliding of rigid indenters of various sizes over the skin surface. A corresponding structurally idealised multilayer skin model was also built for comparison purposes. Microscopic friction specified at skin asperity or microrelief level was an input to the finite element computations. From the contact reaction force measured at the sliding indenter, a homogenised (or apparent) macroscopic friction was calculated. Results demonstrated that the naturally complex geometry of the skin microstructure and surface topography alone can play as significant role in modulating the deformation component of macroscopic friction and can significantly increase it. This effect is further amplified as the ground-state Young's modulus of the stratum corneum is increased (for example, as a result of a dryer environment). In these conditions, the skin microstructure is a dominant factor in the deformation component of macroscopic friction, regardless of indenter size or specified local friction properties. When the skin is assumed to be an assembly of nominally flat layers, the resulting global coefficient of friction is reduced with respect to the local one. This seemingly counter-intuitive effect had already been demonstrated in a recent computational study found in the literature. Results also suggest that care should be taken when assigning a coefficient of friction in computer simulations, as it might not reflect the conditions of microscopic and macroscopic friction one intends to represent. The modelling methodology and simulation tools developed in this study go beyond what current analytical models of skin friction can offer: the ability to accommodate arbitrary kinematics (i.e. finite deformations), nonlinear constitutive properties and the complex geometry of the skin microstructural constituents. It was demonstrated how this approach offered a new level of mechanistic insight into plausible friction mechanisms associated with purely structural effects operating at the microscopic scale; the methodology should be viewed as complementary to physical experimental protocols characterising skin friction as it may facilitate the interpretation of observations and measurements and/or could also assist in the design of new experimental quantitative assays.

SUBMITTER: Leyva-Mendivil MF

PROVIDER: S-EPMC6961497 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Skin Microstructure is a Key Contributor to Its Friction Behaviour.

Leyva-Mendivil Maria F MF Lengiewicz Jakub J Page Anton A Bressloff Neil W NW Limbert Georges G

Tribology letters 20161130 1

Due to its multifactorial nature, skin friction remains a multiphysics and multiscale phenomenon poorly understood despite its relevance for many biomedical and engineering applications (from superficial pressure ulcers, through shaving and cosmetics, to automotive safety and sports equipment). For example, it is unclear whether, and in which measure, the skin microscopic surface topography, internal microstructure and associated nonlinear mechanics can condition and modulate skin friction. This ...[more]

PMID: 32009774

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Project description:Objectives: Proteomics and high connotation functional gene screening (HCS) were used to screen key functional genes that play important roles in the pathogenesis of venous malformation. Furthermore, this study was conducted to analyze and explore their possible functions, establish a gene mutation zebrafish model, and perform a preliminary study to explore their possible pathogenic mechanisms in venous malformation. Methods: Pathological and normal tissues from patients with disseminated venous malformation were selected for Tandem Mass Tag (TMT) proteomics analysis to identify proteins that were differentially expressed. Based on bioinformatics analysis, 20 proteins with significant differential expression were selected for HCS to find key driver genes and characterize the expression of these genes in patients with venous malformations. In vitro experiments were then performed using human microvascular endothelial cells (HMEC-1). A gene mutant zebrafish model was also constructed for in vivo experiments to explore gene functions and pathogenic mechanisms. Results: The TMT results showed a total of 71 proteins that were differentially expressed as required, with five of them upregulated and 66 downregulated. Based on bioinformatics and proteomics results, five highly expressed genes and 15 poorly expressed genes were selected for functional screening by RNAi technology. HCS screening identified ACTA2 as the driver gene. Quantitative polymerase chain reaction (qPCR) and western blot were used to detect the expression of ACTA2 in the pathological tissues of patients with venous malformations and in control tissues, and the experimental results showed a significantly lower expression of ACTA2 in venous malformation tissues (P < 0.05). Cell assays on the human microvascular endothelial cells (HMEC-1) model showed that cell proliferation, migration, invasion, and angiogenic ability were all significantly increased in the ACTA2 over-expression group (P < 0.05), and that overexpression of ACTA2 could improve the inhibitory effect on vascular endothelial cell proliferation. We constructed an ACTA2-knockdown zebrafish model and found that the knockdown of ACTA2 resulted in defective vascular development, disruption of vascular integrity, and malformation of micro vein development in zebrafish. Further qPCR assays revealed that the knockdown of ACTA2 inhibited the Dll4/notch1 signaling pathway, Ephrin-B2 signaling pathway, and vascular integrity-related molecules and activated the Hedgehog signaling pathway. Conclusion: This study revealed that ACTA2 deficiency is an important factor in the pathogenesis of venous malformation, resulting in the disruption of vascular integrity and malformed vascular development. ACTA2 can be used as a potential biomarker for the treatment and prognosis of venous malformations.

Dataset Information

Skin Microstructure is a Key Contributor to Its Friction Behaviour.

Publications

Skin Microstructure is a Key Contributor to Its Friction Behaviour.

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