Cell death induced by mechanical compression on engineered muscle results from a gradual physiological mechanism

Wu, Yabin; Schaft, Dwj Daisy van der; Baaijens, Fpt Frank; Oomens, Cwj Cees

doi:10.1016/j.jbiomech.2016.02.028

Cited by 17 publications

(14 citation statements)

References 39 publications

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“…p38 phosphorylation in MTX-treated and MTX plus vitamin C-treated cells. The MAPK family kinases ERK, JNK and p38 are involved in cell death, cell differentiation, and cell proliferation (46)(47)(48). In the present study, expression levels of EKR, JNK, p38 and their phosphorylated (activated) forms (p-ERK, p-JNK and p-p38) were estimated by western blotting.…”

Section: Mtx-treatment and Combined Mtx Plus Vitamin C Treatment Indumentioning

confidence: 85%

Combined treatment with vitamin C and methotrexate inhibits triple-negative breast cancer cell growth by increasing H2O2 accumulation and activating caspase-3 and p38 pathways

Liu

et al. 2017

Oncology Reports

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Methotrexate (MTX) is widely used as both an anticancer and anti-rheumatoid arthritis drug. Although MTX has been used to inhibit the growth of many cancer cells, it cannot effectively inhibit growth of triple-negative breast cancer cells (TNBC cells). Vitamin C is an antioxidant that can prevent oxidative stress. In addition, vitamin C has been applied as adjunct treatment for growth inhibition of cancer cells. Recent studies indicated that combined treatment with vitamin C and MTX may inhibit MCF-7 and MDA-MB-231 breast cancer cell growth through G2/M elongation. However, the mechanisms remain unknown. The aim of the present study was to determine whether combined treatment with low-dose vitamin C and MTX inhibits TNBC cell growth and to investigate the mechanisms of vitamin C/MTX-induced cytotoxicity. Neither low-dose vitamin C alone nor MTX alone inhibited TNBC cell growth. However, combined low-dose vitamin C and MTX had synergistic anti-proliferative/cytotoxic effects on TNBC cells. In addition, co-treatment increased H2O2 levels and activated both caspase-3 and p38 cell death pathways.

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Section: Mtx-treatment and Combined Mtx Plus Vitamin C Treatment Indumentioning

confidence: 85%

Combined treatment with vitamin C and methotrexate inhibits triple-negative breast cancer cell growth by increasing H2O2 accumulation and activating caspase-3 and p38 pathways

Liu

et al. 2017

Oncology Reports

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“…Friction blisters occur in the viable epidermis as a result of surface shear loads, and while pressure ulcers are related to compression-induced ischaemia and reperfusion of capillary flow, it is likely that excessive shear stresses experienced by living cells of the viable epidermis contribute to their mechanical damage and, subsequently to their death as evidenced for muscle cells [21]. In turn, degradation of the supporting structural and biological constituents of the viable epidermis will compromise skin mechanical integrity and biological functions, thus aggravating the likelihood of developing deeper tissue injuries (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study by Wu, van der Schaft, Baaijens and Oomens [21] showed that the application of shear and compressive stresses to muscle cells can induce cell death. Pig model studies have also shown that interfacial shear up to 70 kPa can also result in skin breakdown [22].…”

Section: Introductionmentioning

confidence: 99%

Implications of Multi-asperity Contact for Shear Stress Distribution in the Viable Epidermis – An Image-based Finite Element Study

et al. 2017

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Understanding load transfer mechanisms from the surface of the skin to its deeper layers is crucial in gaining a fundamental insight into damage phenomena related to skin tears, blisters and superficial/deep tissue ulcers. It is unknown how shear stresses in the viable epidermis are conditioned by the skin surface topography and internal microstructure and to which extent their propagation is conditioned by the size of a contacting asperities.In this computational study, these questions were addressed by conducting a series of contact finite element analyses simulating normal indentation of an anatomically-based two-dimensional multi-layer model of the skin by rigid indenters of various sizes and sliding of these indenters over the skin surface. Indentation depths, local (i.e. microscopic) coefficients of friction and Young's modulus of the stratum corneum were also varied. For comparison purpose and for isolating effects arising purely from the skin microstructure, a geometrically-idealised equivalent multi-layer model of the skin was also considered.The multi-asperity contact induced by the skin topographic features in combination with a non-idealised geometry of the skin layers lead to levels of shear stresses much higher than those produced in the geometrically-idealised case. These effects are also modulated by other system parameters (e.g. local coefficient of friction, indenter radius).These findings have major implications for the design and analyses of finite element studies aiming at modelling the tribology of skin, particularly if the focus is on how surface shear stress leads to damage initiation which is a process known to occur across several length scales.

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“…Ischaemia disrupts nutrient supply and promotes the accumulation of waste products and build-up of acidity [167], which ultimately compromise tissue integrity. Wu et al [168] showed that application of shear and compressive stresses to muscle cells is sufficient to induce cell death. It was reported by Goldstein and Sanders [169] that, in a pig model study, an interfacial shear up to 70 kPa could also result in skin breakdown.…”

Section: Biophysical Response Of Skin Against a Surfacementioning

confidence: 99%

“…It was reported by Goldstein and Sanders [169] that, in a pig model study, an interfacial shear up to 70 kPa could also result in skin breakdown. Excessive shear stresses experienced by living cells of the viable epidermis as a consequence of mechanical forces applied to the surface of the skin can ultimately lead to mechanical damage of their cytoskeleton and other basic cellular units , eventually leading to cell death as evidenced for muscle cells [168]. In turn, degradation of the supporting structural and biological constituents of the viable epidermis can compromise skin mechanical integrity and biological functions, thus increasing the probability of developing deeper tissue injuries (i.e.…”

Section: Biophysical Response Of Skin Against a Surfacementioning

confidence: 99%

Biotribology of the ageing skin—Why we should care

et al. 2019

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Ageing of populations has emerged as one of the most pressing societal, economic and healthcare challenges currently facing most nations across the globe. The ageing process itself results in degradation of physiological functions and biophysical properties of organs and tissues, and more particularly those of the skin. Moreover, in both developed and emerging economies, population ageing parallels concerning increases in lifestyleassociated conditions such as Type 2 diabetes, obesity and skin cancers. When considered together, these demographic trends call for even greater urgency to find clinical and engineering solutions for the numerous age-related deficits in skin function. From a tribological perspective, detrimental alterations of skin bioph ysical properties with age have fundamental consequences on how one interacts with the body's inner and outer environments. This stems from the fact that, besides being the largest organ of the human body, and also nearly covering its entirety, the skin is a multifunctional interface which mediates these interactions. The aim of this paper is to present a focused review to discuss some of the consequences of skin ageing from the viewpoint of biotribology, and their implications on health, well -being and human activities. Current and future research questions/challenges associated with biotribology of the ageing ski n are outlined. They provide the background and motivation for identifying future lines of research that could be taken up by the biotribology and biophysics communities.

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Cell death induced by mechanical compression on engineered muscle results from a gradual physiological mechanism

Cited by 17 publications

References 39 publications

Combined treatment with vitamin C and methotrexate inhibits triple-negative breast cancer cell growth by increasing H2O2 accumulation and activating caspase-3 and p38 pathways

Combined treatment with vitamin C and methotrexate inhibits triple-negative breast cancer cell growth by increasing H2O2 accumulation and activating caspase-3 and p38 pathways

Implications of Multi-asperity Contact for Shear Stress Distribution in the Viable Epidermis – An Image-based Finite Element Study

Biotribology of the ageing skin—Why we should care

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