Desmosomes: adhesive strength and signalling in health and disease

Thomason, Helen A.; Scothern, Anthea; McHarg, Selina; Garrod, David R.

doi:10.1042/bj20100567

Cited by 156 publications

(155 citation statements)

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“…Cite this article as Cold Spring Harb Perspect Biol 2017;9:a029157 and resistance to mechanical strain (Garrod 2010;Thomason et al 2010). In contrast, during regeneration and wound healing, desmosomes become Ca 2þ -dependent resulting in weaker intercellular cohesion, which allows for tissue remodeling (Wallis et al 2000;Kimura et al 2012).…”

Section: Desmosomes and Keratins In Tissue Mechanicsmentioning

confidence: 99%

“…In cultured keratinocytes, desmosomes depend on extracellular Ca 2þ after their formation but undergo a maturation process to become hyperadhesive. Although the mechanism controlling formation of Ca 2þ -insensitive desmosomes is incompletely understood, one model predicts that a highly organized arrangement of the DSG and DSC extracellular domains is induced (Thomason et al 2010), which correlates with a wider intercellular space and the presence of a midline observed in electron microscopic images, whereas Ca 2þ -dependent desmosomes appear to lack this midline (Garrod 2010).…”

Section: Desmosomes and Keratins In Tissue Mechanicsmentioning

confidence: 99%

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Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Hatzfeld

Keil

Magin

2017

Cold Spring Harb Perspect Biol

116

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Adherens junctions (AJs) and desmosomes connect the actin and keratin filament networks of adjacent cells into a mechanical unit. Whereas AJs function in mechanosensing and in transducing mechanical forces between the plasma membrane and the actomyosin cytoskeleton, desmosomes and intermediate filaments (IFs) provide mechanical stability required to maintain tissue architecture and integrity when the tissues are exposed to mechanical stress. Desmosomes are essential for stable intercellular cohesion, whereas keratins determine cell mechanics but are not involved in generating tension. Here, we summarize the current knowledge of the role of IFs and desmosomes in tissue mechanics and discuss whether the desmosome-keratin scaffold might be actively involved in mechanosensing and in the conversion of chemical signals into mechanical strength.

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Section: Desmosomes and Keratins In Tissue Mechanicsmentioning

confidence: 99%

Section: Desmosomes and Keratins In Tissue Mechanicsmentioning

confidence: 99%

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Hatzfeld

Keil

Magin

2017

Cold Spring Harb Perspect Biol

116

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“…Desmosomes are comprised of proteins from at least three distinct gene families: cadherins, armadillo proteins and plakins (Thomason et al, 2010). All desmosomes contain desmoplakin, plakoglobin and at least one isoform of plakophilin as well as the desmosomal cadherins, desmocollin and desmoglein (Thomason et al, 2010). Desmosome function is linked to the tissue integrity, and defects in desmosome assembly and function have been implicated in a number of disease processes including pemphigus vulgaris, arrhythmogenic right ventricular cardiomyopathy and cancer (Thomason et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Desmosomes are multi-protein cell-cell adhesion structures, which act to link the internal keratin intermediate filament cytoskeleton to cadherin family adhesion receptors via linker proteins. Desmosomes are comprised of proteins from at least three distinct gene families: cadherins, armadillo proteins and plakins (Thomason et al, 2010). All desmosomes contain desmoplakin, plakoglobin and at least one isoform of plakophilin as well as the desmosomal cadherins, desmocollin and desmoglein (Thomason et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…All desmosomes contain desmoplakin, plakoglobin and at least one isoform of plakophilin as well as the desmosomal cadherins, desmocollin and desmoglein (Thomason et al, 2010). Desmosome function is linked to the tissue integrity, and defects in desmosome assembly and function have been implicated in a number of disease processes including pemphigus vulgaris, arrhythmogenic right ventricular cardiomyopathy and cancer (Thomason et al, 2010). In addition to a mechanical role there is evidence that plakoglobin, an armadillo family member with homology to b-catenin, can function to regulate gene transcription (Karnovsky and Klymkowsky, 1995;Zhurinsky et al, 2000;Garcia-Gras et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Plakoglobin-dependent regulation of keratinocyte APOPTOSIS by Rnd3

Ryan

Lock

Heath

et al. 2012

Journal of Cell Science

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SummaryThe human epidermis is a self-renewing, stratified epithelial tissue that provides the protective function of the skin. The principal cell type within the epidermis is the keratinocyte, and normal function of the epidermis requires that keratinocyte proliferation, differentiation and cell death be carefully controlled. There is clear evidence that signalling through adhesion receptors such as integrins and cadherins plays a key role in regulating epidermal function. Previous work has shown that Rho family GTPases regulate cadherinand integrin-based adhesion structures and hence epidermal function. In this study, we show that a member of this family, Rnd3, regulates desmosomal cell-cell adhesion in that loss of Rnd3 expression leads to an increase in desmosomes at sites of cell-cell adhesion and altered colony morphology. Loss of Rnd3 expression is also associated with resistance to cisplatin-mediated apoptosis in keratinocytes and this resistance is mediated through the desmosomal protein plakoglobin. We propose a novel plakoglobin-dependent role for Rnd3 in the regulation of keratinocyte cell death.

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Human Disease and the Desmosome

Chidgey

2011

Encyclopedia of Life Sciences

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Desmosomes are intercellular junctions of epithelia and cardiac muscle. They are located at the cell membrane where they act as anchors for intermediate filaments. Desmosomes maintain the structural integrity of tissues and disruption of desmosomal adhesion can have devastating consequences for human health. Arrhythmogenic right ventricular dysplasia, a heart muscle disease that is characterised by life‐threatening arrhythmias and increased risk of sudden heart failure, is caused by mutations in genes encoding desmosomal proteins. Other mutations can result in severe skin blistering, catastrophic fluid loss and early death. Cardiocutaneous syndromes that affect the heart, skin and hair are also caused by mutations in desmosomal genes. Pathogenic autoantibodies against desmogleins, membrane‐spanning proteins of desmosomes, cause the skin blistering diseases pemphigus and staphylococcal scalded skin syndrome. Desmosomes and their constituents could contribute to the progression of cancer. Key Concepts: Desmosomes are intercellular junctions of epithelia and cardiac muscle. Desmosomes maintain the structural integrity of tissues. Mutations in genes encoding desmosomal proteins can result in heart disease and disorders of the skin and hair. Pemphigus is an autoimmune skin blistering disease that is caused by autoantibodies against desmogleins, membrane‐spanning proteins of desmosomes. Desmosomes may be important in cancer.

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Desmosomes: adhesive strength and signalling in health and disease

Cited by 156 publications

References 189 publications

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Desmosomes and Intermediate Filaments: Their Consequences for Tissue Mechanics

Plakoglobin-dependent regulation of keratinocyte APOPTOSIS by Rnd3

Human Disease and the Desmosome

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