Mechanisms of Blister Formation

Stoughton, Richard B.

doi:10.1001/archderm.1957.01550230050008

Cited by 41 publications

(11 citation statements)

References 25 publications

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“…It is a matter of debate whether KIF alterations in response to pemphigus autoantibodies are secondary to changes of the desmosomes or rather cause and contribute to altered desmosome composition and turnover. Indeed, in early ultrastructural studies, it was suggested that the initial changes affect KIFs ( 20 , 28 ). We here demonstrated that changes of the KIF cytoskeleton are visible in HaCaT keratinocytes starting at 60 min after application of autoantibodies.…”

Section: Discussionmentioning

confidence: 99%

Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris

et al. 2018

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Pemphigus vulgaris (PV) is a potentially lethal autoimmune disease characterized by blister formation of the skin and mucous membranes and is caused by autoantibodies against desmoglein (Dsg) 1 and Dsg3. Dsg1 and Dsg3 are linked to keratin filaments in desmosomes, adhering junctions abundant in tissues exposed to high levels of mechanical stress. The binding of the autoantibodies leads to internalization of Dsg3 and a collapse of the keratin cytoskeleton—yet, the relevance and interdependence of these changes for loss of cell–cell adhesion and blistering is poorly understood. In live-cell imaging studies, loss of the keratin network at the cell periphery was detectable starting after 60 min of incubation with immunoglobulin G fractions of PV patients (PV-IgG). These rapid changes correlated with loss of cell–cell adhesion detected by dispase-based dissociation assays and were followed by a condensation of keratin filaments into thick bundles after several hours. Dsg3 internalization started at 90 min of PV-IgG treatment, thus following the early keratin changes. By inhibiting casein kinase 1 (CK-1), we provoked keratin alterations resembling the effects of PV-IgG. Although CK-1-induced loss of peripheral keratin network correlated with loss of cell cohesion and Dsg3 clustering in the membrane, it was not sufficient to trigger the internalization of Dsg3. However, additional incubation with PV-IgG was effective to promote Dsg3 loss at the membrane, indicating that Dsg3 internalization is independent from keratin alterations. Vice versa, inhibiting Dsg3 internalization did not prevent PV-IgG-induced keratin retraction and only partially rescued cell cohesion. Together, keratin changes appear very early after autoantibody binding and temporally overlap with loss of cell cohesion. These early alterations appear to be distinct from Dsg3 internalization, suggesting a crucial role for initial loss of cell cohesion in PV.

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Section: Discussionmentioning

confidence: 99%

Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris

et al. 2018

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“…He likewise theo rizes th a t injurv to epidermal cells from multiple diverse etiologic agents results in an enzym atic degradation process which in turn elicits the vesicle or blister. This author [24] also states th at the presence of a basem ent m em brane at the dermal-epidermal junction is now an established fact and th a t this membrane is an amorphous structure consisting prim arily of mucopolysaccharides which are closely related to if not identical to the ground substance of the der mis. The basem ent m em brane exists normally in a " gel" state and is probably capable of reversible transformation into a " sol" state.…”

Section: Theories Relative To the Blister Formationmentioning

confidence: 97%

“…More recently, Cottini [22] emphasizes the im portance of enzym atic alterations in causation of bullae. Stoughton [23] includes vascular occlusion as a cause of bullae in the various skin disorders characterized by blister formation. He likewise theo rizes th a t injurv to epidermal cells from multiple diverse etiologic agents results in an enzym atic degradation process which in turn elicits the vesicle or blister.…”

Section: Theories Relative To the Blister Formationmentioning

confidence: 99%

Scleroderma with Bullous Lesions

Garb

Sims²

1959

Dermatology

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“…Excessive static normal stress has been shown to cause blood flow occlusion (Daly et al, 1976) which can result in necrosis and ulceration (Levy, 1962). Trauma from dynamic All correspondence to be addressed to J. E. Sanders Ph.D., Center for Bioengineering, WD-12, University of Washington, Seattle, Washington 98195, USA. shear is apparent as separation at the dermalepidermal junction, followed by fluid deposition and blister formation (Stoughton, 1957;Hunter et al, 1974).…”

Section: Introductionmentioning

confidence: 99%

Clinical measurement of normal and shear stresses on a trans-tibial stump

Sanders

Daly

Burgess

1993

Prosthetics &Amp; Orthotics International

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Stresses on the surface of a stump within a prosthetic socket during walking can potentially traumatize stump tissues. To gain insight into stresses and design parameters that affect them, normal and shear interface stresses were measured on three unilateral trans-tibial amputee subjects during walking trials. During stance phase repeated characteristics in wave-form shapes from different subjects were apparent. They included "loading delays", "high frequency events (HFE's)", "first peaks", "valleys", "second peaks", and "push-off". Characteristics did not necessarily occur at the same time from one step to the next but their timings matched well with events in shank force and moment data which were collected simultaneously. For "plantarflexion" and "dorsiflexion" alignment changes, the above wave-form characteristics were still present but their timings within the stance phase changed. The physical meaning and relevance of the characteristics to stump tissue mechanics are discussed.

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Mechanisms of Blister Formation

Cited by 41 publications

References 25 publications

Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris

Keratin Retraction and Desmoglein3 Internalization Independently Contribute to Autoantibody-Induced Cell Dissociation in Pemphigus Vulgaris

Scleroderma with Bullous Lesions

Clinical measurement of normal and shear stresses on a trans-tibial stump

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