Different effects of pemphigus antibody and plasmin on the distribution of keratin intermediate filaments and desmoplakins between cultured oral and epidermal keratinocytes

Jinbu, Yoshinori; Kitajima, Yasuo; Koto, Shigeaki; Akasaka, Yoko; Yaoita, Hideo

doi:10.1016/0923-1811(92)90003-t

Cited by 13 publications

(3 citation statements)

References 13 publications

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“…The primary events after binding of pemphigus antibodies to keratinocytes are changes in the cytoskeleton of keratinocytes with retraction of tonofilaments [17][18][19] and breaking of the bond between tonofilaments and desmosomes culminating in shrinkage of the basal cells. 8,[20][21][22] The detachment of tonofilaments occurs before the desmosomes show any visible alteration 8,23 or loss in adhesion.…”

Section: Nondesmosomal Mechanisms Appear To Be Involved In Pv Acanthomentioning

confidence: 99%

A novel explanation for acantholysis in pemphigus vulgaris: The basal cell shrinkage hypothesis

Bystryn¹,

Grando²

2006

Journal of the American Academy of Dermatology

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Section: Nondesmosomal Mechanisms Appear To Be Involved In Pv Acanthomentioning

confidence: 99%

A novel explanation for acantholysis in pemphigus vulgaris: The basal cell shrinkage hypothesis

Bystryn¹,

Grando²

2006

Journal of the American Academy of Dermatology

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“…First, it has been described that cytokeratin filaments become detached from cell junctions and accumulate in the perinuclear region, a phenomenon commonly referred to as “keratin retraction” (Berkowitz et al 2005 ; Caldelari et al 2001 ; Calkins et al 2006 ; Chernyavsky et al 2007a ; Jinbu et al 1992 ; Kitajima et al 1987 ; Waschke et al 2006 ; Wilgram et al 1961 , 1964 ; Williamson et al 2006 ). It was shown that cytokeratin retraction could be detected as early as 4–6 h after addition of PV-IgG, i.e.…”

Section: Pemphigusmentioning

confidence: 99%

The desmosome and pemphigus

Waschke

2008

Histochem Cell Biol

183

192

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Desmosomes are patch-like intercellular adhering junctions ("maculae adherentes"), which, in concert with the related adherens junctions, provide the mechanical strength to intercellular adhesion. Therefore, it is not surprising that desmosomes are abundant in tissues subjected to signiWcant mechanical stress such as stratiWed epithelia and myocardium. Desmosomal adhesion is based on the Ca 2+ -dependent, homo-and heterophilic transinteraction of cadherin-type adhesion molecules. Desmosomal cadherins are anchored to the intermediate Wlament cytoskeleton by adaptor proteins of the armadillo and plakin families. Desmosomes are dynamic structures subjected to regulation and are therefore targets of signalling pathways, which control their molecular composition and adhesive properties. Moreover, evidence is emerging that desmosomal components themselves take part in outside-in signalling under physiologic and pathologic conditions. Disturbed desmosomal adhesion contributes to the pathogenesis of a number of diseases such as pemphigus, which is caused by autoantibodies against desmosomal cadherins. Beside pemphigus, desmosome-associated diseases are caused by other mechanisms such as genetic defects or bacterial toxins. Because most of these diseases aVect the skin, desmosomes are interesting not only for cell biologists who are inspired by their complex structure and molecular composition, but also for clinical physicians who are confronted with patients suVering from severe blistering skin diseases such as pemphigus. To develop disease-speciWc therapeutic approaches, more insights into the molecular composition and regulation of desmosomes are required.

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“…This is further emphasized by electron microscopic studies which have shown that the keratinocytes separate first at the interdesmosomal areas even before the loss of adhesion of the desmosomes (Hashimoto & Lever, 1967; Wilgram et al, 1961). The second argument is that studies have shown that the binding of autoantibodies to the respective antigens primarily causes the retraction of tonofilaments causing the cell to decrease in size and gain a rounded morphology (Jinbu et al, 1992; Kitajima et al, 1986). This also occurs before the desmosomes can show any visible alteration.…”

Section: Progression Mechanisms (Split Formation)mentioning

confidence: 99%

Critical appraisal of different triggering pathways for the pathobiology of pemphigus vulgaris—A review

et al. 2021

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Pemphigus vulgaris is an autoimmune blistering disease with an increased potential for mortality. The epithelium is key in understanding the pathobiology as it is specialized to perform functions like mechanical protection, immunological defense, and proprioception. In order to perform these array of functions, epithelial integrity is important. This integrity is maintained by a host of molecules which orchestrate the ability of the keratinocytes to function as a single unit. Desmoglein 3 antibodies formed in genetically susceptible individuals are known to cause the disruption of the intact oral mucosa leading to the formation of blisters in pemphigus vulgaris patients. However, there are underlying complex triggering pathways leading to the clinical disease. The aim of the review is to congregate and critically appraise the various triggering pathways which contribute toward the pathobiology of pemphigus vulgaris. Articles relevant to the pathobiology of pemphigus vulgaris were identified from various search databases till the year 2020. The pathogenesis of pemphigus vulgaris is complex, and it involves an in‐depth understanding of the various predisposing factors, provoking factors, and progression mechanisms. Congregation of the various triggering pathways will open our minds to understand pemphigus vulgaris better and in turn develop a reliable treatment in the near future.

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Different effects of pemphigus antibody and plasmin on the distribution of keratin intermediate filaments and desmoplakins between cultured oral and epidermal keratinocytes

Cited by 13 publications

References 13 publications

A novel explanation for acantholysis in pemphigus vulgaris: The basal cell shrinkage hypothesis

A novel explanation for acantholysis in pemphigus vulgaris: The basal cell shrinkage hypothesis

The desmosome and pemphigus

Critical appraisal of different triggering pathways for the pathobiology of pemphigus vulgaris—A review

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