Discriminating roles of desmosomal cadherins: Beyond desmosomal adhesion

Dusek, Rachel L.; Godsel, Lisa M.; Green, Kathleen J.

doi:10.1016/j.jdermsci.2006.10.006

Cited by 118 publications

(121 citation statements)

References 120 publications

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“…Therefore, the reasons for a decrease in desmosomal expression in skinks with noninvasive epitheliochorial placentae remain unclear. An increase in the number of desmosomes in uterine epithelium of a noninvasive placenta might be expected during pregnancy to provide greater cell-cell adhesion of the heavily stressed uterine epithelia of both oviparous and viviparous species as the conceptus increases in size (Dusek et al, 2007). Similarly, in other desmosome functional studies, an increase in the number of desmosomes had a profound effect on tumor suppression (Tselepis et al, 1998) as elevated desmosomal adhesion prevented tumor invasion into other tissue.…”

Section: Discussionmentioning

confidence: 91%

“…Desmosomes are a series of ''spot welds'' that attach adjoining epithelial cells along the lateral plasma membrane (Farquhar and Palade, 1963) and occur principally in heavily stressed tissue, such as the heart and the epidermis, that experience distension forces (Dusek et al, 2007). Desmosomal adhesion molecules comprise four desmogleins (Dsg1-4) and three desmocollins (Dsc 1-3), which are Ca 2þ -binding desmosomal cadherins responsible for the filamentous appearance of the extracellular region between two desmosomal plaques (Burdett, 1998;Bazzi and Christiano, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Desmosomes in the Uterine Epithelium of Noninvasive Skink Placentae

Biazik

Thompson

Murphy

2010

The Anatomical Record

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Australian species of viviparous skinks have noninvasive epitheliochorial placentation where there is no breeching or interruption of the uterine epithelial cell barrier. This is contrary to some African and South American species of skinks which exhibit invading chorionic cells and a localized endotheliochorial placenta. The desmosomes, which maintain the adhesive properties of the junctional complex between uterine epithelial cells, were found to decrease as gestation progressed in the uterus of two highly placentotrophic Australian skinks, but no changes in desmosomal numbers were present in the uterus of two Australian oviparous skinks or viviparous skinks with a simple placenta. In mammals, desmosomes decrease in the uterine epithelium of species with invasive hemochorial placentation, where less chemical and mechanical adhesion between cells assists the invading trophoblast at the time of implantation. However, Australian viviparous skinks do not have an invasive trophoblast; yet, similarities in decreasing lateral cellular adhesion exist in the uterus of both invasive and noninvasive placental types. This similarity in cellular mechanisms suggests a conservation of plasma membrane changes across placentation irrespective of reptilian or mammalian origin. Anat Rec, 293:502-512, 2010. V V C 2010 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Desmosomes in the Uterine Epithelium of Noninvasive Skink Placentae

Biazik

Thompson

Murphy

2010

The Anatomical Record

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“…In this respect, different permutations are possible between different desmosomal cadherins in order to adjust the level of adhesiveness of desmosomes. However, an emerging view is that desmosomes, like the classical adherens junctions, are involved in signaling pathways that dictate or maintain the differentiation status or program of the cells [1]. Due to its functional similarity to β-catenin in desmosomes, the armadillo protein PKG, also called γ-catenin, has been at the center of investigation with ample evidence to support a signaling role besides its adhesive role [37,38].…”

Section: Models and Cancermentioning

confidence: 99%

“…In recent years, elegant research from many different laboratories has provided definitive evidence that desmosomes, the "welding spots" of cell-cell junctions, are essential for the morphogenesis, differentiation, and maintenance of tissues that are subjected to high mechanical stress such as the skin and heart [1]. The highly electron dense and symmetric desmosomes are abundant between the keratinocytes of the skin epidermis and its appendages, as well as the myocytes of the heart, but can also be found in some specialized cells of the meninges and lymph nodes [2].…”

Section: Introductionmentioning

confidence: 99%

Broken hearts, woolly hair, and tattered skin: when desmosomal adhesion goes awry

Bazzi

Christiano

2007

Current Opinion in Cell Biology

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Desmosomal cadherins constitute the adhesive core of desmosomes. The different types of these cadherins are differentially expressed in a tissue specific as well as differentiation dependent manner. The skin and the heart are two examples of tissues whose vital functions require the ability to endure mechanical stress, and therefore, the integrity of desmosomal adhesion. When this adhesion is compromised via mutations in genes encoding desmosomal cadherins or associated plaque proteins, both tissues can suffer the consequences. Open questions revolve around whether the resulting phenotypes are solely due to physical disruption of cell adhesion, or whether these events are coupled with signaling mechanisms that influence many additional cellular processes. In this review, we focus on new developments in desmosomal adhesion with an emphasis on the skin, hair and heart.

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“…These discoveries have often highlighted novel or unusual phenotypes, including abnormal skin barrier function, alterations in epidermal differentiation, and developmental anomalies of various ectodermal appendages, especially hair, as well as a range of extracutaneous pathologies. The human diseases thus provide intriguing insight into the biological complexities of cell-cell contact and intercellular communication [59,60]. …”

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confidence: 99%

Diseases of epidermal keratins and their linker proteins

Uitto

Richard

McGrath³

2007

Experimental Cell Research

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Epidermal keratins, a diverse group of structural proteins, form intermediate filament networks responsible for the structural integrity of keratinocytes. The networks extend from the nucleus of the epidermal cells to the plasma membrane where the keratins attach to linker proteins which are part of desmosomal and hemidesmosomal attachment complexes. The expression of specific keratin genes is regulated by differentiation of the epidermal cells within the stratifying squamous epithelium. Progress in molecular characterization of the epidermal keratins and their linker proteins has formed the basis to identify mutations which are associated with distinct cutaneous manifestations in patients with genodermatoses. The precise phenotype of each disease apparently reflects the spatial level of expression of the mutated genes, as well as the types and positions of the mutations and their consequences at mRNA and protein levels. Identification of specific mutations in keratinization disorders has provided the basis for improved diagnosis and subclassification with prognostic implications and has formed the platform for prenatal testing and preimplantation genetic diagnosis. Finally, precise knowledge of the mutations is a prerequisite for development of gene therapy approaches to counteract, and potentially cure, these often devastating and currently intractable diseases. KeywordsEpidermal keratins; intermediate filaments; epidermal differentiation; hemidesmosomes; desmosomes; genodermatoses; skin fragility; epidermolysis bullosa; epidermolytic hyperkeratosis; ichthyosis Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. BIOLOGY OF EPIDERMAL KERATINSKeratins NIH Public Access Author ManuscriptExp Cell Res. Author manuscript; available in PMC 2008 November 4. Published in final edited form as:Exp Cell Res. 2007 June 10; 313(10): 1995-2009. doi:10.1016/j.yexcr.2007.03.029. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript dimensional and highly dynamic cytoskeleton spanning between the nucleus and the cell membrane, where they are anchored by interactions with desmosomal and hemidesmosomal linker proteins (Fig. 1). This organization provides both structural stability and flexibility, and ensures the mechanical integrity of different epithelial tissues. Keratins are expressed as obligate heterodimers of acidic (type I) and basic (type II) proteins, which assemble, through a multi-step process, into intermediate filaments (Fig. 2). The genes encoding type I and type II keratins cluster on chromosomal regions 17q12-q21 and 12q11-q13, respectively. Keratin ...

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Discriminating roles of desmosomal cadherins: Beyond desmosomal adhesion

Cited by 118 publications

References 120 publications

Desmosomes in the Uterine Epithelium of Noninvasive Skink Placentae

Desmosomes in the Uterine Epithelium of Noninvasive Skink Placentae

Broken hearts, woolly hair, and tattered skin: when desmosomal adhesion goes awry

Diseases of epidermal keratins and their linker proteins

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