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Journal articles on the topic 'Desmosomal disruption'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Garrod, David, and Tomomi E. Kimura. "Hyper-adhesion: a new concept in cell–cell adhesion." Biochemical Society Transactions 36, no. 2 (2008): 195–201. http://dx.doi.org/10.1042/bst0360195.

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We have developed a new concept of cell–cell adhesion termed ‘hyper-adhesion’, the very strong adhesion adopted by desmosomes. This uniquely desmosomal property accounts for their ability to provide the intercellular links in the desmosome–intermediate filament complex. These links are targeted by diseases, resulting in disruption of the complex with severe consequences. Hyper-adhesion is characteristic of desmosomes in tissues and is believed to result from a highly ordered arrangement of the extracellular domains of the desmosomal cadherins that locks their binding interaction so that it is

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Li, Jifen, and Glenn L. Radice. "A New Perspective on Intercalated Disc Organization: Implications for Heart Disease." Dermatology Research and Practice 2010 (2010): 1–5. http://dx.doi.org/10.1155/2010/207835.

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Adherens junctions and desmosomes are intercellular adhesive junctions and essential for the morphogenesis, differentiation, and maintenance of tissues that are subjected to high mechanical stress, including heart and skin. The different junction complexes are organized at the termini of the cardiomyocyte called the intercalated disc. Disruption of adhesive integrity via mutations in genes encoding desmosomal proteins causes an inherited heart disease, arrhythmogenic right ventricular cardiomyopathy (ARVC). Besides plakoglobin, which is shared by adherens junctions and desmosomes, other desmos

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Zen, Ke, Brian A. Babbin, Yuan Liu, John B. Whelan, Asma Nusrat, and Charles A. Parkos. "JAM-C Is a Component of Desmosomes and a Ligand for CD11b/CD18-mediated Neutrophil Transepithelial Migration." Molecular Biology of the Cell 15, no. 8 (2004): 3926–37. http://dx.doi.org/10.1091/mbc.e04-04-0317.

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Neutrophil (PMN) transepithelial migration is dependent on the leukocyte β2integrin CD11b/CD18, yet the identity of epithelial counterreceptors remain elusive. Recently, a JAM protein family member termed JAM-C was implicated in leukocyte adhesive interactions; however, its expression in epithelia and role in PMN-epithelial interactions are unknown. Here, we demonstrate that JAM-C is abundantly expressed basolaterally in intestinal epithelia and localizes to desmosomes but not tight junctions. Desmosomal localization of JAM-C was further confirmed by experiments aimed at selective disruption o

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Bogner, P., P. Skehan, S. Kenney, E. Sainz, M. A. Akeson, and S. J. Friedman. "Stabilization of intercellular contacts in MDCK cells during Ca2+ deprivation. Selective effects of monocarboxylic acids on desmosomes." Journal of Cell Science 103, no. 2 (1992): 463–73. http://dx.doi.org/10.1242/jcs.103.2.463.

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Short-chain monocarboxylic acids (MCAs) selectively protect desmosomal junctions of MDCK cells from disruption by chelating agents and low calcium medium. This effect occurs in the millimolar concentration range and increases inversely with carbon chain length (formate &gt; acetate = propionate &gt; butyrate &gt; isobutyrate &gt; isovalerate). The relative activity of MCAs does not correlate with their overall hydrophobicity or ability to chelate ions, or their effectiveness in lowering cytosolic pH. It exhibits chemical specificity and is dependent upon postconfluency culture

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Stappenbeck, T. S., and K. J. Green. "The desmoplakin carboxyl terminus coaligns with and specifically disrupts intermediate filament networks when expressed in cultured cells." Journal of Cell Biology 116, no. 5 (1992): 1197–209. http://dx.doi.org/10.1083/jcb.116.5.1197.

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Specific interactions between desmoplakins I and II (DP I and II) and other desmosomal or cytoskeletal molecules have been difficult to determine in part because of the complexity and insolubility of the desmosome and its constituents. We have used a molecular genetic approach to investigate the role that DP I and II may play in the association of the desmosomal plaque with cytoplasmic intermediate filaments (IF). A series of mammalian expression vectors encoding specific predicted domains of DP I were transiently expressed in cultured cells that form (COS-7) and do not form (NIH-3T3) desmosom

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Allen, E., Q. C. Yu, and E. Fuchs. "Mice expressing a mutant desmosomal cadherin exhibit abnormalities in desmosomes, proliferation, and epidermal differentiation." Journal of Cell Biology 133, no. 6 (1996): 1367–82. http://dx.doi.org/10.1083/jcb.133.6.1367.

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Desmogleins are members of the cadherin superfamily which form the core of desmosomes. In vitro studies indicate that the cytoplasmic domain of desmogleins associates with plakoglobin; however, little is known about the role of this domain in desmosome recognition or assembly in vivo, or about the possible relation of desmoglein mutations to epidermal differentiation and disease. To address these questions we used transgenic mouse technology to produce an NH2-terminally truncated desmoglein (Pemphigus Vulgaris Antigen or Dsg3) in cells known to express its wild-type counterpart. Within 2 d, ne

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Jones, J. C., K. M. Yokoo, and R. D. Goldman. "Further analysis of pemphigus autoantibodies and their use in studies on the heterogeneity, structure, and function of desmosomes." Journal of Cell Biology 102, no. 3 (1986): 1109–17. http://dx.doi.org/10.1083/jcb.102.3.1109.

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Pemphigus is an autoimmune disease that causes blistering of human epidermis. We have recently shown that autoantibodies in the serum of three pemphigus patients bind to desmosomes (Jones, J. C. R., J. Arnn, L. A. Staehelin, and R. D. Goldman, 1984, Proc. Natl. Acad. Sci. USA., 81:2781-2785), and we suggested that pemphigus blisters form, at least in part, from a specific antibody-induced disruption of desmosomes in the epidermis. In this paper, experiments are described that extend our initial observations. 13 pemphigus serum samples, which include four known pemphigus vulgaris (Pv) and four

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8

de Bruin, Alain, Reto Caldelari, Lina Williamson, et al. "Plakoglobin-dependent disruption of the desmosomal plaque in pemphigus vulgaris." Experimental Dermatology 16, no. 6 (2007): 468–75. http://dx.doi.org/10.1111/j.1600-0625.2007.00557.x.

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9

Chavez, Miquella G., Christian A. Buhr, Whitney K. Petrie, Angela Wandinger-Ness, Donna F. Kusewitt, and Laurie G. Hudson. "Differential Downregulation of E-Cadherin and Desmoglein by Epidermal Growth Factor." Dermatology Research and Practice 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/309587.

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Modulation of cell : cell junctions is a key event in cutaneous wound repair. In this study we report that activation of the epidermal growth factor (EGF) receptor disrupts cel : cell adhesion, but with different kinetics and fates for the desmosomal cadherin desmoglein and for E-cadherin. Downregulation of desmoglein preceded that of E-cadherinin vivoand in an EGF-stimulatedin vitrowound reepithelialization model. Dual immunofluorescence staining revealed that neither E-cadherin nor desmoglein-2 internalized with the EGF receptor, or with one another. In response to EGF, desmoglein-2 entered

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Caldelari, Reto, Alain de Bruin, Dominique Baumann, et al. "A Central Role for the Armadillo Protein Plakoglobin in the Autoimmune Disease Pemphigus Vulgaris." Journal of Cell Biology 153, no. 4 (2001): 823–34. http://dx.doi.org/10.1083/jcb.153.4.823.

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In pemphigus vulgaris (PV), autoantibody binding to desmoglein (Dsg) 3 induces loss of intercellular adhesion in skin and mucous membranes. Two hypotheses are currently favored to explain the underlying molecular mechanisms: (a) disruption of adhesion through steric hindrance, and (b) interference of desmosomal cadherin-bound antibody with intracellular events, which we speculated to involve plakoglobin. To investigate the second hypothesis we established keratinocyte cultures from plakoglobin knockout (PG−/−) embryos and PG+/+ control mice. Although both cell types exhibited desmosomal cadher

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Orzan, Olguța Anca, Liliana Gabriela Popa, Iulia Badiu, et al. "The Transition from Pemphigus Foliaceus to Pemphigus Vegetans—An Intriguing Phenomenon within the Spectrum of Autoimmune Blistering Diseases: A Case Report." Dermato 4, no. 2 (2024): 60–71. http://dx.doi.org/10.3390/dermato4020007.

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Pemphigus vegetans and pemphigus foliaceus are rare autoimmune blistering diseases characterized by the disruption of desmosomal adhesion proteins, particularly desmoglein 3 and desmoglein 1. We report the case of a 62-year-old male who presented initially with scaly red plaques posing several diagnostic challenges. A histopathological examination revealed subcorneal acantholysis, matching the suspected clinical diagnosis of pemphigus foliaceus. The patient progressed, developing vegetating plaques, and a new biopsy was performed. The new histopathological and direct immunofluorescence exams w

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12

Chidgey, Martyn, Cord Brakebusch, Erika Gustafsson, et al. "Mice lacking desmocollin 1 show epidermal fragility accompanied by barrier defects and abnormal differentiation." Journal of Cell Biology 155, no. 5 (2001): 821–32. http://dx.doi.org/10.1083/jcb.200105009.

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The desmosomal cadherin desmocollin (Dsc)1 is expressed in upper epidermis where strong adhesion is required. To investigate its role in vivo, we have genetically engineered mice with a targeted disruption in the Dsc1 gene. Soon after birth, null mice exhibit flaky skin and a striking punctate epidermal barrier defect. The epidermis is fragile, and acantholysis in the granular layer generates localized lesions, compromising skin barrier function. Neutrophils accumulate in the lesions and further degrade the tissue, causing sloughing (flaking) of lesional epidermis, but rapid wound healing prev

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Ojakian, G. K., D. R. Ratcliffe, and R. Schwimmer. "Integrin regulation of cell-cell adhesion during epithelial tubule formation." Journal of Cell Science 114, no. 5 (2001): 941–52. http://dx.doi.org/10.1242/jcs.114.5.941.

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The extracellular matrix plays an important role in regulation of epithelial development and organization. To determine more precisely the function of extracellular matrix in this process, the initial steps in collagen-mediated formation of epithelial tubules were studied using a model cell culture system. Previous studies have demonstrated that incubation of Madin-Darby canine kidney (MDCK) epithelial cells with a collagen gel overlay induces (beta)1 integrin-regulated epithelial remodeling accompanied by extensive cell rearrangements and formation of epithelial tubules. During epithelial rem

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14

Godsel, Lisa M., Adi D. Dubash, Amanda E. Bass-Zubek, et al. "Plakophilin 2 Couples Actomyosin Remodeling to Desmosomal Plaque Assembly via RhoA." Molecular Biology of the Cell 21, no. 16 (2010): 2844–59. http://dx.doi.org/10.1091/mbc.e10-02-0131.

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Plakophilin 2 (PKP2), an armadillo family member closely related to p120 catenin (p120ctn), is a constituent of the intercellular adhesive junction, the desmosome. We previously showed that PKP2 loss prevents the incorporation of desmosome precursors enriched in the plaque protein desmoplakin (DP) into newly forming desmosomes, in part by disrupting PKC-dependent regulation of DP assembly competence. On the basis of the observation that DP incorporation into junctions is cytochalasin D–sensitive, here we ask whether PKP2 may also contribute to actin-dependent regulation of desmosome assembly.

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15

Gasymov, E. K., R. V. Shadlinskaya та S. A. Israfilova. "Light and electron-microscopic study of epithelium covering free gingiva at various stages of chronic gingivitis in patients with β-thalassemia major". Kazan medical journal 99, № 4 (2018): 598–605. http://dx.doi.org/10.17816/kmj2018-598.

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Aim. Study of the nature and severity of reorganization of the structural elements of gingival epithelium in remission and exacerbation of chronic catarrhal sclerosing gingivitis in patients with β-thalassemia major at the light-microscopic and ultrastructural levels. Methods. From araldite-epon blocks of gingival biopsy specimens taken from 18 patients with β-thalassemia major, the semithin (1-2 μm) and ultrathin (35-70 nm) sections were obtained by means of ultramicrotome. Semi-thin sections were stained by trichrome. Viewing of stained and unstainted ultrathin sections was performed on an e

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16

Arden, Warwick A., Ronald F. Slocombe, John A. Stick, and Andrew H. Parks. "Morphologic and ultrastructural evaluation of effect of ischemia and dimethyl sulfoxide on equine jejunum." American Journal of Veterinary Research 51, no. 11 (1990): 1784–91. http://dx.doi.org/10.2460/ajvr.1990.51.11.1784.

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SUMMARY Morphologic changes in equine jejunal segments subjected to 1 hour of ischemia and 1 hour of reperfusion, and protective effects of systemic administration of dimethyl sulfoxide (dmso; 1 g/kg of body weight) were investigated in 18 ponies, using light microscopy and scanning and transmission electron microscopy. Ponies were allotted to 4 groups: group 1—control (n = 3); group 2—dmso (n = 3); group 3—ischemia (n = 6); and group 4—ischemia and dmso (n = 6). In each pony, 2 jejunal sections were evaluated. The first section was obtained prior to induction of ischemia, and the second was o

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Kim, Joon-Chul, Marta Pérez-Hernández, Francisco J. Alvarado, et al. "Disruption of Ca 2+ i Homeostasis and Connexin 43 Hemichannel Function in the Right Ventricle Precedes Overt Arrhythmogenic Cardiomyopathy in Plakophilin-2–Deficient Mice." Circulation 140, no. 12 (2019): 1015–30. http://dx.doi.org/10.1161/circulationaha.119.039710.

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Background: Plakophilin-2 (PKP2) is classically defined as a desmosomal protein. Mutations in PKP2 associate with most cases of gene-positive arrhythmogenic right ventricular cardiomyopathy. A better understanding of PKP2 cardiac biology can help elucidate the mechanisms underlying arrhythmic and cardiomyopathic events consequent to PKP2 deficiency. Here, we sought to capture early molecular/cellular events that can act as nascent arrhythmic/cardiomyopathic substrates. Methods: We used multiple imaging, biochemical and high-resolution mass spectrometry methods to study functional/structural pr

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Bandyopadhyay, Sheila, Edward M. Bonder, and Nan Gao. "Desmosome Disruption by Enteropathogenic E coli." Cellular and Molecular Gastroenterology and Hepatology 6, no. 2 (2018): 225–26. http://dx.doi.org/10.1016/j.jcmgh.2018.05.001.

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Mruk, Dolores D., Michele Bonanomi та Bruno Silvestrini. "Lonidamine-ethyl ester-mediated remodelling of the Sertoli cell cytoskeleton induces phosphorylation of plakoglobin and promotes its interaction with α-catenin at the blood–testis barrier". Reproduction, Fertility and Development 29, № 5 (2017): 998. http://dx.doi.org/10.1071/rd15378.

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Several compounds affect male fertility by disrupting the adhesion of germ cells to Sertoli cells, which results in the release of undeveloped germ cells into the seminiferous tubule lumen that are incapable of fertilising the ovum. Indazole carboxylic acids are one class of compounds exhibiting such effects and they have been investigated as non-hormonal contraceptives for potential human use. The aims of this study were to investigate the effects of lonidamine-ethyl ester, an indazole carboxylic acid, on spermatogenesis and cell junctions, in particular, desmosomes. We found two doses of lon

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Denning, M. F., A. P. Kowalczyk, J. E. Borgwardt, and K. J. Green. "Disruption of desmosomes by activated SRC family kinases." Journal of Dermatological Science 16 (March 1998): S3. http://dx.doi.org/10.1016/s0923-1811(98)83013-2.

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Stappenbeck, T. S., E. A. Bornslaeger, C. M. Corcoran, H. H. Luu, M. L. Virata, and K. J. Green. "Functional analysis of desmoplakin domains: specification of the interaction with keratin versus vimentin intermediate filament networks." Journal of Cell Biology 123, no. 3 (1993): 691–705. http://dx.doi.org/10.1083/jcb.123.3.691.

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We previously demonstrated that truncated desmoplakin I (DP I) molecules containing the carboxyl terminus specifically coalign with and disrupt both keratin and vimentin intermediate filament (IF) networks when overexpressed in tissue culture cells (Stappenbeck, T. S., and K. J. Green. J. Cell Biol. 116:1197-1209). These experiments suggested that the DP carboxyl-terminal domain is involved either directly or indirectly in linking IF with the desmosome. Using a similar approach, we have now investigated the behavior of ectopically expressed full-length DP I in cultured cells. In addition, we h

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Todorovic´, Viktor, Jennifer L. Koetsier, Lisa M. Godsel, and Kathleen J. Green. "Plakophilin 3 mediates Rap1-dependent desmosome assembly and adherens junction maturation." Molecular Biology of the Cell 25, no. 23 (2014): 3749–64. http://dx.doi.org/10.1091/mbc.e14-05-0968.

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The pathways driving desmosome and adherens junction assembly are temporally and spatially coordinated, but how they are functionally coupled is poorly understood. Here we show that the Armadillo protein plakophilin 3 (Pkp3) mediates both desmosome assembly and E-cadherin maturation through Rap1 GTPase, thus functioning in a manner distinct from the closely related plakophilin 2 (Pkp2). Whereas Pkp2 and Pkp3 share the ability to mediate the initial phase of desmoplakin (DP) accumulation at sites of cell–cell contact, they play distinct roles in later steps: Pkp3 is required for assembly of a c

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Sumigray, Kaelyn, Kang Zhou, and Terry Lechler. "Cell-Cell Adhesions and Cell Contractility Are Upregulated upon Desmosome Disruption." PLoS ONE 9, no. 7 (2014): e101824. http://dx.doi.org/10.1371/journal.pone.0101824.

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Mao, Xuming, Eun Jung Choi, and Aimee S. Payne. "Disruption of Desmosome Assembly by Monovalent Human Pemphigus Vulgaris Monoclonal Antibodies." Journal of Investigative Dermatology 129, no. 4 (2009): 908–18. http://dx.doi.org/10.1038/jid.2008.339.

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DiColandrea, Teresa, Tadashi Karashima, Arto Määttä, and Fiona M. Watt. "Subcellular Distribution of Envoplakin and Periplakin." Journal of Cell Biology 151, no. 3 (2000): 573–86. http://dx.doi.org/10.1083/jcb.151.3.573.

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Envoplakin and periplakin are two plakins that are precursors of the epidermal cornified envelope. We studied their distribution and interactions by transfection of primary human keratinocytes and other cells. Full-length periplakin localized to desmosomes, the interdesmosomal plasma membrane and intermediate filaments. Full length envoplakin also localized to desmosomes, but mainly accumulated in nuclear and cytoplasmic aggregates with associated intermediate filaments. The envoplakin rod domain was required for aggregation and the periplakin rod domain was necessary and sufficient to redistr

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Nedelcu, Roxana, Alexandra Dobre, Gabriela Turcu, et al. "Grover’s Disease Association with Cutaneous Keratinocyte Cancers: More than a Coincidence?" International Journal of Molecular Sciences 25, no. 17 (2024): 9713. http://dx.doi.org/10.3390/ijms25179713.

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Better mechanistic understanding of desmosome disruption and acantholysis in Grover’s disease (GD) may improve management of this disease. Recent molecular studies highlighted promising pathways to be explored by directly comparing GD and selected features of associated skin diseases. The association between GD and cutaneous keratinocyte carcinomas, the most prevalent non-melanoma skin cancers (NMSC), is not completely characterized. To review the medical literature regarding GD-associated cutaneous keratinocyte cancers, focusing on molecular features, pathophysiological mechanisms, and diseas

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Springer, Michael, Zeynep Aydin Burakgazi, Anastasiia Domukhovska та ін. "HIF-1α-Mediated Disruption of Cellular Junctions: The Impact of Hypoxia on the Tumor Microenvironment and Invasion". International Journal of Molecular Sciences 26, № 11 (2025): 5101. https://doi.org/10.3390/ijms26115101.

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Hypoxia is a critical factor affecting tissue homeostasis that dramatically alters the tumor microenvironment (TME) through genetic, metabolic, and structural changes, promoting tumor survival and proliferation. Hypoxia-inducible factor-1α (HIF-1α) plays a central role in this process by regulating hundreds of genes involved in the processes of tumorigenesis, angiogenesis, metabolic reprogramming, and immune evasion. This review provides a comprehensive examination of the role of HIF-1α in hypoxia and how hypoxia weakens intercellular junctions—including gap junctions, adherens junctions, tigh

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Alhajj, Mandy, and Sathees Chandra. "Pemphigus Vulgaris: A Comprehensive Presentation of the Desmosomal Adhesion Disrupting and Oral Blister Causing Multifactorial Autoimmune Disease." Journal of Experimental and Integrative Medicine 6, no. 4 (2016): 151. http://dx.doi.org/10.5455/jeim.020916.rw.017.

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Leclerc, E. A., A. Huchenq, N. R. Mattiuzzo, et al. "Corneodesmosin gene ablation induces lethal skin-barrier disruption and hair-follicle degeneration related to desmosome dysfunction." Journal of Cell Science 122, no. 15 (2009): 2699–709. http://dx.doi.org/10.1242/jcs.050302.

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Mahaparea, APK, G. Srinivas, D.V. Ramanjaneyulu, et al. "Etiology, Epidemiology, Pathophysiology, Histopathology, Diagnosis, Differential Diagnosis, Treatment and Prognosis of Squamous Cell Carcinoma in Human Beings." Journal of Advancement in Immunology 2, no. 1 (2025): 1–9. https://doi.org/10.5281/zenodo.15261332.

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<em>The incidence of squamous cell carcinoma, the second most prevalent skin cancer, is steadily increasing annually, which is a serious public health problem, especially in the United States. Mortality rates for cutaneous squamous cell carcinoma are comparable to those of melanoma, renal carcinoma, and oro</em><em> pharyngeal carcinoma in the central and southern regions of the United States. Timely surveillance, early diagnosis, and prompt treatment are </em><em>crucial to minimize morbidity </em><em>as well as mortality risks. </em><em> The mainstay of therapy is still surgical excisio

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Tilwani, Sarika, Karan Gandhi, Satya Narayan, Sri Rama Koti Ainavarapu та Sorab Nariman Dalal. "Disruption of desmosome function leads to increased centrosome clustering in 14‐3‐3γ‐knockout cells with supernumerary centrosomes". FEBS Letters 595, № 21 (2021): 2675–90. http://dx.doi.org/10.1002/1873-3468.14204.

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Andl, Claudia D. "The Misregulation of Cell Adhesion Components during Tumorigenesis: Overview and Commentary." Journal of Oncology 2010 (2010): 1–9. http://dx.doi.org/10.1155/2010/174715.

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Cell adhesion complexes facilitate attachment between cells or the binding of cells to the extracellular matrix. The regulation of cell adhesion is an important step in embryonic development and contributes to tissue homeostasis allowing processes such as differentiation and cell migration. Many mechanisms of cancer progression are reminiscent of embryonic development, for example, epithelial-mesenchymal transition, and involve the disruption of cell adhesion and expression changes in components of cell adhesion structures. Tight junctions, adherens junctions, desmosomes, and focal adhesion be

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Tervonen, Topi A., Shishir M. Pant, Johanna Englund, and Juha Klefström. "Abstract 5817: LKB1 overcomes RAS pathway-mediated loss of epithelial integrity." Cancer Research 83, no. 7_Supplement (2023): 5817. http://dx.doi.org/10.1158/1538-7445.am2023-5817.

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Abstract Oncogenic RAS pathway disassembles cell-cell and cell-basement membrane junctions, thus promoting epithelial cell motility and invasion. To find tumor proteomic changes responsible for the disrupting effects of RAS on epithelial integrity, we explored cBioportal cell line proteomics data across all cancer types for correlations between oncogenic KRAS or HRAS mutations and possible regulators of epithelial integrity. We found inverse correlation between these RAS mutations and tumor suppressor LKB1 protein levels in a cohort where LKB1 was not inactivated by a mutation. Furthermore, LK

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Madazimov, M. M., M. G. Teshaboev, and Z. Q. Raximov. "Structural features of face and neck skin in intraoperative cylinder tension." Traditional Medicine and Modern Medicine 02, no. 04 (2019): 165–69. http://dx.doi.org/10.1142/s2575900019500125.

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Objective: Recently, significant attention has been paid to the aesthetics of the skin, which has led to the emergence and development, in addition to traditional medical cosmetology, of areas such as aesthetic and plastic skin surgery, surgical cosmetology, and others. Methods: For light microscopy, samples from various sections of the skin of the face and neck (total 57 samples) subjected to stretching, obtained during surgery, were fixed in a 10–12% solution of neutral formalin. After appropriate treatment, the samples were poured into paraffin and 5–7-[Formula: see text]m-thick sections we

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Wang, Lan-Min, Yu-Ting Wang, and Wan-Xi Yang. "Engineered nanomaterials induce alterations in biological barriers: focus on paracellular permeability." Nanomedicine 16, no. 30 (2021): 2725–41. http://dx.doi.org/10.2217/nnm-2021-0165.

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Engineered nanoparticles (ENPs) are widely used in medical diagnosis and treatment, as food additives and as energy materials. ENPs may exert adverse or beneficial effects on the human body, which may be linked to interactions with biological barriers. In this review, the authors summarize the influences of four typical metal/metal oxide nanomaterials (Ag, TiO2, Au, ZnO nanoparticles) on the paracellular permeability of biological barriers. Disruptions on tight junctions, adhesion junctions, gap junctions and desmosomes via complex signaling pathways, such as the MAPK, PKC and ROCK signaling p

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Takahashi, K., J. Folmer, and P. A. Coulombe. "Increased expression of keratin 16 causes anomalies in cytoarchitecture and keratinization in transgenic mouse skin." Journal of Cell Biology 127, no. 2 (1994): 505–20. http://dx.doi.org/10.1083/jcb.127.2.505.

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Injury to epidermis and other stratified epithelia triggers profound but transient changes in the pattern of keratin expression. In postmitotic cells located at the wound edge, a strong induction of K6, K16, and K17 synthesis occurs at the expense of the keratins produced under the normal situation. The functional significance of these alterations in keratin expression is not known. Here, we report that overexpression of a wild-type human K16 gene in a tissue-specific fashion in transgenic mice causes aberrant keratinization of the hair follicle outer root sheath and proximal epidermis, and it

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Potempa, Sandra, and Anne J. Ridley. "Activation of Both MAP Kinase and Phosphatidylinositide 3-Kinase by Ras Is Required for Hepatocyte Growth Factor/Scatter Factor–induced Adherens Junction Disassembly." Molecular Biology of the Cell 9, no. 8 (1998): 2185–200. http://dx.doi.org/10.1091/mbc.9.8.2185.

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Hepatocyte growth factor/scatter factor (HGF/SF) stimulates the motility of epithelial cells, initially inducing centrifugal spreading of colonies followed by disruption of cell–cell junctions and subsequent cell scattering. In Madin–Darby canine kidney cells, HGF/SF-induced motility involves actin reorganization mediated by Ras, but whether Ras and downstream signals regulate the breakdown of intercellular adhesions has not been established. Both HGF/SF and V12Ras induced the loss of the adherens junction proteins E-cadherin and β-catenin from intercellular junctions during cell spreading, an

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Koch, P. J., M. G. Mahoney, G. Cotsarelis, K. Rothenberger, R. M. Lavker, and J. R. Stanley. "Desmoglein 3 anchors telogen hair in the follicle." Journal of Cell Science 111, no. 17 (1998): 2529–37. http://dx.doi.org/10.1242/jcs.111.17.2529.

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Little is known about the function of desmosomes in the normal structure and function of hair. Therefore, it was surprising that mice without desmoglein 3 (the autoantigen in pemphigus vulgaris) not only developed mucous membrane and skin lesions like pemphigus patients, but also developed hair loss. Analysis of this phenotype indicated that hair was normal through the first growth phase (‘follicular neogenesis’). Around day 20, however, when the hair follicles entered the resting phase of the hair growth cycle (telogen), mice with a targeted disruption of the desmoglein 3 gene (DSG3-/-) lost

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Toivola, D. M., R. D. Goldman, D. R. Garrod, and J. E. Eriksson. "Protein phosphatases maintain the organization and structural interactions of hepatic keratin intermediate filaments." Journal of Cell Science 110, no. 1 (1997): 23–33. http://dx.doi.org/10.1242/jcs.110.1.23.

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The importance of protein phosphatases in the maintenance of cytoskeletal structure is supported by the serious liver injury caused by microcystin-LR, a hepatotoxic inhibitor of type-1 and type-2A serine/threonine protein phosphatases. We used the microcystin-LR-induced cell injury as a model to study the roles of protein dephosphorylation in maintaining cytoskeletal structure and cellular interactions in primary rat hepatocyte cultures. Confocal microscopy revealed that the first visible effect of microcystin-LR is disruption of desmoplakin organization at the cell surface, indicating dissoci

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Arnoux, Valerie, Mayssaa Nassour, Annie L'Helgoualc'h, Robert A. Hipskind, and Pierre Savagner. "Erk5 Controls Slug Expression and Keratinocyte Activation during Wound Healing." Molecular Biology of the Cell 19, no. 11 (2008): 4738–49. http://dx.doi.org/10.1091/mbc.e07-10-1078.

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Reepithelialization during cutaneous wound healing involves numerous signals that result in basal keratinocyte activation, spreading, and migration, all linked to a loosening of cell–cell adhesion structures. The transcription factor Slug is required for this process, and EGF treatment of human keratinocytes induced activating phosphorylation of Erk5 that coincides with slug transcription. Accordingly, ectopic activation of Erk5 led to increased Slug mRNA levels and faster wound healing, whereas keratinocyte migration was totally blocked by Erk5 pathway inhibition. Expression of a shRNA specif

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Sumigray, Kaelyn D., Henry P. Foote, and Terry Lechler. "Noncentrosomal microtubules and type II myosins potentiate epidermal cell adhesion and barrier formation." Journal of Cell Biology 199, no. 3 (2012): 513–25. http://dx.doi.org/10.1083/jcb.201206143.

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During differentiation, many cells reorganize their microtubule cytoskeleton into noncentrosomal arrays. Although these microtubules are likely organized to meet the physiological roles of their tissues, their functions in most cell types remain unexplored. In the epidermis, differentiation induces the reorganization of microtubules to cell–cell junctions in a desmosome-dependent manner. Here, we recapitulate the reorganization of microtubules in cultured epidermal cells. Using this reorganization assay, we show that cortical microtubules recruit myosin II to the cell cortex in order to engage

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Vijayaraj, Preethi, Cornelia Kröger, Ursula Reuter, Reinhard Windoffer, Rudolf E. Leube, and Thomas M. Magin. "Keratins regulate protein biosynthesis through localization of GLUT1 and -3 upstream of AMP kinase and Raptor." Journal of Cell Biology 187, no. 2 (2009): 175–84. http://dx.doi.org/10.1083/jcb.200906094.

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Keratin intermediate filament proteins form cytoskeletal scaffolds in epithelia, the disruption of which affects cytoarchitecture, cell growth, survival, and organelle transport. However, owing to redundancy, the global function of keratins has not been defined in full. Using a targeted gene deletion strategy, we generated transgenic mice lacking the entire keratin multiprotein family. In this study, we report that without keratins, embryonic epithelia suffer no cytolysis and maintain apical polarity but display mislocalized desmosomes. All keratin-null embryos die from severe growth retardati

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Sowińska, Agnieszka, Yasser Morsy, Elżbieta Czarnowska, et al. "Transcriptional and Ultrastructural Analyses Suggest Novel Insights into Epithelial Barrier Impairment in Celiac Disease." Cells 9, no. 2 (2020): 516. http://dx.doi.org/10.3390/cells9020516.

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Disruption of epithelial junctional complex (EJC), especially tight junctions (TJ), resulting in increased intestinal permeability, is supposed to activate the enhanced immune response to gluten and to induce the development of celiac disease (CD). This study is aimed to present the role of EJC in CD pathogenesis. To analyze differentially expressed genes the next-generation mRNA sequencing data from CD326+ epithelial cells isolated from non-celiac and celiac patients were involved. Ultrastructural studies with morphometry of EJC were done in potential CD, newly recognized active CD, and non-c

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Labudova, Martina, Jana Tomaskova, Ludovit Skultety, Jaromir Pastorek, and Silvia Pastorekova. "The Nucleoprotein of Lymphocytic Choriomeningitis Virus Facilitates Spread of Persistent Infection through Stabilization of the Keratin Network." Journal of Virology 83, no. 16 (2009): 7842–49. http://dx.doi.org/10.1128/jvi.00309-09.

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ABSTRACT Lymphocytic choriomeningitis virus (LCMV) is a prototypic arenavirus containing a bisegmented single-stranded RNA genome with an ambisense coding strategy. MX is a noncytolytic LCMV strain with an in vitro host range restricted to only few cell lines. MX LCMV spreads via cell-cell contacts and causes persistent infection with high production of viral nucleoprotein (NP). Using a proteomic approach, we identified keratin 1 (K1), an intermediate filament network component, as a binding partner of the viral NP. The functional significance of this interaction has been examined by chemical

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Nolan, D. T., R. H. Hadderingh, F. AT Spanings, H. A. Jenner, and S. E. Wendelaar Bonga. "Acute temperature elevation in tap and Rhine water affects skin and gill epithelia, hydromineral balance, and gill Na+/K+-ATPase activity of brown trout (Salmo trutta) smolts." Canadian Journal of Fisheries and Aquatic Sciences 57, no. 4 (2000): 708–18. http://dx.doi.org/10.1139/f99-252.

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The effects of a 3-h temperature elevation of 7°C were studied for 29 days on the brown trout (Salmo trutta) smolt in tap water and in water from the lower Rhine. The effects in the skin were apparent at 3 h and included depletion of electron-dense vesicles and increased numbers of heavily stained desmosomes in the filament cells of the upper epidermis. Increased levels of apoptosis and necrosis occurred and were associated with leukocyte infiltration of the epidermis. Similar effects in the gill epithelium were mainly confined to the chloride cells. Highest levels of necrosis in skin and gill

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Koch, Peter J., M. G. Mahoney, Hiroyasu Ishikawa, et al. "Targeted Disruption of the Pemphigus Vulgaris Antigen (Desmoglein 3) Gene in Mice Causes Loss of Keratinocyte Cell Adhesion with a Phenotype Similar to Pemphigus Vulgaris." Journal of Cell Biology 137, no. 5 (1997): 1091–102. http://dx.doi.org/10.1083/jcb.137.5.1091.

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In patients with pemphigus vulgaris (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell–cell adhesion of keratinocytes in the basal and immediate suprabasal layers of stratified squamous epithelia. The pathology, at least partially, may depend on protease release from keratinocytes, but might also result from antibodies interfering with an adhesion function of Dsg3. However, a direct role of desmogleins in cell adhesion has not been shown. To test whether Dsg3 mediates adhesion, we genetically engineered mice with a targeted disruption of the DSG3 gene. DSG3 −/− mice had no DSG

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Roxas, Jennifer Lising, and V. K. Viswanathan. "Modulation of Intestinal Paracellular Transport by Bacterial Pathogens." Comprehensive Physiology 8, no. 2 (2018): 823–42. https://doi.org/10.1002/j.2040-4603.2018.tb00025.x.

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ABSTRACTThe passive and regulated movement of ions, solutes, and water via spaces between cells of the epithelial monolayer plays a critical role in the normal intestinal functioning. This paracellular pathway displays a high level of structural and functional specialization, with the membrane‐spanning complexes of the tight junctions, adherens junctions, and desmosomes ensuring its integrity. Tight junction proteins, like occludin, tricellulin, and the claudin family isoforms, play prominent roles as barriers to unrestricted paracellular transport. The past decade has witnessed major advances

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Trang, Phan Thi Thuc, Tran Van Anh, Tran Ngoc Dung, et al. "Ultrastructural characteristics of keloid: before and after surface irradiation with X-ray." Romanian Medical Journal 72, no. 2 (2025): 251–57. https://doi.org/10.37897/rmj.2025.2.20.

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Background and objectives. Keloid is a benign fibroproliferative disorder that commonly develops following skin trauma, often resulting in considerable physical and psychological distress. Despite numerous treatment modalities, recurrence rates remain high and outcomes suboptimal. This study aimed to characterize the ultrastructural features of keloid tissue and examine the effects of surface X-ray irradiation. Materials and methods. Eight keloid samples were obtained from patients at the Vietnam National Institute of Burns, with some undergoing surgical excision alone and others receiving add

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Kopan, R., G. Traska, and E. Fuchs. "Retinoids as important regulators of terminal differentiation: examining keratin expression in individual epidermal cells at various stages of keratinization." Journal of Cell Biology 105, no. 1 (1987): 427–40. http://dx.doi.org/10.1083/jcb.105.1.427.

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When human epidermal cells were seeded on floating rafts of collagen and fibroblasts, they stratified at the air-liquid interface. The suprabasal cells synthesized the large type II (K1) and type I (K10/K11) keratins characteristic of terminal differentiation in skin. At earlier times in culture, expression of the large type II keratins appeared to precede the expression of their type I partners. At later times, all suprabasal cells expressed both types, suggesting that the accumulation of a critical level of K1 keratin may be a necessary stimulus for K10 and K11 expression. Expression of the

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Eshel, I., N. Savion, and J. Shoham. "Analysis of thymic stromal cell subpopulations grown in vitro on extracellular matrix in defined medium. I. Growth conditions and morphology of murine thymic epithelial and mesenchymal cells." Journal of Immunology 144, no. 5 (1990): 1554–62. http://dx.doi.org/10.4049/jimmunol.144.5.1554.

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Abstract We report here the successful selective cultivation of murine thymic mesenchymal reticular cells (MTMC) and murine thymic epithelial cells (MTEC) grown on extracellular matrix in the presence of defined medium. The selective growth of these two cell types was based on 1) conditions of tissue disruption and 2) differential growth requirements. Both cell types were dependent on transferrin, high density lipoproteins, insulin, hydrocortisone, and epidermal growth factor, whereas MTMC was dependent also on selenium and 3,5,3'-triiodothyronine. The elimination of single factors or extracel

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