Disease relevance of Dsp

• To elucidate the changes, we conducted experimental infarction in rats and performed 3-dimensional analysis of the localization of gap junctions (connexin43), desmosomes (desmoplakin), adherens junctions (cadherin), and integrins (beta(1)-integrin) by immunoconfocal microscopy [1].

High impact information on Dsp

• Redistribution of adducin after addition of extracellular Ca++ is independent of formation of desmosomal and adherens junctions since assembly of adducin at contact sites requires lower concentrations of Ca++ and occurs more rapidly than redistribution of desmoplakin or vinculin [2].
• It is shown that the desmoplakin-containing structures are often associated with IF stained by antibodies to desmin, i.e., the characteristic type of IF present in these cells [3].
• Connexin43, desmoplakin, and cadherin were localized between grafted cardiomyocytes themselves and between grafted and host cardiomyocytes [4].
• In addition, we show that the sequence requirements for the recruitment of desmoplakin, another desmosomal plaque protein, differ and that a short (10 aa) segment of the desmocollin 1a tail, located close to the plasma membrane, is also required for the binding of plakoglobin, as well as of desmoplakin, and also for IF anchorage [5].
• Immunostaining for connexin 43 (Cx43) and for cell adhesion junction proteins (N-cadherin, catenins, and desmoplakin) in single- and double-label techniques was analyzed and quantified by confocal and electron microscopy [6].

Biological context of Dsp

• Keratin 8, keratin 18 and desmoplakin I/II are the major cytoskeleton-associated targets for microcystin-LR-induced phosphorylation [7].
• Specifically, we found that DHT treatment of CA25 cells resulted in a striking change in cell architecture, localization of desmoplakin to cell-cell boundaries, and an increase in alpha 6p integrin levels, a newly described marker of cell differentiation [8].
• Exposure of the renal epithelial cell lines NRK-52E and LLC-PK1 to 400 microM Bi(3+) also resulted in the disappearance of N-cadherin expression after 1 h, whereas ZO-1, E-cadherin, and Desmoplakin expression did not resolve before cell death at 24 h, thus confirming in vivo results [9].

Anatomical context of Dsp

• These observations show that anchorage at desmosomal plaques is not restricted to IF of the cytokeratin type and that IF composed of either cytokeratin or desmin, specifically attach, in a lateral fashion, to desmoplakin-containing regions of the plasma membrane [3].
• The newly formed ID, observed after 5 days, showed the presence of N-cadherin, catenins, and desmoplakin, low levels of Cx43, and absence of ultrastructurally discernible gap junctions [6].
• To examine this question, we have used immunoelectron and immunoconfocal microscopy to analyze the spatial distributions of gap junctional (connexin43), desmosomal (desmoplakin), and adherens junctional (N-cadherin) components during maturation of rodent and canine left ventricular myocardium [10].
• Confocal microscopy revealed that the first visible effect of microcystin-LR is disruption of desmoplakin organization at the cell surface, indicating dissociation of desmosomes [7].
• Rhodamine phalloidin was used to monitor the organizational state of the myofibrils and antibodies to desmoplakin and vinculin were used as markers for the presence of desmosomes and fasciae adherentes, respectively [11].

Other interactions of Dsp

• The localization of actin, myosin, tropomyosin, alpha-actinin, vinculin, and desmoplakin I/II was visualized by immunofluorescence microscopy [12].
• Immunocytochemical findings indicated that all cells expressed epithelial cell markers including cytoskeletal (cytokeratin and actin), basement membrane (laminin and collagen type IV) and junctional complex (ZO-1 and desmoplakin I+II) proteins at 33 degrees C. All cells expressed mRNA of cathepsin E, a pit cell marker [13].
• Changes in cytokeratin, vimentin and desmoplakin distribution during the repair of irradiation-induced lung injury in adult rats [14].

Analytical, diagnostic and therapeutic context of Dsp

• After treatment with NiCl2 (150 micrograms/ml) for 24 hr, the cytokeratin filaments and desmoplakin became focally detached from the cell cortex and retracted to form an aggregate around the nucleus [15].

References