Biomedical subjects

P Petzelbauer

Publications and source records attributed to P Petzelbauer.

At least 19 recordsLinked to original sources

PubMed2001

Clinical and histopathological aspects of cutaneous mastocytosis.

The organ most frequently involved in mastocytosis is the skin. Cutaneous mastocytosis (CM) is classified according to clinical presentation and is further defined by onset of disease. CM tends to appear early in life but adult onset CM occurs. CM in children has a low incidence of systemic involvement whereas systemic mastocytosis occurs in >25% of CM in adults. Almost all patients with CM belong into the indolent category of the consensus revised classification (Valent et al., Diagnostic criteria and classification of mastocytosis: a consensus proposal. Leukemia Research 2001;25:603-625.) and thus have a good prognosis. CM of infancy and childhood frequently involutes spontaneously, CM of adults does not. The prevalence of the disease is unknown and familiar occurrence is very rare.

Adult↗

PubMed2001

Dimethylfumarate inhibits tumor-necrosis-factor-induced CD62E expression in an NF-kappa B-dependent manner.

Fumaric acid esters are thought to improve psoriasis by altering leukocyte, keratinocyte, and/or endothelial functions. To determine specificity, kinetics, and molecular mechanisms of different fumaric acid esters in their ability to inhibit endothelial cell activation, we analyzed CD62E and CD54 expression in endothelial cells in vivo and in vitro. In lesional skin of psoriatic patients, oral fumaric acid ester treatment resulted in a marked reduction of CD62E but not CD54 expression on dermal microvessels. Using human umbilical vein endothelial cells, dimethylfumarate almost completely inhibited tumor-necrosis-factor-induced CD62E, but not CD54 expression at concentrations < or = 70 microM, mimicking the situation in vivo. A 60 min dimethylfumarate preincubation was sufficient to block tumor-necrosis-factor-induced CD62E expression for up to 24 h. In contrast, equimolar concentrations of methylhydrogenfumarate, the hydrolysis product of dimethylfumarate, did not suppress tumor-necrosis-factor-induced CD62E expression. Likewise, all fumaric acid esters other than dimethylfumarate were ineffective. Using CD62E, NF-kappa B, or AP-1-responsive promoter constructs, dimethylfumarate inhibited tumor-necrosis-factor-induced activation of the CD62E and the NF-kappa B but not the AP-1 promoter construct. In summary, at a dose range < or = 70 microM, dimethylfumarate appeared to be a specific inhibitor of CD62E expression in an NF-kappa B-dependent manner.

Capillaries↗

PubMed2001

Residual expression of functional MHC class II molecules in twin brothers with MHC class II deficiency is cell type specific.

We examined major histocompatibility complex (MHC) class II expression in B cells, peripheral blood monocytes, activated T cells, epidermal Langerhans cells, monocyte-derived dendritic cells, dermal microvascular endothelial cells (DMEC) and fibroblasts of twin brothers with MHC class II deficiency. Although residual human leucocyte antigen (HLA)-DR expression was found on a subpopulation of epidermal Langerhans cells and a subset of peripheral blood monocyte-derived dendritic cells, the patients' B cells, monocytes and activated T cells were HLA-DR negative. After treatment with interferon-gamma (IFN-gamma), the patients' DMEC expressed HLA-DR but not -DP and -DQ at the protein and mRNA level, whereas IFN-gamma failed to induce HLA-DR expression on dermal fibroblasts. The patients' monocyte-derived dendritic cells were capable of processing and presenting tetanus toxoid to autologous T cells, and patient-derived DMEC induced the proliferation of allogeneic CD4(+) T cells in an MHC class II-restricted fashion, indicating that the observed residual MHC class II surface expression was functional. The findings reported show that the defect encountered in these patients is not necessarily expressed to the same extent in different cell lineages, which is relevant for the understanding of the patients' phenotype and also illustrates that only small amounts of MHC class II are needed to mount a functional cellular immune response in vivo.

Child↗

PubMed2001

Platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin cooperatively regulate fibroblast growth factor-induced modulations of adherens junction functions.

Cellular adherens junctions are formed by cadherins linked to proteins of the catenin family. In endothelial cells, not only vascular endothelial cadherin but also platelet endothelial cell adhesion molecule-1 localizes into junctions and associates with beta-catenin. To explore a putative cooperation of platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin, we analyzed transfectants expressing either platelet endothelial cell adhesion (CD31 cells) or vascular endothelial cadherin (CD144 cells) or both molecules (CD31/CD144 cells), and, for comparison, human umbilical vein endothelial cells. Basic fibroblast growth factor completely dissociated vascular endothelial cadherin/beta-catenin complexes and robustly moved beta-catenin into the nucleus in CD144 cells, whereas in CD31/CD144 cells as well as in human umbilical vein endothelial cells, fibroblast growth factor only partially dissociated the junctional complex followed by a significantly reduced nuclear translocation of beta-catenin. In contrast, in CD31 cells, the subcellular distribution of beta-catenin remained unaffected by fibroblast growth factor. As a functional consequence, fibroblast growth factor induced a complete collapse of the F-actin network in CD144 cells, a limited rearrangement of F-actin fibers in CD31/CD144 cells and no F-actin rearrangement in CD31 cells. We also analyzed the effect of fibroblast growth factor-induced rearrangement of junctions on junction permeability for leukocytes: in line with our observation that vascular endothelial cadherin was required for cells to respond to fibroblast growth factor, only in CD31/CD144 cells, but not in CD31 cells, leukocyte transmigration was significantly enhanced by fibroblast growth factor. In conclusion platelet endothelial cell adhesion molecule-1 cooperates with vascular endothelial cadherin in a mutual fashion; platelet endothelial cell adhesion molecule-1 reduces and temporarily limits fibroblast growth factor-induced dissociation of vascular endothelial cadherin/beta-catenin complexes, but requires vascular endothelial cadherin to control leukocyte transmigration in dependence of fibroblast growth factor.

Adherens Junctions↗

PubMed2001

Localized syringolymphoid hyperplasia with alopecia and anhidrosis.

We describe a female patient with a localized form of syringolymphoid hyperplasia with alopecia and anhidrosis (SLHA). This woman is the eleventh patient with this disease so far reported in the literature. She suffered from a slowly but continuously progressing single lesion on her right ankle. It took 7 years until the diagnosis of SLHA could be established. Many divergent diagnoses were assumed and different treatments were performed during this time. The final diagnosis was established by histopathology revealing syringotropic T-cell infiltrates. Clinical features were scattered brownish papules, which formed a sharply demarcated erythematous patch lacking hairs and sweat production. The progressive course of the disease and the unresponsiveness to treatments support the current view that SLHA is a syringotropic variant of mucinosis follicularis and therefore should be viewed as a facultative precursor lesion of mycosis fungoides. In our patient, during a 7-year follow-up, no T-cell lymphoma occurred. This case emphasizes the difficulties of establishing the diagnosis of SLHA, which requires cooperation between the dermatologist and dermatopathologist.

Adult↗

PubMed2001

A unique case of a benign disseminated angioproliferation combining features of Kaposi's sarcoma and diffuse dermal angioendotheliomatosis.

A female patient undergoing chronic hemodialysis had disseminated, violaceous, and partly ulcerated plaques develop on the trunk. Lesions had erupted simultaneously over a period of 4 weeks and resolved within 5 months after steroid treatment. By histopathology, the papillary dermis was densely filled with blood vessels lined by a single layer of differentiated endothelial cells, a growth pattern resembling diffuse dermal angioendotheliomatosis. In some areas, endothelial cells were spindle shaped and formed discontinuous lumina. Red blood cells were interspersed within these slits, giving the lesions a kaposiform appearance. By immunohistochemistry, endothelial cells reacted with the antibodies anti-von Willebrand factor, anti-CD31, and anti-CD34 and with the lectin Ulex europaeus-1. The course of the disease combined with the unusual histopathology makes this case a unique form of a benign disseminated kaposiform angioproliferation.

Disease Progression↗

PubMed2001

The prefabricated scapula flap consists of syngeneic bone, connective tissue, and a self-assembled epithelial coating.

The reconstruction of maxillary defects is a challenge in plastic surgery. The so-called prefabricated scapula flap consists of syngeneic bone covered with syngeneic dermis and is used to reconstruct maxillary defects. After placing these flaps into the oral cavity, they are reepithelialized within a short time period, raising the question of the cellular origin of the "neomucosa." We therefore obtained sequential biopsy samples of the prefabricated flap and of the flap after being placed into the oral cavity and analyzed the keratin expression profile of epithelial cells. We expected that after placing the prefabricated flap into the oral cavity, keratinocytes from adnexal structures of the dermal component of the graft would migrate onto the surface and reepithelialize the flap. Unexpectedly, reepithelialization occurred earlier. The flap had acquired a mucosa-like epithelium at the interface between the Gore-Tex coating and the dermis while still being positioned within the scapular region. The keratin expression profile of this epithelium was very similar to that of mucosal epithelium. Thus, the prefabricated scapula flap not only consisted of bone covered with connective tissue, but was also covered with epithelial cells derived from adnexal structures of the dermal graft. This seems to be the reason for the rapid restoration of an intact mucosa and the excellent outcome achieved with this surgical technique.

Adult↗

PubMed2000

Dermal microvascular endothelial cells express the 180-kDa macrophage mannose receptor in situ and in vitro.

Expression of the 180-kDa mannose receptor (MR) is mainly found on cells of the macrophage lineage. MR mediates the uptake of micro-organisms and host-derived glycoproteins. We demonstrate that endothelium of the human skin in situ and dermal microvascular endothelial cells (DMEC) in vitro expressed MR at both the protein and mRNA levels. In contrast, HUVEC were consistently negative for MR expression. DMEC internalized dextran as well as Escherichia coli by the way of MR into acidic phagosomes, only a few of which fused with CD63- and lysosomal-associated membrane glycoprotein-2-positive lysosomes. This contrasts with the situation in monocyte-derived dendritic cells, where almost all of the MR-Ag complexes reached CD63- and lysosomal-associated membrane glycoprotein-2-positive compartments, indicating differences in the phagolysosomal fusion rate between DMEC and dendritic cells. In conclusion, DMEC express functional MR, a finding that corroborates a role of skin endothelium in Ag capture/clearing.

Cell Membrane↗

PubMed2000

Endothelial adherens junctions.

The principle of the molecular organization of adherens junctions follows a uniform pattern, which is found in epithelial, muscular, neuroneal as well as in endothelial cells and is highly conserved among species. Transmembrane molecules of the cadherin family link to catenins, which anchor the adhesion plaque to the cytoskeleton. The kind of cadherin used in adherens junctions is cell-type specific, vascular endothelial (VE)-cadherin is specific for endothelial cells. The assembly and disassembly of the cadherin/catenin complex is dynamic and regulated by growth factors. The functional status of adherens junctions controls endothelial cell-to-cell adhesion, cell scattering, vessel morphogenesis and has intracellular signaling properties, thereby playing an important role in vasculogenesis and angiogenesis.

Adherens Junctions↗

PubMed1999

A standardized, a computer-assisted in vitro assay for the assessment of neutrophil transmigration across endothelial monolayers.

We describe an automated, observer-independent and highly reproducible assay for the quantification of transmigrated neutrophils across endothelial monolayers. Endothelial cells grown on collagen gels were loaded with a dye emitting red fluorescence. Neutrophils loaded with dye emitting green fluorescence were allowed to adhere to and transmigrate across endothelial monolayers. For quantification of adherent and migrated cells, randomly selected fields were scanned by confocal laser scan microscopy at defined depths within and below the endothelial monolayers. The images obtained were transferred into the public domain NIH image program and numbers and distribution of cells within scanned sectors were automatically calculated. We demonstrate that adherent neutrophils are easily discriminated from transmigrated cells; absolute numbers of migrated cells can be reproducibly calculated by counting cells at a depth of -20 microm, thus permitting evaluation of large-scale experiments: the efficacy of neutrophil transmigration depends on the level of endothelial activation after TNF stimulation and mAbs to cell surface adhesion molecules interfere with migration in a manner similar to that previously shown in in vivo experiments. This assay lends itself to the identification of molecules influencing in cell migration in each phase of EC activation and to the screening of pro- and anti-migratory properties of biological or pharmacological reagents.

Animals↗

PubMed1999

Immune complexes from vasculitis patients bind to endothelial Fc receptors independent of the allelic polymorphism of FcgammaRIIa.

UNLABELLED: Cutaneous leukocytoclastic vasculitis is characterized by the deposition of circulating immune complexes, neutrophil extravasation, and vessel destruction, but mechanisms of circulating immune complexes capture within postcapillary venules are unknown. We demonstrate that circulating immune complexes from sera of vasculitis patients bind to cultured endothelium in an Fc gamma receptor IIa-dependent fashion. In lesional skin, endothelial cells bind immunoglobulin G2 > immunoglobulin G3 and immunoglobulin G4, but not immunoglobulin G1, even before obvious neutrophil transmigration and vessel damage. As the human Fc gamma receptor IIa proteins exist in two allotypes (one with a histidine at position 131, which binds immunoglobulin G1, 2, 3 and the other with an arginine at position 131, which binds immunoglobulin G1, and 3, but is unable to bind immunoglobulin G2), we expected an altered prevalence of histidine 131 forms in vasculitis patients. Sequence analysis, however, revealed an equal distribution of allotypes in patients and controls. In conclusion, circulating immune complex binding to endothelial Fc gamma receptor IIa is among the initial steps in the development of vasculitis. Although immunoglobulin G2 is the predominant subtype precipitated at endothelial surfaces, it is not required for fixing circulating immune complexes to endothelium, because patients homozygote for Fc gamma receptor IIa-arginine 131 equally develop leukocytoclastic vasculitis as those bearing the Fc gamma receptor IIa-histidine 131 allele. As immunoglobulin G1 is virtually absent in leukocytoclastic vasculitis lesions and immunoglobulin G4 does not bind to both Fc gamma receptor IIa alleles, these complexes, in addition to immunoglobulin G2, should contain immunoglobulin G3 in order to fix to vascular Fc gamma receptor IIa, at least in persons homozygous for Fc gamma receptor IIa-arginine 131. KEYWORDS: CD32/immunoglobulin G subtypes/leukocytoclastic vasculitis/microvessels.

Alleles↗

PubMed1999

Peripheral lymph node addressins are expressed on skin endothelial cells.

The term "peripheral node addressins" describes a set of several endothelial adhesion molecules, which collectively bind to L-selectin and react with monoclonal antibody MECA-79. They regulate lymphocyte recirculation through peripheral nodes. Their expression is thought to be restricted to a specialized vascular segment within the node, called the high endothelial venule. In certain chronic skin diseases, however, postcapillary venules of the skin may also acquire a high endothelial venule-like morphology. Employing immunohistochemistry on cryostat sections, we found these skin endothelial cells - like peripheral node high endothelial venules - to be reactive with monoclonal antibody MECA-79. Tissue lysates from the same specimens were then analyzed by immunoprecipitation using recombinant human L-selectin Fc-chimeras followed by immunoblotting using monoclonal antibody MECA-79. In contrast to peripheral node endothelium, which mainly expressed peripheral node addressin moieties of molecular sizes 90-110 kDa and 160 kDa, endothelial cells in cutaneous T cell lymphoma skin lesions expressed an additional and not yet defined 220 kDa peripheral node addressin-like molecule. Most surprisingly, even in normal skin specimens, we found a distinct subset of endothelial cells located around hair follicles constitutively expressing 90-110 kDa peripheral node addressin-like moieties. It is intriguing to speculate that - in analogy to the role of peripheral node addressins in peripheral nodes - the induced expression of peripheral node addressins in chronic T cell mediated skin diseases is responsible for a sustained lymphocyte recruitment. The constitutive expression of peripheral node addressins on perifollicular endothelium may serve for a continuous lymphocyte recirculation through normal skin.

Antigens, Surface↗

PubMed1999

Vascular-endothelial cadherin (CD144)- but not PECAM-1 (CD31)-based cell-to-cell contacts convey the maintenance of a quiescent endothelial monolayer.

BACKGROUND: In vivo, all blood vessels are lined by a single layer of flattened noncycling endothelial cells. We tested the hypothesis that the maintenance of such a quiescent endothelial monolayer depends on homotypic contacts between not yet defined growth-inhibitory molecules located at interendothelial junctions. METHODS: ECV304 cells, which lack endogenous vascular endothelial cadherin (VE cadherin) or CD31 expression, were transfected with cDNA encoding for the respective proteins or with the empty vector. RESULTS: In VE cadherin transfectants, beta-catenin was targeted to junctional regions and the F-actin-based cytoskeleton formed parallel bundles reaching from one cell border to the other. In contrast, in CD31 transfectants and in empty vector cells, beta-catenin was dispersed throughout the cytoplasm, and F-actin formed short, plump and criss-cross bundles. On a two-dimensional plastic matrix, both, VE cadherin and CD31 transfectants formed clusters of polygonal cells, whereas in three-dimensional gels, only VE cadherin cells were able to form tubes. Empty vector cells grew in a fibroblast-like pattern and neither formed clusters nor tubes. Most importantly, whereas CD31 and empty vector cells grew on top of each other, formed polylayers and maintained cycling even after reaching confluence, VE cadherin cells strictly maintained a single layer of flattened cells and the numbers of cycling cells dramatically dropped after reaching a continuous monolayer. CONCLUSION: The insertion of VE cadherin into ECV304 cells produces a cell type which mimics endothelial growth characteristics seen in vivo.

Antigens, CD↗

PubMed1998

Fc epsilon receptor I on dendritic cells delivers IgE-bound multivalent antigens into a cathepsin S-dependent pathway of MHC class II presentation.

In this study, we elucidate the Fc epsilon RI-mediated Ag uptake and presentation mechanisms of dendritic cells (DC). We found that Fc epsilon RI-bound IgE, after polyvalent but not after monovalent ligation, is efficiently internalized into acidic, proteolytic compartments, degraded, and delivered into organelles containing MHC class II, HLA-DM, and lysosomal proteins. To follow the fate of the fragmented ligand, we sought to interfere with invariant chain (Ii) degradation, a process critical for peptide loading of nascent MHC class II molecules. We found DC to express cathepsin (Cat) S, a cysteine protease involved in Ii processing by B cells. Exposure of DC to a specific, active-site inhibitor of Cat S resulted in the loss of anti-Cat S immunoreactivity, led to the appearance of an N-terminal Ii remnant, and decreased the export of newly synthesized MHC class II to the DC surface. Furthermore, inactivation of Cat S as well as blockade of protein neosynthesis by cycloheximide strongly reduced IgE/Fc epsilon RI-mediated Ag presentation by DC. Thus, multimeric ligands of Fc epsilon RI, instead of being delivered into a recycling MHC class H pathway, are channeled efficiently into MIIC (MHC class II compartment)-like organelles of DC, in which Cat S-dependent Ii processing and peptide loading of newly synthesized MHC class II molecules occur. This IgE/Fc epsilon RI-dependent signaling pathway in DC may be a particularly effective route for immunization and a promising target for interfering with the early steps of allergen presentation.

Animals↗

PubMed1998

Interferon enhances tumor necrosis factor-induced vascular cell adhesion molecule 1 (CD106) expression in human endothelial cells by an interferon-related factor 1-dependent pathway.

Tumor necrosis factor (TNF) and interleukin 1 are known to initiate endothelial vascular cell adhesion molecule (VCAM)-1 transcription primarily by activating nuclear factor (NF)-kappaB, which translocates to the nucleus. In addition to two NF-kappaB elements found within the minimal cytokine-inducible VCAM-1 promoter, an interferon-related factor (IRF) element (IRF-1) has been identified close to the transcription initiation site, suggesting that cytokines that induce IRF-1 might affect VCAM-1 expression levels. We therefore investigated the effects of interferons (IFNs), which strongly induce IRF-1, on VCAM-1 transcription and expression. We show that IFN-alpha and -gamma enhance TNF-induced VCAM-1 mRNA transcription and protein expression in human endothelial cells. IFN enhancement of TNF-induced expression is also seen using chloramphenicol acetyl transferase reporter genes linked to the minimal cytokine inducible VCAM-1 promoter. Nuclear IRF-1 is the molecular basis of IFN enhancement, because (a) IFN plus TNF-treated cells displayed increased nuclear IRF-1 levels and increased IRF-1 binding to the VCAM-1 promoter, compared with cells treated with TNF alone; (b) kinetics of nuclear IRF-1 levels correlated with VCAM-1 mRNA levels; (c) transfection with an IRF-1 construct substituted for IFN treatment; and (d) transfection with an expression construct encoding IRF-2, a competitive inhibitor of IRF-1, reduced TNF-induced VCAM-1 expression. Our experiments show that IFN amplifies TNF-induced VCAM-1 expression at the transcriptional level by an IRF-1-dependent pathway.

Cell Compartmentation↗

PubMed1998

Granulocyte/macrophage colony-stimulating factor increases wound-fluid interleukin 8 in normal subjects but does not accelerate wound healing.

Granulocyte/macrophage colony-stimulating factor (GM-CSF) is thought to play an important part under conditions of impaired wound healing. This is not confirmed and it is also unknown whether GM-CSF affects wound healing in healthy subjects. We conducted a randomized, double-blind, placebo-controlled pilot study in 10 healthy volunteers. Triplicate wounds (10 x 10 x 0.5 mm) on the right and left upper thigh were made by a razor blade and injected with GM-CSF or a solvent control. Four of the 10 volunteers were re-examined after 2 months by investigating the healing of a new set of triplicate wounds injected with solvent control alone (controls). Factors measured were wound healing time, wound-fluid cytokines by enzyme-linked immunosorbent assay, wound-fluid inflammatory cells and dermal thickness by ultrasonography. Intradermal injection with 20 micrograms GM-CSF per wound caused significantly higher wound-fluid GM-CSF and interleukin 8 (IL-8) levels than in controls, but did not affect the time needed for wound closure (mean 11 days in all groups), dermal thickness, wound-fluid inflammatory cells or other wound-fluid cytokines, e.g. vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). Transforming growth factor (TGF) beta 1 and beta 2, epidermal growth factor (EGF), and beta-fibroblast growth factor (beta-FGF) were not measurable in any wound fluid. The lack of efficacy of exogenously delivered GM-CSF on wound healing in healthy subjects is probably based on the failure of GM-CSF to induce 'wound-healing cytokines' like PDGF, FGF, TGF, EGF or VEGF. However, GM-CSF increases IL-8 release, which is a potent chemotactic cytokine, indicating that GM-CSF might be of therapeutic value under conditions of impaired chemotaxis.

Adult↗

PubMed1998

MCP-1 and MIP-1alpha are most efficient in recruiting T cells into the skin in vivo.

To analyze T cell recruitment by chemokines in vivo, we used SCID mice grafted with human skin onto their backs and human T cells into their peritoneal cavities. rh MIP-1alpha and rh MCP-1, as well as mouse MCP-1, attracted significant amounts of human T cells into human skin grafts, whereas effects of rh RANTES, rh SDF-1, or rh IP-10 were minimal. Human T cells were found in a striking perivascular position exclusively at sites of human endothelium. None of the chemokines recruited human T cells across mouse endothelial barriers. For control purposes, chemokines were injected into the abdominal wall directly above the peritoneal cavity, where human T cells had been injected and were not subjected to flow. At this site all tested chemokines attracted human T cells to an equal extent. In summary, our experiments point towards an important role for MCP-1 and MIP-1alpha as T cell chemoattractants for skin inflammatory conditions.

Animals↗

PubMed1997

Endothelial cell tube formation depends on cadherin 5 and CD31 interactions with filamentous actin.

Capillary tube formation represents a specialized endothelial cell function and is a prerequisite for the establishment of a continuous vessel lumen. Tube formation is thought to depend on cell-cell adhesion molecules, but whereas cadherins, Ig superfamily proteins, and integrins have been considered as potential candidates, the specific proteins subserving this function are unknown. We identified cadherin 5 and CD31 as two molecules critical for endothelial cell tube formation. Using human dermal microvascular endothelial cells or human umbilical vein endothelial cells for an in vitro capillary tube formation assay or, for comparison, an in vivo wound healing model in SCID mice, we show that tube formation in vivo and in vitro were prevented by adhesion-blocking mAbs to both proteins when used in conjunction but not by either mAb alone. In addition, both mAbs but not each individual mAb blocked cytoplasmic filamentous actin (F-actin) reorganization that resulted in cytoplasmic F-actin clumps similar to those induced by cytochalasin D, suggesting that cadherin 5 and CD31 tune tube formation in concert with F-actin. Indeed, cytochalasin D blocked capillary tube formation but colchicine did not, the latter inhibiting microtubule but not F-actin assembly. Using immunoprecipitation methods, we show for the first time that not only cadherin 5 but also a portion of CD31 connects to beta-catenin, which is part of the adherens junction complex known to be linked to F-actin. In conclusion, we provide evidence that cadherin 5, CD31, beta-catenin, and F-actin shape a functional complex that controls endothelial cell tube formation.

Actin Cytoskeleton↗