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Angio-modulation in endothelial cells: an unexpected role of desmoglein-2 in regulating actin dynamics and its relevance to angiogenesis deregulation in systemic sclerosis

ABSTRACT: Gene expression study of DSG2 silenced human microvascular endothelial cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE21547 | GEO | 2012/10/01

SECONDARY ACCESSION(S): PRJNA126213

REPOSITORIES: GEO

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Angio-modulation in endothelial cells: an unexpected role of desmoglein-2 in regulating actin dynamics and its relevance to angiogenesis deregulation in systemic sclerosis

Project description:Gene expression study of DSG2 silenced human microvascular endothelial cells Affymetrix GeneChip Human Genome U133 Plus 2.0 Array were used to examine differentially expressed genes between normal microvascular endothelial cells and DSG2 silenced microvascular endothelial cells

2012-10-01 | E-GEOD-21547 | biostudies-arrayexpress

Desmoglein-2-integrin Beta-8 interaction regulates actin assembly in endothelial cells: deregulation in systemic sclerosis.

Project description:BackgroundThe inability of endothelial cells of patients affected by the diffuse form of Systemic sclerosis (SSc) to perform angiogenesis is a marker of the disease. We previously demonstrated that desmoglein-2 reduction is a major difference between (SSc)-microvascular endothelial cells (MVECs) and normal (N)-MVECs. Here we investigated the role of desmoglein-2 in human N-MVECs and SSc-MVECs angiogenesis.Methodology/principal findingsAngiogenesis was studied by Matrigel invasion, capillary morphogenesis in vitro and Matrigel plug assay in vivo. Gene profiling was studied by Affymetrix technology and signal transduction by Western blotting. Colocalization was validated by immunoprecipitation and confocal microscopy. SiRNAs were used to validate the roles of specific molecules. We observed that desmoglein-2 co-localizes with integrin-beta8 in N-MVECs. This complex is required to signal through Rac, FAK, SMAD1/5 and MAP-kinases, promoting an angiogenic program. Inhibition of desmoglein-2 by DSG2-siRNA impaired actin stress fibres formation, capillary morphogenesis in vitro and angiogenesis in vivo. Transcriptome profiling after DSG2 inhibition revealed alterations of several genes involved in actin organization. siRNA inhibition of integrin-beta8 and RAC2 also resulted into capillary morphogenesis impairment in N-MVECs, due to reduced expression of the same actin-assembly genes that were down-regulated by DSG2 silencing. SSc-MVECs showed down-regulation of the same genes in DSG2-siRNA treated N-MVECs, suggesting that impairment of desmoglein-2/integrin-beta8 complex contributes to angiogenesis derangement in SSc. Transfection of DSG2 in SSc-MVEC partially restored their angiogenic properties in vitro.Conclusions/significanceWe have shown that impairment of actin assembly as a result of desmoglein-2/integrin-beta8 complex formation is a major factor contributing to angiogenesis deregulation in Systemic sclerosis.

| S-EPMC3708925 | biostudies-literature

Desmoglein 2 is a crucial receptor for adenovirus infection of epithelial cells

Project description:We have identified desmoglein 2 (DSG2) as the primary high-affinity receptor used by adenovirus (Ad) serotypes Ad3, Ad7, and Ad14. These serotypes represent important human pathogens causing respiratory tract infections. In epithelial cells, adenovirus binding to DSG2 triggers events reminiscent of epithelial-to-mesenchymal transition, leading to transient opening of intercellular junctions. This improves access to receptors, e.g. CD46 and Her2/neu, that are trapped in intercellular junctions. In addition to complete virions, dodecahedral particles (PtDd) formed by viral penton and fiber in excess during viral replication, can trigger DSG2-mediated opening of intercellular junctions as shown by studies with recombinant Ad3 PtDd. Our findings shed light on adenovirus biology and pathogenesis and have implications for cancer therapy.

2010-12-08 | GSE24138 | GEO

Desmoglein 2 is a crucial receptor for adenovirus infection of epithelial cells

2010-12-08 | E-GEOD-24138 | biostudies-arrayexpress

Electrophysiological defects in a novel patient-derived stem cell model of desmoglein-2 mutant ARVC

Project description:Here we developed a novel human induced pluripotent stem cell (hiPSC) model of ARVC to gain insight into the electrical and biomolecular effects of desmoglein-2 (DSG2) mutation in cardiomyocytes. hiPSC-derived cardiomyocytes (hiPSC-CMs) were generated from peripheral blood mononuclear cells donated by an ARVC patient with a pathogenic variant in DSG2, c.2358delA.

2021-06-06 | GSE176209 | GEO

Cell-cycle and cancer-associated gene networks activated by Dsg2: evidence of cystatin A deregulation and a potential role in cell

Project description:Our recently generated transgenic mouse model in which Dsg2 is overexpressed in the epidermis observed notable epidermal hyperplasia. We described how Dsg2 altered a number of genes important in epithelial cell growth including the cysteine protease inhibitor cystatin A. We offer a novel pathway of cystatin A regulation involving Dsg2 and a potential crosstalk between Dsg2 and CSTA that modulates cell adhesion.

2014-10-30 | GSE62814 | GEO

Angiogenesis Dysregulation in the Pathogenesis of Systemic Sclerosis.

Project description:Systemic sclerosis is a chronic autoimmune connective tissue disease characterized by vascular injury and fibrosis and by an impaired angiogenesis which cannot ensure an efficient vascular recovery. Vascular injury is responsible for hypoxia and tissual ischemia which are the primary triggers for angiogenesis and are not able to induce a compensatory angiogenesis. This review article is focused on current knowledge on the mechanisms responsible for angiogenesis dysregulation in systemic sclerosis.

| S-EPMC5534276 | biostudies-literature

Transcription profiling of human microvascular endothelial cells in systemic sclerosis

Project description:Patients with the diffuse avascular form of Systemic Sclerosis (SSc) and healthy controls (N) were used as sources of microvascular endothelial cells (MVEC). MVEC were obtained from biopsies of involved skin of the hands in 6 SSc patients and from 6 healthy patients undergoing surgery for traumatic events at the hands. The controls were matched by age and sex to the SSc cases. All patients fulfilled the American College of Rheumatology criteria for SSc, as well as the criteria for the diffuse form of the disease.

2005-08-30 | E-MEXP-417 | biostudies-arrayexpress

Clinical Relevance of Liver Involvement in the Clinical Course of Systemic Sclerosis.

Project description:Liver involvement in systemic sclerosis (SSc) is rare. We evaluated the prevalence of liver fibrosis and hepatic autoimmunity in SSc patients in a retrospective observational cohort (97 SSc or mixed connective tissue disease with sclerodermic manifestations patients undergoing transient elastography, evaluating liver stiffness (LS) and controlled attenuation parameter (CAP), due to clinical indications along with biochemistry assessments and major antibodies associated to liver autoimmunity). Among them, 11 had LS ≥ 7.5 kPa and 5 showed an LS compatible with cirrhosis (LS ≥ 12.5 kPa). Predictors of LS ≥ 7.5 fibrosis were alcohol consumption (>14 or >7 alcoholic units/week for men and women, respectively), waist circumference (>102 or >88 cm for men and women, respectively), elevated alkaline phosphatase, and anti-La and anti-mitochondrial antibody (AMA) positivity. Six patients had CAP values compatible with severe steatosis (≥280 dB/m). Waist circumference, body mass index and diabetes mellitus were significant predictors of steatosis. Out of 97 patients, 19 were positive for AMA, 4 for anti-Sp100, 1 for anti-Gp210 and 7 were diagnosed with primary biliary cholangitis. Among SSc patients, hepatic fibrosis biomarkers and AMA prevalence are relatively high, suggesting the opportunity of performing a transient elastography and a screening for hepatic autoimmunity at diagnosis and/or during disease progression.

| S-EPMC8879679 | biostudies-literature

RNA-Sequencing of heart tissue obtained from cardiac specific-Dsg2-/- and wild-type (Dsg2+/+) mice at 2-weeks and 10-weeks of age

Project description:We studied how loss of the desmosome associated protein, desmoglein-2 (Dsg2), in the heart leads to Arrhythmogenic Cardiomyopathy with particular interest in the early stages of disease progression. Mice expressing the cardiac αMHC-Cre promoter were crossed with Dsg2 floxed mice in which exon 4-5 of the Dsg2 gene was flanked by loxP sites, resulting in Cre-mediated excision of Dsg2 in cardiac myocytes. Wild type Dsg2+/+ (Cre-, Dsg2flx/flx) and knockout Dsg2-/- (Cre+, Dsg2flx/flx) mice were generated. RNA-seq was performed on heart tissue obtained from wild-type and Dsg2-/- mice at 2-weeks and 10-weeks of age.

2021-07-22 | GSE153124 | GEO

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