Expression of beta 2 integrin (CD18) in embryonic mouse and chicken heart

Oliveira, Laser Antônio Machado; Baker, Robert K.; Klewer, Scott E.; Kitten, Gregory T.

doi:10.1590/s0100-879x2010000100005

Cited by 5 publications

(7 citation statements)

References 37 publications

(43 reference statements)

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“…Over the last decades, as evidence demonstrated, CD11c + DCs may involve in angiogenesis. α X β2 Integrin expression in endothelial cells was already reported both in vitro and in vivo . Coukos et al reported that CD11c + DCs may contribute to ovarian carcinogenesis by exhibiting simultaneous expression of both endothelial and leukocyte markers.…”

Section: Introductionmentioning

confidence: 94%

“…α X β2 Integrin expression in endothelial cells was already reported both in vitro 18 and in vivo. 19 Coukos et al 20 reported that CD11c + DCs may contribute to ovarian carcinogenesis by exhibiting simultaneous expression of both endothelial and leukocyte markers. Salvi et al 21 found that CD11c + DCs may serve as the main VEGF-A-producing cells in human reactive secondary lymphoid organs, promoting the inflammatory angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Integrin alpha x stimulates cancer angiogenesis through PI3K/Akt signaling–mediated VEGFR2/VEGF‐A overexpression in blood vessel endothelial cells

Wang

Yang

Fan

et al. 2018

J of Cellular Biochemistry

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Integrin alpha x (ITGAX), a member of the integrin family, usually serves as a receptor of the extracellular matrix. Recently, accumulating evidence suggests that ITGAX may be involved in angiogenesis in dendritic cells. Herein, we report a direct role of ITGAX in angiogenesis during tumor development. Overexpression of ITGAX in human umbilical vein endothelial cells (HUVECs) enhanced their proliferation, migration, and tube formation and promoted xenograft ovarian tumor angiogenesis and growth. Further study showed that overexpression of ITGAX activated the PI3k/Akt pathway, leading to the enhanced expression of c‐Myc, vascular endothelial growth factor‐A (VEGF‐A), and VEGF receptor 2 (VEGFR2), whereas, the treatment of cells with PI3K inhibitor diminished these effects. Besides, c‐Myc was observed to bind to the VEGF‐A promoter. By Co‐Immunoprecipitation (Co‐IP) assay, we manifested the interaction between ITGAX and VEGFR2 or the phosphorylated VEGFR2. Immunostaining of human ovarian cancer specimens suggested that endothelial cells of micro–blood vessels displayed strong expression of VEGF‐A, c‐Myc, VEGFR2, and the PI3K signaling molecules. Also, overexpression of ITGAX in HUVECs could stimulate the spheroid formation of ovarian cancer cells. Our study uncovered that ITGAX stimulates angiogenesis through the PI3K/Akt signaling–mediated VEGFR2/VEGF‐A overexpression during cancer development.

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Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Integrin alpha x stimulates cancer angiogenesis through PI3K/Akt signaling–mediated VEGFR2/VEGF‐A overexpression in blood vessel endothelial cells

Wang

Yang

Fan

et al. 2018

J of Cellular Biochemistry

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“…They consist of non-covalently linked heterodimers, which are composed of α and β subunits. The β2 integrin subfamily consists of the β2 subunit (also termed CD18) in combination with one of four different α (CD11) subunits: αL (CD11a), αM (CD11b), αX (CD11c), or αD (CD11d) (Oliveira et al, 2010). The β2 integrin is encoded by ITGB2.…”

Section: Discussionmentioning

confidence: 99%

Identification and validation of immune-related genes and immune cell infiltration in preeclampsia

Chen

Han

Zhang

et al. 2022

Preprint

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Preeclampsia (PE) is a complex multisystem disease, and its etiology remains unclear. The aim of this study was to identify potential immune-related diagnostic genes for PE, analyze the role of immune cell infiltration in PE. We used the dataset GSE25906 from Gene Expression Omnibus and immune-related genes from the ImmPort database. The differentially expressed genes (DEGs) were identified using the “limma” package, and the differentially expressed immune-related genes (DEIGs) were extracted from the DEGs and immune-related genes using Venn diagrams. The potential functions of DEIGs were determined. Furthermore, the protein–protein interaction network was obtained from the STRING database, and it was visualized using the Cytoscape software. Least absolute shrinkage and selection operator logistic regression and seven machine learning algorithms were used to verify the diagnostic markers of PE and build a predicting model. The model was validated using datasets GSE66273 and GSE75010. Finally, CIBERSORT was used to evaluate the infiltration of immune cells in PE tissues. Six genes (ACTG1, ENG, IFNGR1, ITGB2, NOD1, and SPP1) were identified. Datasets GSE66273 and GSE75010 were used to validate the model, and the area under the curve was 0.77 and 0.82, respectively. Immune cell infiltration analysis revealed an increase in plasma cells and gamma delta T cells and a decrease in resting natural killer cells in the high score group according to the predictive model risk values. We developed a risk model to predict PE and proved that immune imbalance at the maternal–fetal interface plays a key role in the pathogenesis of PE.

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Section: Discussionmentioning

confidence: 99%

Identification and Validation of Immune-Related Genes and Immune Cell Infiltration in Preeclampsia

Chen

Han

Zhang

et al. 2021

Preprint

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Background Preeclampsia (PE) is a complex multisystem disease and its etiology remains unclear. The aim of this study was to identify potential immune-related diagnostic genes for PE, analyze the role of immune cell infiltration in PE, and explore the mechanism underlying PE-induced disruption of immune tolerance at the maternal-fetal interface. Methods We used the PE dataset GES25906 from Gene Expression Omnibus and immune-related genes from ImmPort database. The differentially expressed genes (DEGs) were identified using the “limma” package, and the differentially expressed immune-related genes (DEIGs) were extracted from the DEGs and immune-related genes using Venn diagrams. The potential functions of DEIGs were determined by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Furthermore, the protein–protein interaction network was obtained from the STRING database, and it was visualized using Cytoscape software. Least absolute shrinkage and selection operator logistic regression was used to verify the diagnostic markers of PE and build a predicting model. The model was validated using datasets GSE66273 and GSE75010. Finally, CIBERSORT was used to evaluate the infiltration of immune cells in PE tissues. Results Six genes (ACTG1, ENG, IFNGR1, ITGB2, NOD1, and SPP1) enriched in Th17 cell differentiation, cytokine-cytokine receptor interaction, innate immune response, and positive regulation of MAPK cascade pathways were identified, and a predicting model was built. Datasets GSE66273 and GSE75010 were used to validate the model, and the area under the curve was 0.8333 and 0.8107, respectively. Immune cell infiltration analysis revealed an increase in plasma cells and gamma delta T cells and a decrease in resting natural killer cells in the high score group according to the predictive model risk values. Conclusions We developed a risk model to predict PE and proved that immune imbalance at the maternal-fetal interface plays a key role in the pathogenesis of PE.

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Expression of beta 2 integrin (CD18) in embryonic mouse and chicken heart

Cited by 5 publications

References 37 publications

Integrin alpha x stimulates cancer angiogenesis through PI3K/Akt signaling–mediated VEGFR2/VEGF‐A overexpression in blood vessel endothelial cells

Integrin alpha x stimulates cancer angiogenesis through PI3K/Akt signaling–mediated VEGFR2/VEGF‐A overexpression in blood vessel endothelial cells

Identification and validation of immune-related genes and immune cell infiltration in preeclampsia

Identification and Validation of Immune-Related Genes and Immune Cell Infiltration in Preeclampsia

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