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BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

ABSTRACT: BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

PROVIDER: PRJNA1080533 | ENA |

REPOSITORIES: ENA

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BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

Project description:Retinal pathological angiogenesis (PA) is a common hallmark in proliferative retinopathies, including age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and retinopathy of prematurity (ROP). The mechanisms underlying PA is complex and incompletely understood. Using oxygen-induced retinopathy (OIR) mouse as a model, the role of extracellular matrix (ECM) protein biglycan (BGN) in PA was studied. Significant upregulation of BGN in the retina of OIR mice and in neovascular proliferative membranes of PDR patients was found. The reduction of BGN expression by Bgn-specific small interfering RNA (siRNA) effectively diminished retinal PA in OIR mouse. Subsequent analysis of the mouse OIR retinal single-cell RNA sequencing data from the Gene Expression Omnibus dataset (GSE150703) suggested pericyte as a source of BGN. This was verified using cultured retinal capillary pericytes. BGN expression in pericytes was highly sensitive to hypoxic stimulation. BGN stimulated retinal PA via the upregulation of C-X-C motif chemokine ligand 12 (CXCL12). Inhibition of the CXCL12-CXCR4 axis effectively diminished PA in OIR mouse. In conclusion, this study demonstrated the stimulatory role of BGN in retinal PA, identified the link between BGN and CXCL12 expression, and further highlighted the role of pericytes in retinal PA.

2025-02-10 | GSE259255 | GEO

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

2025-02-10 | GSE259254 | GEO

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

Project description:BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (mouse)

| PRJNA1080537 | ENA

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

Project description:BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes (human)

| PRJNA1080538 | ENA

BGN stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-02-10 | GSE259256 | GEO

Study on the mechanism of BGN in progression and metastasis of ccRCC

Project description:Based on multiple public databases, we investigated the expression level of BGN in ccRCC, its clinical significance, and its association with immune cells. Real-time fluorescence quantitative PCR was employed to validate BGN expression in tumor and adjacent normal tissues. Differential gene analysis, GO-KEGG analysis, and GSEA analysis were performed by RNA sequencing to elucidate the underlying signaling pathways. BGN knockdown cells were generated through lentiviral transfection to examine the impact of BGN on ccRCC. Cell proliferation, migration, and invasion were assessed using CCK8, colony formation, wound healing, Transwell migration, and invasion assays, respectively. Results: Our findings from database analysis and polymerase chain reaction (PCR) revealed a significant upregulation of BGN expression in kidney cancer tissues compared to normal tissues. Further analysis demonstrated a correlation between high BGN expression and ccRCC progression and immune infiltration. In vitro experiments confirmed that BGN silencing effectively inhibited cell proliferation, migration, and invasion of ccRCC. Mechanistically, these effects may be mediated through the MAPK signaling pathway. Conclusion: BGN potentially plays a pivotal role in the progression and metastasis of ccRCC, possibly acting through the MAPK signaling pathway. Therefore, BGN holds promise as a potential therapeutic target for ccRCC.

2024-09-01 | GSE264075 | GEO

Research on Downstream Binding Proteins of PlexinB1 in Human Brain Vascular Pericytes

Project description:Age-related macular degeneration (AMD) is a prevalent neuroinflammation condition and the leading cause of irreversible blindness among the elderly population. Smoking significantly increases AMD risk, yet the mechanisms remain unclear. Here, we investigated the role of Sema4D-PlexinB1 axis in the progression of AMD, in which Sema4D-PlexinB1 is highly activated by smoking. Using patient-derived samples and mouse models, we discovered that smoking increased the presence of Sema4D on the surface of CD8+ T cells that migrated into the choroidal neovascularization (CNV) lesion via CXCL12-CXCR4 axis and interacted with its receptor PlexinB1 on choroidal pericytes. This led to ROR2-mediated PlexinB1 phosphorylation and pericytes activation, hence disrupted vascular homeostasis and promoted neovascularization. Inhibition of Sema4D reduced CNV and improved the benefit of anti-VEGF treatment. In conclusion, this study unveils the molecular mechanisms through which smoking exacerbates AMD pathology, and presents a potential therapeutic strategy by targeting Sema4D to augment current AMD treatments.

2025-01-26 | PXD059165 | Pride

Comparative bulk RNAseq analysis of CXCL12-deficient bone marrow stromal cells (BMSCs), Cxcl12-GFP+ BMSCs versus CXCL12-deficient Cxcl12-GFP+ BMSCs.

Project description:We revealed the unique molecular signature characterizing CXCL12-deficient Cxcl12-GFP+ bone marrow stromal cells.

2020-10-27 | GSE160158 | GEO

Comparative bulk RNAseq analysis of CXCL12-deficient bone marrow stromal cells (BMSCs), Cxcl12-GFP+ BMSCs versus CXCL12-deficient Cxcl12-GFP+ BMSCs.

Project description:Comparative bulk RNAseq analysis of CXCL12-deficient bone marrow stromal cells (BMSCs), Cxcl12-GFP+ BMSCs versus CXCL12-deficient Cxcl12-GFP+ BMSCs.

| PRJNA672120 | ENA

BGN promotes epithelial migration in mammary gland development and breast cancer metastasis through activation of WNT signaling

Project description:This study investigates the role of Biglycan (BGN) in promoting epithelial migration during mammary gland development and breast cancer metastasis. Using in vitro and in vivo models, including a 3D organoid migration assay and single-cell RNA sequencing, we demonstrate that BGN enhances the interaction between WNT3A and FZD6, activating the WNT signaling pathway. This activation promotes epithelial cell migration and breast cancer metastasis. The findings provide new insights into breast cancer metastasis mechanisms and identify BGN as a potential therapeutic target.

2024-10-19 | GSE279436 | GEO

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