Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119715 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We generated the transcriptional regulatory footprint of phthalimide neovascular factor 1 (PNF1)—a novel synthetic small molecule that exhibits significant in vitro endothelial potency and significant in vivo microvascular network expansion—by performing comparative microarray analysis on PNF1-stimulated (versus control) human microvascular endothelial cells (HMVEC) spanning 1-48 h post-supplementation. We subsequently applied network analysis tools (including substantial libraries of information regarding known associations among network components) to elucidate key signaling components and pathways involved in the PNF1 mechanism-of-action. We identified that PNF1 first induces function of the tumor necrosis factor-alpha (TNF-α) signaling pathway, which in turn affects transforming growth factor-beta (TGF-β) signaling.
2009-07-17 | GSE17119 | GEO
Project description:We report that decreased expression and activity of AhR exacerbates murine neovascular age-related macular degeneration, and increases cell migration and tube formation. The mechanism involves increased expression of pro-angiogenic mediators and altered matrix degradation. The results of our study suggest that the AhR signaling pathway may be important in multiple AMD related pathways. Gene expression analysis in the retinal pigment epithelium (RPE)-choroid tissue from AhR knockout mice contrasted against wild-type age-matched controls.
2015-01-01 | E-GEOD-56983 | biostudies-arrayexpress
Project description:We report that decreased expression and activity of AhR exacerbates murine neovascular age-related macular degeneration, and increases cell migration and tube formation. The mechanism involves increased expression of pro-angiogenic mediators and altered matrix degradation. The results of our study suggest that the AhR signaling pathway may be important in multiple AMD related pathways.
2015-01-01 | GSE56983 | GEO
Project description:Introduction: Autologous platelet concentrates (APC) are pro-angiogenic and can promote wound healing and tissue repair, also in combination with other biomaterials. However, challenging defect situations remain demanding. 3D bioprinting of an APC based bioink encapsulated in a hydrogel could overcome this limitation with enhanced physio-mechanical interface, growth factor retention/secretion and defect-personalized shape to ultimately enhance regeneration. Methods: This study used extrusion-based bioprinting to create a novel bioink of alginate/cellulose hydrogel loaded with thrombocyte concentrate. Chemico-physical testing exhibited an amorphous structure characterized by high shape fidelity. Cytotoxicity assay and incubation of human osteogenic sarcoma cells (SaOs2) exposed excellent biocompatibility. ELISA analysis confirmed pro-angiogenic growth factor release of the printed constructs, and co-incubation with HUVECS displayed proper cell viability and proliferation. Chorioallantoic membrane (CAM) assay explored the pro-angiogenic potential of the prints in vivo. Detailed proteome and secretome analysis revealed a substantial amount and homologous presence of pro-angiogenic proteins in the 3D construct. Results: This study demonstrated a 3D bioprinting approach to fabricate a novel bioink of alginate/cellulose hydrogel loaded with thrombocyte concentrate with high shape fidelity, biocompatibility, and substantial pro-angiogenic properties. Conclusion: This approach may be suitable for challenging physiological and anatomical defect situations when translated into clinical use.
2024-06-23 | PXD050629 | Pride
Project description:Neovascular AMD (nAMD) causes vision loss from destructive angiogenesis, termed choroidal neovascularization (CNV). Cx3cr1-/- mice display non-classical monocyte and microglia alterations, and increased CNV size, suggesting that non-classical monocytes may inhibit CNV formation. While Nr4a1-/- mice are deficient in non-classical monocytes, results are confounded by macrophage hyper-activation. Nr4a1se2/se2 mice lack a transcriptional activator, resulting in non-classical monocyte loss, without macrophage hyper-activation. We subjected Nr4a1-/- and Nr4a1se2/se2 mice to the laser-induced CNV model and performed multi-parameter flow cytometry. We found that both models lack non-classical monocytes, but only Nr4a1-/- mice displayed increased CNV area. Additionally, CD11c+ macrophages were increased in Nr4a1-/- mice. Single-cell transcriptomic analysis uncovered that CD11c+ macrophages were enriched from Nr4a1-/- mice and expressed a pro-angiogenic transcriptomic profile that was disparate from prior reports of macrophage hyper-activation. These results suggest that non-classical monocytes are dispensable during laser-induced CNV, and NR4A1 deficiency shifts the transcriptional profile toward a pro-angiogenic phenotype.
2024-02-28 | GSE239941 | GEO
Project description:The standard treatment for neovascular age-related macular degeneration (nAMD) consists of intravitreal anti-vascular endothelial growth factors (VEGF). However, for some patients, even maximal anti-VEGF treatment does notentirely suppress exudative activity. The goal of this study was to identify molecular biomarkers in nAMD with incomplete response to anti-VEGF treatment. Aqueous humor (AH) samples were collected from three groups of patients: 18 patients with nAMD responding incompletely to anti-VEGF, 19 patients affected by nAMD with normal treatment response, and 14 control patients without any retinopathy. Proteomic and multiplex analyses were performed on these samples. Proteomic analyses showed that nAMD patients with incomplete anti-VEGF response displayed an increased inflammatory response, complement activation, cytolysis, protein-lipid complex, and vasculature development pathways. Multiplex analyses revealed a significant increase of soluble vascular cell adhesion molecule-1 (sVCAM-1) [p=0.001], interleukin-6 (IL-6) [p=0.009], bioactive interleukin-12 (IL-12p40) [p=0.03], plasminogen activator inhibitor type 1 (PAI-1) [p=0.004], and hepatocyte growth factor (HGF)[p=0.004] levels in incomplete responders in comparison to normal treatment response. Interestingly, The same biomarkers showed a high intercorrelation with r2 values between 0.58 and 0.94. In addition, we confirmed by AlphaLISA the increase of sVCAM-1 [p<0.0001] and IL-6 [p=0.043] in incomplete responder group. Incomplete responders in nAMD are associated with activated angiogenic and inflammatory pathways. The residual exudative activity of nAMD despite maximal anti-VEGF treatment may be related to both angiogenic and inflammatory responses requiring specific adjuvant therapy.
2021-01-18 | PXD022471 | Pride
Project description:CYTL1 is a bona fide pro-angiogenic factor produced by endothelial colony forming cells (ECFCs), which mediates high angiogenic sprouting of ECFCs and vessel wall endothelial cells by autocrine and paracrine stimulation, respectively. To evaluate whether the signaling response to CYTL1 mimics the response to VEGF-A or induces unique signaling pathways in endothelial cells, we performed transcriptional profiling to compare the gene repertoire induced by CYTL1 to the repertoire triggered by VEGF-A in HUVEC under standard normoxic conditions or angiogensis stimulating hypoxic conditions.
2018-05-01 | GSE71967 | GEO
Project description:We generated the transcriptional regulatory footprint of phthalimide neovascular factor 1 (PNF1)—a novel synthetic small molecule that exhibits significant in vitro endothelial potency and significant in vivo microvascular network expansion—by performing comparative microarray analysis on PNF1-stimulated (versus control) human microvascular endothelial cells (HMVEC) spanning 1-48 h post-supplementation. We subsequently applied network analysis tools (including substantial libraries of information regarding known associations among network components) to elucidate key signaling components and pathways involved in the PNF1 mechanism-of-action. We identified that PNF1 first induces function of the tumor necrosis factor-alpha (TNF-α) signaling pathway, which in turn affects transforming growth factor-beta (TGF-β) signaling. HMVEC (Cambrex, Walkersville, MD, USA) were cultured in endothelial growth medium 2-microvascular (bulletkit, BioWhittaker, Walkersville, MD, USA) supplemented as directed with 5% fetal bovine serum. The cells (passage 9) were plated at 2.5 x 104 cells/cm2 at 37 degrees Celsius in a humidified chamber with 5% carbon dioxide. They were grown to confluence. After confluence, medium was refreshed, and 30 µM PNF1 or 0.6% dimethyl sulfoxide (DMSO) vehicle control was added to the sample. Total RNA from the PNF1 (n=1 at each timepoint) and control (n=1 at each timepoint) samples was isolated 1, 2, 4, 8, 16, 24 and 48 h post-supplementation using an RNeasy kit (Qiagen, Inc., Valencia, CA, USA) according to the manufacturer's protocol.
2009-07-17 | E-GEOD-17119 | biostudies-arrayexpress
Project description:Suppression of the FOXM1 transcriptional program via novel small molecule inhibition
| PRJNA253038 | ENA
Project description:We used single cell RNA-seq to comprehensively map all retinal microglia populations in a mouse model of oxygen-induced PR. We unveiled several unique types of PR-associated microglia (PRAM) and identified markers, signaling pathways, and regulons associated with these cells. Among these microglial subpopulations, we found a highly proliferative subset of cells with a high self-renewal capacity and a subset of cells with hypermetabolism that expresses high levels of activating microglia markers, glycolytic enzymes, and pro-angiogenic insulin-like growth factor 1. Immunohistochemical staining shows that PRAMs were spatially located within neovascular tufts. These unique microglial subtypes have the potential to promote retinal angiogenesis, which may have important implications for the future treatment of PR and other ocular diseases characterized by pathological angiogenesis.
2023-01-17 | GSE199792 | GEO