Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell Transcriptomes of RPE-specific AAV-GFP/AAV-PDGF-D mouse RPE-choroid complex

ABSTRACT: Purpose: PDGF-D is a potent angiogenic and immune-related factor. It has been demonstrated that PDGF-D play roles in the pathological process of ocular angiogenesis and degenerative diseases. In our previous study, we established a retinal pigment epithelial (RPE) cell-specifc AAV-PDGF-D/GFP mouse model to study PDGF-D's role in age-related macular degeneration (AMD). In this study, we utilized the single-cell transcriptiome seqeuncing technique to explore the cell types of immune cells attracted by PDGF-D overepxression using the same animal models, with emphases on the impact of PDGF-D overexpression on individual cell's behaviour.

ORGANISM(S): Mus musculus

PROVIDER: GSE193002 | GEO | 2023/12/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single-cell Transcriptomes of RPE-specific AAV-GFP/AAV-PDGF-D mouse RPE-choroid complex

Project description:Single-cell Transcriptomes of RPE-specific AAV-GFP/AAV-PDGF-D mouse RPE-choroid complex

| PRJNA794114 | ENA

Mouse RPE-Choroids mRNA profiles of 4-week subretinal injection of AAV-GFP/PDGF-D

Project description:Wet age-related macular degeneration (AMD) is a progressive degenerative disease and a leading cause of blindness in elderly population. AMD pathogenesis initiated by several signals generates cellular and molecular cross-talk, including complement pathway-mediated inflammation, macrophage activation, and upregulation of angiogenic and cytokine/chemokine pathways. However, the mechanism by which the complement system is activated in AMD is not well understood, although its components are found in the neovascular lesions of wet AMD patients. Here, we show that increased PDGF-D expression engaged both classical and alternative complement pathways and markedly increased chemokine and cytokine responses to activate macrophages, thereby triggering neuroinflammatory milieu and exacerbating pathological neovascularization. Pharmacological targeting of the complement C3a receptor using SB290157 alleviated neuroinflammation by blocking macrophage polarization and by inhibiting pathological choroidal neovascularization (CNV). Our study thus suggests that therapeutic strategies targeting both PDGF-D and complement-mediated inflammatory signals may open up new possibilities for the treatment of neovascular diseases.

2021-06-01 | GSE164972 | GEO

Mouse RPE-Choroids mRNA profiles of 4-week subretinal injection of AAV-GFP/PDGF-D

Project description:Mouse RPE-Choroids mRNA profiles of 4-week subretinal injection of AAV-GFP/PDGF-D

| PRJNA692714 | ENA

PDGF-hSyn Synaptosomes (vGlut FASS) nanoLC-MS/MS

Project description:This project studies the differential abundance of proteins at excitatory synapses of PDGF-hSyn mice (Masliah et al., 2000, Science), which are a model for Parkinson’s disease/dementia with Lewy bodies. The mice overexpress human alpha synuclein under the human PDGF promoter. Synapses were purified from animals expressing fluorescently tagged vGlut1 (vGlut1-Venus) using fluorescence activated synapse sorting (FASS; cf. Biesemann et al., 2014, EMBO J).

2019-09-02 | PXD006812 | Pride

PDGF and FGF treatment in E13.5 MEPMs II

2015-05-07 | GSE66484 | GEO

PDGF and FGF treatment in E13.5 MEPMs II

Project description:PDGF and FGF treatment in E13.5 MEPMs. 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates) 4 hr PDGF treated MEPMs (3 replicates), 4 hr FGF treated MEPMs (3 replicates), 1 hr PDGF + PD325901 treated MEPMs (2 replicates), 4 hr PDGF + PD325901 treated MEPMs (2 replicates), 1 hr FGF + PD325901 treated MEPMs (2 replicates), 4 hr FGF + PD325901 treated MEPMs (2 replicates), 1 hr PDGF + LY294002 treated MEPMs (2 replicates), 4 hr PDGF + LY294002 treated MEPMs (2 replicates), 1 hr FGF + LY294002 treated MEPMs (2 replicates), 4 hr FGF + LY294002 treated MEPMs (2 replicates)

2015-05-07 | E-GEOD-66484 | biostudies-arrayexpress

Gene expression profiling regulated by PDGF in pBSMCs

Project description:To explore global molecular changes in smooth muscle in response to PDGFR activation, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h. Total RNA were prepared, and analyzed using expression profiling, and subjected to bioinformatic and functional interrogation. To identify molecular signatures of bladder smooth muscle peturbed by PDGF, primary human bladder smooth muscle cells were treated with 1 nM PDGF-BB (hereafter PDGF) for 0, 4 or 24 h.

2014-10-06 | E-GEOD-52488 | biostudies-arrayexpress

A gene expression signature of PDGF-stimulated fibroblasts

Project description:Analysis of platelet-derived growth factor (PDGF)-stimulated fibroblasts. Results provide insight into novel pro-tumorigenic factors induced by PDGF-activation of fibroblasts.

2012-09-10 | GSE40720 | GEO

Dose-dependent dual roles of PDGF-BB–PDGFR-? in vascular remodeling and opposing effects of anti-PDGF drug-induced metastasis

Project description:Anti-PDGF agents are routinely used as a key component in front-line therapy for the treatment of various cancers. However, molecular mechanisms underlying their impact on vascular remodeling in relation to the dose issue remain poorly understood. Here we show that in high PDGF-BB-producing tumors, anti-PDGF drugs significantly inhibited tumor growth and metastasis by preventing pericyte (PC) loss and vascular permeability. Surprisingly, the same anti-PDGF-BB drugs promoted tumor cell dissemination and metastasis in PDGF-BB-low-producing or negative tumors by ablating PCs from tumor vessels. At the molecular level, we show that the PDGFR-? signaling pathway in PCs mediated the opposing effects and persistent exposure of PCs to PDGF-BB led to marked downregulation of PDGFR-?. Inactivation of the PDGFR-? signaling system led to decreased levels of integrin ?1?1, resulted in impaired adhesion of PCs to collagen I, IV and laminin, two principal extracellular matrix components in blood vessels for interaction with these integrins. Our data suggest that tumor PDGF-BB levels may serve as an important biomarker for selection of tumor-bearing hosts for beneficial therapy and unsupervised practice of this group of drugs could potentially promote tumor invasion and metastasis. Pericytes were isolated and treated with PDGF-BB or control for 5 days.

2013-07-22 | E-GEOD-46564 | biostudies-arrayexpress

Effect of PDGF-Ddstimulation on human tonsil ILC1

Project description:The effect of PDGF-DD on the gene expression of human tonsil ILC1 is unknown. We used microarray to determine the transcriptional differences between unstimulated and PDGF-DD-stimulated human tonsil ILC1.

2018-02-01 | GSE107043 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data