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Human fibroblast stimulation with PDGF-BB or b-FGF

ABSTRACT: We analyzed gene expression in human fibroblasts stimulated by platelet-derived growth factor-BB (PDGF-BB) or basic fibroblast growth factor (bFGF) for 1h and 24h. The results of two independent experiments were merged. SAM analysis identified 116 relevant probe sets. Hierarchical clustering of these probe sets showed divergent early gene regulation by PDGF and FGF but overlapping late response. We first analyzed genes commonly regulated by PDGF-BB and b-FGF more than 2 fold after 24h of stimulation and we found that these two growth factors repressed FOXO. We then focused on the early gene expression response induced by both growth factors. We performed a fold change analysis and found 114 probe sets regulated by PDGF-BB and 42 probe sets regulated by b-FGF, 37 of which were shared between the two gene lists . Keywords: Time course, cell Treatment comparison

ORGANISM(S): Homo sapiens

PROVIDER: GSE14256 | GEO | 2009/03/16

SECONDARY ACCESSION(S): PRJNA111211

REPOSITORIES: GEO

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Transcription profiling of human fibroblasts stimulated with PDGF-BB or b-FGF

Project description:We analyzed gene expression in human fibroblasts stimulated by platelet-derived growth factor-BB (PDGF-BB) or basic fibroblast growth factor (bFGF) for 1h and 24h. The results of two independent experiments were merged. SAM analysis identified 116 relevant probe sets. Hierarchical clustering of these probe sets showed divergent early gene regulation by PDGF and FGF but overlapping late response. We first analyzed genes commonly regulated by PDGF-BB and b-FGF more than 2 fold after 24h of stimulation and we found that these two growth factors activated SREBP and E2F and repressed FOXO. We then focused on the early gene expression response induced by both growth factors. We performed a fold change analysis and found 114 probe sets regulated by PDGF-BB and 42 probe sets regulated by b-FGF, 37 of which were shared between the two gene lists . We found by data mining that both PDGF-BB and b-FGF activated AP-1 and NF-kB. Next we analyzed genes specifically regulated by PDGF-BB and found that STATs are specifically activated by PDGF and not by FGF. Experiment Overall Design: Human foreskin fibroblasts (AG01518) were cultured (1.5E6 cells/10 cm dish) in MEM medium with 10% fetal calf serum and glutamine for 24h, then washed and incubated for 47h in serum-free medium. Cells were stimulated for 1h by PDGF-BB (25ng/ml) or b-FGF (10ng/ml, + heparine 50 microg/ml). Alternatively, cells were incubated for 24h in starvation medium and treated for 24h with growth factors, or left untreated for 48h in serum-free medium (control treatment). Experiment Overall Design: Two biological replicates were performed

2009-03-20 | E-GEOD-14256 | biostudies-arrayexpress

PDGF-BB modulates hematopoiesis and tumor angiogenesis by inducing erythropoietin production in stromal cells.

Project description:The platelet-derived growth factor (PDGF) signaling system contributes to tumor angiogenesis and vascular remodeling. Here, we show PDGF-BB markedly induces erythropoietin (EPO) mRNA and protein expression by targeting the PDGFR-beta+ stromal and perivascular compartments. In mouse tumor models, PDGF-BB-induced EPO promotes tumor growth via two mechanisms: 1) paracrine stimulation of tumor angiogenesis by directly inducing endothelial cell proliferation, migration, sprouting and tube formation; and 2) endocrine stimulation of extramedullary hematopoiesis leading to increased oxygen perfusion and protection against tumor-associated anemia. Similarly, delivery of an adenovirus-PDGF-BB to tumor-free mice markedly increases EPO production and hematopoietic parameters. An EPO blockade specifically attenuates PDGF-BB-induced tumor growth, angiogenesis and hematopoiesis. At the molecular level, we show that the PDGF-BB-PDGFR-beta signaling system activates EPO promoter via in part transcriptional regulation of ATF3 by possible association with c-Jun and SP1. These findings uncover a novel mechanism of PDGF-BB-induced tumor growth, angiogenesis and hematopoiesis.

2011-12-04 | GSE33717 | GEO

PDGF-BB modulates hematopoiesis and tumor angiogenesis by inducing erythropoietin production in stromal cells.

2011-12-04 | E-GEOD-33717 | biostudies-arrayexpress

Dose-dependent dual roles of PDGF-BB–PDGFR-β 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-β signaling pathway in PCs mediated the opposing effects and persistent exposure of PCs to PDGF-BB led to marked downregulation of PDGFR-β. Inactivation of the PDGFR-β signaling system led to decreased levels of integrin α1β1, 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.

2013-07-22 | GSE46564 | 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

Next Generation Sequencing Fascilitates Quantitative Analysis of Differential Gene Expression in Human Pericytes treated with PDGF-BB

Project description:PDGF-BB:PDGFRβ signalling in brain pericytes is critical to the development, maintenance and function of a healthy blood-brain barrier (BBB). Furthermore, BBB impairment and pericyte loss in Alzheimer’s disease (AD) is well documented. We used tissue microarrays from control and AD brains to determine if PDGF-BB:PDGFRβ signalling components were altered in AD, and found that there was a reduction in vascular expression of PDGFB. We hypothesised that reduced PDGF-BB:PDGFRβ signalling in pericytes may have an impact on functions related to the BBB. We therefore tested the effects of PDGF-BB on primary human brain pericytes in vitro to define important signalling pathways and outcomes related to BBB function. Pericytes demonstrate a biphasic response to PDGF-BB, predominantly dependent on Akt and ERK. We determined that the actions of PDGF-BB are on-target at PDGFRβ, leading to internalisation and degradation of PDGFRβ. Using pharmacological inhibitors, we dissected distinct aspects of the PDGF-BB response that are controlled by ERK and Akt pathways. PDGF-BB promotes the proliferation of pericytes and protection from toxic stimuli through ERK signalling. In contrast, PDGF-BB:PDGFRβ signalling through Akt and NF-κB augments pericyte-derived inflammatory secretions. It may therefore be possible to supplement PDGF-BB or small molecule agonists to stabilise the cerebrovasculature in AD.

2021-11-30 | GSE189712 | GEO

Genes induced by PDGF-BB in cells lacking Signal Transducer and Activator of Transcription-1 (Stat1)

Project description:Comparison of gene expression between Stat1+/- and Stat1-/- dermal fibroblasts or vascular smooth muscle cells after treatment with PDGF-BB for one hour.

2020-06-13 | GSE152342 | GEO

The gene expression profile of PDGF-treated neural stem cells corresponds to partially differentiated neurons and glia

Project description:Understanding and controlling stem cell differentiation in vitro is critical for the development of stem cell-based therapies. We have previously shown that platelet-derived growth factor AA (PDGF-AA) stimulates the expansion of neuronal progenitors from neural stem cells, but is unable to replace fibroblast-growth factor 2 (FGF-2) as a stem cell mitogen. In the present study, we compared gene expression in neural stem cells that were grown in the presence of FGF-2 to that of cells cultured with PDGF-AA or in the absence of growth factor, which induces differentiation. Most of the transcripts enriched in FGF-2-treated cells were connected to cell division (70%) and showed limited overlap with previously described stem cell transcriptional signatures. PDGF-AA significantly regulated 156 genes, 146 of which were also modified by differentiation in the absence of growth factor. The latter condition affected the expression of 153 additional genes which were regulated less than two fold by PDGF-AA. Among the genes induced by differentiation was the PDGF-A gene itself, suggesting that in the absence of exogenously added growth factors, cells make their own PDGF-AA in an autocrine manner. In addition, we identified several poorly characterized transcripts that were highly regulated and may play a role in stem cell differentiation. Our results suggest that the genetic program elicited by PDGF-AA is not unique, but an intermediate between the ones of FGF-2-cultured stem cells and differentiated cells. These observations are compatible with the hypothesis that PDGF-AA induces a partial differentiation of neural stem cells, which retain the ability to proliferate. Keywords: treatment comparison

2006-03-12 | GSE3251 | GEO

Microassay analysis of the lncRNAs expression profile in human aortic vascular smooth muscle cells(hAoSMCs) treated with PDGF-BB at 24 h.

Project description:Atherosclerosis is the most important mechanism of cardiovascular and cerebrovascular diseases and has become one of the most serious diseases that threaten human health. Vascular smooth muscle cells (VSMCs) are the main cellular components that constitute the structure of the blood vessel wall. The excessive proliferation and migration are pivotal pathological basis of atherosclerosis, in-stent restenosis, pulmonary hypertension and other vascular proliferative diseases. PDGF-BB is a potent proliferative agent for VSMCs, but the specific mechanism of PDGF-BB signaling pathway involved in biological processes such as proliferation and migration of VSMCs is not elusive.

2023-10-22 | GSE186313 | GEO

Role of ZHX2 in VSMCs [RNA-seq]

Project description:Primary rat VSMCs were infected with Ad-Control and Ad-ZHX2 and stimulated with PDGF-BB of 24h. RNAseq and differential expression analysis were performed to investigate the role of ZHX2 in VSMCs.

2023-10-07 | GSE244564 | GEO

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