PDGF induction of immediate early genes in NIH3T3 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE2196 | GEO | 2005/02/23
SECONDARY ACCESSION(S): PRJNA91261
REPOSITORIES: GEO
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Project description:This experiment was performed to identify immediate early genes that were induced by PDGF specifically through Src family kinases (SFKs), MEK1/2, or PI 3-K.
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Project description:Liver cirrhosis is a strong risk factor for the development of hepatocellular carcinoma (HCC), yet the mechanisms by which cirrhosis predisposes patients to tumorigenesis are not well understood. Transgenic mice expressing platelet-derived growth factor C (Pdgf-c) under the control of the albumin promoter provide a unique animal model that mimics the step-wise disease progression in humans from fibrosis to HCC. The livers of Pdgf-c Tg mice show evidence of liver injury, including inflammation, proliferation, fibrosis and steatosis, and as the mice age, angiogenesis and dysplasia. Eighty-five percent of these mice develop HCC spontaneously, and have reduced survival that is related to their liver pathology. Through measurement of protein, RNA, and histological markers, we provide evidence to support the hypothesis that changes in liver stromal cells play an essential role in tumorigenesis in this model. A paracrine signaling model is proposed where ectopic expression of Pdgf-c in hepatocytes results in activation of hepatic stellate cells, which subsequently activates endothelial and Kupffer cells. Activation of these non-parenchymal cells promotes the release of hepatocyte growth factors that, together with changes in extracellular matrix, lead to the formation of HCC. Pdgf-c Tg mice provide a useful pre-clinical model in which to test novel drugs for chronic liver disease and HCC that focus on blocking the processes that alter the liver's fibrotic microenvironment. Two strains of mice, C57BL/6 and C57/BL6 Pdgf-c transgenic, were analyzed to see if liver stromal cells play an essential role in tumorigenesis.
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Project description:Liver cirrhosis is a strong risk factor for the development of hepatocellular carcinoma (HCC), yet the mechanisms by which cirrhosis predisposes patients to tumorigenesis are not well understood. Transgenic mice expressing platelet-derived growth factor C (Pdgf-c) under the control of the albumin promoter provide a unique animal model that mimics the step-wise disease progression in humans from fibrosis to HCC. The livers of Pdgf-c Tg mice show evidence of liver injury, including inflammation, proliferation, fibrosis and steatosis, and as the mice age, angiogenesis and dysplasia. Eighty-five percent of these mice develop HCC spontaneously, and have reduced survival that is related to their liver pathology. Through measurement of protein, RNA, and histological markers, we provide evidence to support the hypothesis that changes in liver stromal cells play an essential role in tumorigenesis in this model. A paracrine signaling model is proposed where ectopic expression of Pdgf-c in hepatocytes results in activation of hepatic stellate cells, which subsequently activates endothelial and Kupffer cells. Activation of these non-parenchymal cells promotes the release of hepatocyte growth factors that, together with changes in extracellular matrix, lead to the formation of HCC. Pdgf-c Tg mice provide a useful pre-clinical model in which to test novel drugs for chronic liver disease and HCC that focus on blocking the processes that alter the liver's fibrotic microenvironment.
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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)
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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.
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