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Hedgehog and PDGF signaling intersect during postnatal lung development

ABSTRACT: Hedgehog and PDGF signaling intersect during postnatal lung development

PROVIDER: PRJNA853385 | ENA |

REPOSITORIES: ENA

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Primary lung fibroblasts treated with hedgehog agonist, purmorphamine

Project description:Postnatal tissue quiescence is generally thought to be a default state in the absence of a proliferative stimulus such as injury. We now demonstrate that in the lung, quiescence in the adult is an actively maintained state and is regulated by paracrine hedgehog signaling. Epithelial-specific deletion of Sonic Hedgehog during normal homeostasis results in a proliferative expansion of the adjacent lung mesenchyme. Injury to the lung epithelium results in decreased hedgehog activation, accompanied by proliferative expansion of the adjacent mesenchyme. Moreover, reconstitution of Hedgehog signaling during epithelial injury attenuated the proliferative expansion of the adjacent mesenchyme. Hedgehog signaling maintains lung quiescence by attenuating PDGF signaling through blocking post-translational processing of PDGF receptor Î±/Î² into the mature isoforms. These results indicate that in postnatal tissues, epithelial cells can actively maintain mesenchymal quiescence via paracrine hedgehog activation, and that imbalances in this pathway could lead to aberrant mesenchymal expansion and postnatal disease. Fibroblasts were isolated from mouse lungs and grown in culture in triplicate wells. Samples were treated with vehicle or purmorphamine 5um for 24 hours and RNA was isolated for microarray.

2016-07-03 | E-GEOD-61026 | biostudies-arrayexpress

Primary lung fibroblasts treated with hedgehog agonist, purmorphamine

Project description:Postnatal tissue quiescence is generally thought to be a default state in the absence of a proliferative stimulus such as injury. We now demonstrate that in the lung, quiescence in the adult is an actively maintained state and is regulated by paracrine hedgehog signaling. Epithelial-specific deletion of Sonic Hedgehog during normal homeostasis results in a proliferative expansion of the adjacent lung mesenchyme. Injury to the lung epithelium results in decreased hedgehog activation, accompanied by proliferative expansion of the adjacent mesenchyme. Moreover, reconstitution of Hedgehog signaling during epithelial injury attenuated the proliferative expansion of the adjacent mesenchyme. Hedgehog signaling maintains lung quiescence by attenuating PDGF signaling through blocking post-translational processing of PDGF receptor α/β into the mature isoforms. These results indicate that in postnatal tissues, epithelial cells can actively maintain mesenchymal quiescence via paracrine hedgehog activation, and that imbalances in this pathway could lead to aberrant mesenchymal expansion and postnatal disease.

2016-01-01 | GSE61026 | GEO

Hedgehog and PDGF signaling intersect during postnatal lung development

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

2023-01-26 | GSE207062 | GEO

Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [scRNA-seq]

Project description:HH inhibition reproduces the lung phenotype of PDGF pathway knockout lungs and results in profound effects on differentiation and gene expression of Pdgfra-expressing alveolar mesenchymal cells, in particular myofibroblasts.

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Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [bulk RNA-seq]

2023-01-26 | GSE207051 | GEO

Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [scRNA-seq]

Project description:Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [scRNA-seq]

| PRJNA853388 | ENA

Primary lung fibroblasts activated with constitutively active Smo

Project description:Postnatal tissue quiescence is generally thought to be a default state in the absence of a proliferative stimulus such as injury. We now demonstrate that in the lung, quiescence in the adult is an actively maintained state and is regulated by paracrine hedgehog signaling. Epithelial-specific deletion of Sonic Hedgehog during normal homeostasis results in a proliferative expansion of the adjacent lung mesenchyme. Injury to the lung epithelium results in decreased hedgehog activation, accompanied by proliferative expansion of the adjacent mesenchyme. Moreover, reconstitution of Hedgehog signaling during epithelial injury attenuated the proliferative expansion of the adjacent mesenchyme. Hedgehog signaling maintains lung quiescence by attenuating PDGF induced activation. These results indicate that in postnatal tissues, epithelial cells can actively maintains mesenchymal quiescence via paracrine hedgehog activation, and that imbalances in this pathway could lead to aberrant mesenchymal expansion and postnatal disease.

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Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [bulk RNA-seq]

Project description:Hedgehog signaling affects platelet-derived growth factor signaling mediated alveolar septum formation during postnatal lung development [bulk RNA-seq]

| PRJNA853371 | ENA

Indian Hedgehog Signaling in the Postnatal Growth Plate

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Platelet-derived growth factor receptor signaling is required for postnatal tendon growth

Project description:Platelet-derived growth factor receptor (PDGFR) signaling plays an important role in the embryonic formation of many different tissues. There is a family of PDGF isoforms which signal through the PDGF receptors α (PDGFRα) and β (PDGFRβ). PDGF regulates many key cellular processes of mesenchymal cell function including proliferation, differentiation, migration and extracellular matrix (ECM) synthesis. While PDGF has been used to enhance flexor tendon healing in vivo, its role in postnatal tendon growth has remained largely unexplored. To determine the importance of PDGFR signaling in postnatal tendon growth, we performed pharmacological blockade of PDGFRα and PDGFRβ, and then induced tendon growth via mechanical overload using the hindlimb synergist ablation model. Our hypothesis was that inhibition of PDGFR signaling will restrict normal growth of tendon tissue in response to mechanical loading.

2017-03-08 | GSE95794 | GEO

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