Hedgehog-regulated genes in the chick coelomic epithelium
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA615212 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11424489.fastq.gz | Fastqsanger.gz | |||
| SRR11424490.fastq.gz | Fastqsanger.gz | |||
| SRR11424491.fastq.gz | Fastqsanger.gz | |||
| SRR11424492.fastq.gz | Fastqsanger.gz | |||
| SRR11424493.fastq.gz | Fastqsanger.gz |
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Project description:In the experimental group, the coelomic cavity of HHStage 12-13 chick embryos was electroporated with a plasmid expressing PatchedDLoop2 (a dominant negative hedgehog pathway inhibitor) and GFP. In the control group, a plasmid expressing GFP alone was electroporated. After 14 hours, embryos were dissociated into single cells, FACS sorted, and processed for RNAseq.
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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. 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
Project description:Coelomic epithelium (CE), or coelothelium, is a mesodermal-derived tissue lining coelomic cavities and enveloping inner organs in all coelomates, including vertebrates, where it forms both peritoneum and pericardium, as well as pleura, in mammals. Due to its histogenetic potential, CE is considered a key-tissue characterized by unique features. At present, in adult echinoderms, CE is supposed to play fundamental key roles acting as: 1) source of stem/multipotent cells (undifferentiated coelomocytes), particularly during regenerative phenomena (Candia Carnevali et al., 2009; Candia Carnevali and Burighel, 2010; Hernroth et al., 2010; García-Arrarás et al., 2011). 2) haematopoietic tissue, being the direct source of circulating elements (differentiated coelomocytes) including immune cells, indispensable elements during the first repair events of clotting and defence against pathogens (Boassche and Jangoux, 1976; Munoz-Chapuli et al., 2005; Pinsino et al., 2007). Despite these indications, the histological approach alone, microscopic or ultrastructural, is not sufficient to fully attribute a haematopoietic role to the CE and even the presumptive production/release process of stem/pluripotent cells from coelothelium during regeneration need to be confirmed as well. As a matter of fact, it is still unclear if the intense proliferation detectable in regenerating CE is functional to the production of wandering coelomocytes necessary to restore the post-traumatic fluid loss or rather to produce truly regeneration-competent cells used as building blocks of the regenerating tissues. In order to overcome some of these issues and deeply understand the complex physiological role of this epithelial tissue in echinoderm biology, it is important to integrate morphological evidences with detailed molecular data. In particular, proteomics is becoming a powerful tool to deepen the problem of cell and tissue functions during both tissue homeostasis and regeneration by depicting the existing protein activities involved in the regrowth processes. However, proteomics investigations focussed on echinoderm CE are quite limited. Specific molecular information are due to the works by Gabre and co-workers (2015) and by Kim and co-workers (2018), which are addressed to the characterization of CE transcriptome from the clonal starfish Coscinasterias muricata and the blue bat starfish Patiria pectinifera, respectively. The analysis of the biological processes associated to the transcripts identified in these studies suggests the involvement of CE in the development of anatomical units. More recently the CE proteome of the common starfish Asterias rubens was also published (Sharlaimova et al., 2021). Despite these evidences, there is a great lack of integrated multidisciplinary studies that can contribute to unravel the complex roles exerted by this tissue both in regeneration and other physiological processes. In order to partially unravel this gap, the present work is addressed to analyse the CE of the starfish Marthasterias glacialis in both standard physiological (homeostatic) and regenerating conditions, by combining histological/ultrastructural analyses with appropriate proteomics approaches, the former to provide a detailed cell and tissue perspective, the latter to contribute a base-line molecular view of CE multifunctional implications. This integrated approach can significantly help to shed new light into the intriguing role of this apparently simple but fundamental tissue.
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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.
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Project description:Epithelial Hedgehog (Hh) ligands regulate several aspects of fetal intestinal organogenesis and emerging data implicate the Hh pathway in inflammatory signaling in adult colon. We investigated the effects of chronic Hh inhibition in vivo and profiled molecular pathways acutely modulated by Hh signaling in the intestinal mesenchyme. Experiment Overall Design: E18.5 intestinal mesenchyme was isolated and cultured. Mesenchyme was treated with Sonic (Shh) or Indian (Ihh) hedgehog ligand or Vehicle (control) acutely to identify targets regulated by Hh signaling in intestinal mesenchyme.
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