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Late chick lung development

ABSTRACT: Type IV collagen is the main component of the basement membrane which gives strength to the blood-gas barrier. In avians the formation of the blood-gas barrier happens rapidly and before hatching. We have performed a microarray expression analysis in late chick lung development and found that COL4A1 and COL4A2 were among the most significantly upregulated genes during the formation of the avian blood-gas barrier. Our study showed that type IV collagen and therefore the basement membrane play fundamental roles in coordinating alveolar morphogenesis. Four developmental stages of chick lung maturation (E14, E15, E16, E18). Three biological replicates per time point.

ORGANISM(S): Gallus gallus

SUBMITTER: Maria Loscertales

PROVIDER: E-GEOD-72385 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Late chick lung development

Project description:Type IV collagen is the main component of the basement membrane which gives strength to the blood-gas barrier. In avians the formation of the blood-gas barrier happens rapidly and before hatching. We have performed a microarray expression analysis in late chick lung development and found that COL4A1 and COL4A2 were among the most significantly upregulated genes during the formation of the avian blood-gas barrier. Our study showed that type IV collagen and therefore the basement membrane play fundamental roles in coordinating alveolar morphogenesis.

2015-11-01 | GSE72385 | GEO

Caspase-3 cleaves extracellular vesicle proteins during auditory brainstem development

Project description:Sound localization requires extremely precise development of auditory brainstem circuits, the molecular mechanisms of which are largely unknown. We previously demonstrated a novel requirement for non-apoptotic activity of the protease caspase-3 in chick auditory brainstem development. Here, we used mass spectrometry to identify proteolytic substrates of caspase-3 during chick auditory brainstem development. Functional annotation analysis revealed that our caspase-3 substrates were enriched more than two-fold for proteins associated with extracellular vesicles (EVs), membrane-bound nanoparticles that function in intercellular communication. The proteome of EVs isolated from the auditory brainstem contained caspase-3 and was highly enriched for the caspase-3 substrates identified here. Additionally, we identified two caspase-3 substrates with known functions in axon guidance, namely Neural Cell Adhesion Molecule (NCAM) and Neuronal-glial Cell Adhesion Molecule (Ng-CAM), that were found in auditory brainstem EVs and expressed in the auditory pathway alongside cleaved caspase-3. Taken together, these data suggest a novel developmental mechanism whereby caspase-3 influences auditory brainstem circuit formation through the proteolytic cleavage of EV proteins.

2020-10-16 | PXD021728 | Pride

T7-SAGE transcriptome of cleft versus end bud epithelial cells of embryonic mouse salivary glands

Project description:Mus musculus embryonic submandibular salivary glands from embryonic day 12.5 embryos were laser microdissected to isolate epithelial cells from regions adjacent to forming clefts or from the peripheral end bud region. The isolated region-specific samples were then subjected to T7-SAGE transcriptome analysis. Toluidine blue-stained cryostat sections of embryonic day 12.5 submandibular salivary glands were used for laser microdissection using an LMD system (Leica) with a pulsed UV laser on an upright automated microscope. A total of approximately 500 cells from a region immediately adjacent to a forming cleft or from a peripheral end bud region were excised by the laser and transferred to caps of 0.5 ml PCR tubes. SAGE libraries were constructed from the microdissected cleft and bud epithelia cells. SAGE tags were identified using the National Center for Biotechnology Information (NCBI) tag map set for UniGene.

2010-06-16 | E-GEOD-22374 | biostudies-arrayexpress

Transcription profiling of human stromal samples prepared from 15 normal/DCIS and 7 IDC tumor specimens reveals bone-marrow-derived mesenchymal stem cells promote breast cancer metastasis

Project description:tumor microenviroment facilitates metastatic spread by eliciting reversible changes in the phenotypes of cancer cells Experiment Overall Design: expression array of stromal samples prepared from 15 normal/DCIS and 7 IDC tumor specimans

2009-03-14 | E-GEOD-8977 | biostudies-arrayexpress

Transcription profiling of human breast tissue tumors vs. normal tissue

Project description:bulk breast tumor RNA from patient; Abstract: Sporadic basal-like cancers (BLC) are a distinct class of human breast cancers that are phenotypically similar to BRCA1-associated cancers. Like BRCA1-deficient tumors, most BLC lack markers of a normal inactive X chromosome (Xi). Duplication of the active X chromosome and loss of Xi characterized almost half of BLC cases tested. Others contained biparental but nonheterochromatinized X chromosomes or gains of X chromosomal DNA. These abnormalities did not lead to a global increase in X chromosome transcription but were associated with overexpression of a small subset of X chromosomal genes. Other, equally aneuploid, but non-BLC rarely displayed these X chromosome abnormalities. These results suggest that X chromosome abnormalities contribute to the pathogenesis of BLC, both inherited and sporadic. total 62 sample incudes 43 tumor, 7 normal breast and 12 normal organelle Experiment Overall Design: compare expression of tumor to normal breast tissue

2008-06-16 | E-GEOD-7904 | biostudies-arrayexpress

Ash1 ChIP-chip data from murine Embyonic Stem cells

Project description:Ash1 is a Trithorax Group (TrxG) protein with histone methyl transferase activity that is associated with gene activation. Here we use ChIP-chip to determine the occupancy of Ash1 at promoters in murine embryonic stem cells. This dataset includes singlet ChIP-chip data targeting Ash1 in murine Embryonic stem cells.

2010-05-14 | E-GEOD-20063 | biostudies-arrayexpress

RNAseq of epidermis reconstructed from TSG-6-/- and TSG-6+/+ immortalized N/TERT keratinocytes and stimulated or not with interleukins 4 and 13 for 48h

Project description:TNFα-stimulated gene 6 (TSG-6) is an anti-inflammatory protein. In human epidermis, TSG-6 is secreted in extracellular matrix where it interacts with hyaluronan (HA). However, their functions are not well understood. In this study, immortalized N/TERT keratinocytes were edited by CRISPR/Cas9, used to reconstruct in vitro epidermis (RHE) and stimulated or not with interleukins 4 and 13 for 48h to mimic atopic dermatitis (AD). Two TSG-6-/- clones (respectively TSG-6-/- (a) and TSG-6-/- (b)) harboring major deletions in both alleles were selected and compared to TSG-6+/+ cells. Epidermis reconstructed from TSG-6-/- (a) and TSG-6-/- (b) exhibit normal differentiation process and morphology but show an increased HA leakage in the underlying culture medium of both TSG-6-/- RHE compared to TSG-6+/+ tissues, especially in conditions that mimic AD. While IL-4/13 treatment of RHE induces regulation of genes associated with AD, the absence of TSG-6 don’t seem to show any major transcriptomic regulation.

2021-12-30 | E-MTAB-10095 | biostudies-arrayexpress

The Skin Barrier Defects Caused by Keratinocyte-Specific Deletion of ADAM17 or EGFR are Based on Highly Similar Proteome and Degradome Alterations

Project description:ADAM17 and EGFR are essential key players for epidermal integrity. Keratinocyte-specific deletion of ADAM17 in mice results in pronounced alterations in terminal differentiation of keratinocytes leading to severe epidermal barrier defects with enhanced transepidermal water loss. Thereby, mice deficient for ADAM17 in keratinocytes phenocopy mice with a keratinocyte-specific deletion of EGFR, highlighting the role of ADAM17 as a “ligand sheddase”, as it sheds membrane bound EGFR ligands from the cell surface and finally modulates EGFR signaling. In this study we aim for the first proteomic / degradomic approach to characterize the disruption of the ADAM17-EGFR signaling axis and its consequences for epidermal barrier formation. Proteomic profiling of the epidermal proteome of mice deficient for either ADAM17 or EGFR in keratinocytes at postnatal days 3 and 10 revealed highly similar protein alterations for ADAM17 and EGFR deficiency. These include massive proteome alterations of structural and regulatory components important for barrier formation, like transglutaminases, involucrin, S100 protein family members and S100 fused-type proteins, such as filaggrin, filaggrin-2 and hornerin. Cleavage site analysis using TAILS reveals, among other ADAM17 dependent cleavage sites, increased proteolytic processing of S100 fused-type proteins, including filaggrin-2. Alterations in proteolytic processing are supported by altered protein abundance of numerous proteases upon keratinocyte-specific Adam17 or Egfr deletion, among them kallikreins, cathepsins and their inhibitors. In addition, N-terminal proteomics indicated usage of alternative translation start sites. This study highlights the essential role of proteolytic processing for maintenance of a functional epidermal barrier. Furthermore it suggests that most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR.

2016-04-20 | PXD002597 | Pride

Transcription profiling of mouse embryonic stem cells with inducible Oct-3/4 or Tcl1 expression or Tcl1 knock out using siRNA

Project description:POU transcription factor Pou5f1 (Oct3/4) is required to maintain ES cells in an undifferentiated state. Here we show that global expression profiling of Oct3/4-manipulated ES cells delineates the downstream target genes of Oct3/4. Combined with data from genome-wide chromatin-immunoprecipitation assays, this analysis identifies not only primary downstream targets of Oct3/4, but also secondary or tertiary targets. Furthermore, the analysis also reveals that downstream target genes are regulated either positively or negatively by Oct3/4. Identification of a group of genes that show both activation and repression depending on Oct3/4 expression levels provides a possible mechanism for the requirement of appropriate Oct3/4 expression to maintain undifferentiated ES cells. As a proof-of-principle study, one of the downstream genes, Tcl1, has been analyzed in detail. We show that Oct3/4 binds to the promoter region of Tcl1 and activates its transcription. We also show that Tcl1 is involved in the regulation of proliferation, but not differentiation, in ES cells. These findings suggest that the global expression profiling of gene-manipulated ES cells can help to delineate the structure and dynamics of gene regulatory networks.

2006-11-30 | E-MNIA-61 | biostudies-arrayexpress

An organ-specific angiogenic control mechanism for endothelial tailoring

Project description:Each organ of the human body requires locally-adapted blood vessels. The gain of such organotypic vessel specializations is often deemed molecularly unrelated to the process of organ vascularization. Opposing this model, we reveal a molecular mechanism for brain-specific angiogenesis, that operates under the control of Wnt7a/b ligands, well-known blood-brain barrier maturation signals. The control mechanism relies on Wnt7a/b-dependent expression of Mmp25 in brain endothelial cells. This hitherto poorly characterized GPI-anchored matrix metalloproteinase is selectively required in endothelial tip cells to enable their initial migration across the pial basement membrane lining the brain surface, which distinctive molecular composition is controlled by embryonic pial fibroblasts. Mechanistically, Mmp25 confers brain invasive competence by cleaving the pial basement membrane-enriched Col4a5/6 within a short non-collagenous region of the central helical part of the heterotrimer. Upon genetic interference with pial basement membrane composition, the Wnt/β-catenin-dependent organotypic control of brain angiogenesis is lost, resulting in properly patterned, yet blood-brain barrier-defective cerebrovasculatures. This work reveals an organ-specific angiogenesis mechanism, sheds light on tip cell mechanistic angiodiversity, and thereby illustrates how organs, by imposing local constraints on angiogenic tip cells, can select vessels matching their distinctive physiological requirements.

2024-02-08 | GSE233662 | GEO

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