Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Profiling Motility Signal-Induced Genes in Human Keratinocytes

ABSTRACT: In an acute skin wound, newly released serum growth factors in the wound bed drive lateral migration of human keratinocytes (HKs) to re-epithelialize the wound. However, profiling the migration signal-specific genes has long been challenged by pleiotropic effects of a given growth factor, including proliferation, migration and factor-specific responses. To overcome these technical problems, we 1) took advantage of a unique response of HKs to transforming growth factor-beta (TGFbeta) to selectively suppress growth signal-responding genes and identify motility-specific genes and 2) employed dual stimulation of HKs with TGFalpha and insulin to identify the common genes and eliminate factor-specific genes. Under these conditions, DNA microarray analyses were utilized to study the profiles of both TGFalpha-regualted and insulin-regulated immediate early (IE, 30 min), early (E, 60 min) and delayed early (DE, 120 min) genes. Keywords: time course, growth factor response

ORGANISM(S): Homo sapiens

PROVIDER: GSE8531 | GEO | 2007/08/15

SECONDARY ACCESSION(S): PRJNA101663

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human keratinocytes treated with TGFalpha and insulin

Project description:In an acute skin wound, newly released serum growth factors in the wound bed drive lateral migration of human keratinocytes (HKs) to re-epithelialize the wound. However, profiling the migration signal-specific genes has long been challenged by pleiotropic effects of a given growth factor, including proliferation, migration and factor-specific responses. To overcome these technical problems, we 1) took advantage of a unique response of HKs to transforming growth factor-beta (TGFbeta) to selectively suppress growth signal-responding genes and identify motility-specific genes and 2) employed dual stimulation of HKs with TGFalpha and insulin to identify the common genes and eliminate factor-specific genes. Under these conditions, DNA microarray analyses were utilized to study the profiles of both TGFalpha-regualted and insulin-regulated immediate early (IE, 30 min), early (E, 60 min) and delayed early (DE, 120 min) genes. Experiment Overall Design: HKs were seeded on collagen I pre-coated tissue culture plates (150 mm) around 45% confluence (~ 2.5 X 106 cells) in complete medium and incubated overnight. Next day, the cells (~ 4.5 X 106 cells) were deprived of any supplemental GFs and incubated in serum-free medium for 16 hours to rest the cells at G0/G1 phase. The cells were then washed with pre-warmed serum-free medium and incubated in fresh serum-free medium containing 20 ng/ml TGFbeta for 20 min at 37oC to block expression of growth signal-related genes. TGFalpha or insulin was added to separate plates (in the continued presence of TGFbeta) for 30 min, 60 min and 120 min. At the end of each stimulation time points, the cells were washed with ice-cold PBS to holt the stimulation and subjected to RNA isolation.

2008-06-16 | E-GEOD-8531 | biostudies-arrayexpress

Bioactive insulin-loaded electrospun wound dressings for localized drug delivery and stimulation of protein expression associated with wound healing

Project description:Effective therapy of wounds is difficult, especially for chronic, non-healing wounds, and novel therapeutics are urgently needed. This challenge can be addressed with bioactive wound dressings providing a microenvironment and facilitating cell proliferation and migration, ideally incorporating actives which initiate and/or progress effective healing upon release. In this context, electrospun scaffolds loaded with growth factors emerged as promising wound dressings due to their biocompatibility, similarity to the extracellular matrix and potential for controlled drug release. In this study, electrospun core-shell fibers were designed composed of a combination of polycaprolactone and polyethylene oxide. Insulin, a proteohormon with growth factor characteristics, was successfully incorporated into the core and was released in a controlled manner. The fibers exhibited favorable mechanical properties and a surface guiding cell migration for wound closure in combination with a high uptake capacity for wound exudate. Biocompatibility and significant wound healing effects were shown in interaction studies with human skin cells. As a new approach, analysis of the wound proteome in treated ex vivo human skin wounds clearly demonstrated a remarkable increase in wound healing biomarkers. Based on these findings, insulin-loaded electrospun wound dressings bear a high potential as effective wound healing therapeutics overcoming current challenges in the clinics.

2022-12-19 | PXD034076 | Pride

VEGF Study in Primary Human Endothelial Cells

Project description:The process of angiogenesis is under complex regulation in adult organisms, particularly as it often occurs in an inflammatory post-wound environment. As such, there are many impacting factors that will regulate the generation of new blood vessels which include not only pro-angiogenic growth factors such as vascular endothelial growth factor, but also angiostatic factors. During initial post-wound hemostasis, a large initial bolus of platelet factor 4 is released into localized areas of damage prior to progression of wound healing toward tissue homeostasis. Due to its early presence and high concentration, the angiostatic chemokine platelet factor 4, which can induce endothelial anoikis, can strongly affect angiogenesis. In our work, we explored signaling crosstalk interactions between vascular endothelial growth factor and platelet factor 4 using phosphotyrosine-enriched mass spectrometry methods on human dermal microvascular endothelial cells cultured under conditions facilitating migratory sprouting into collagen gel matrices. We developed new methods to enable mass spectrometry-based phosphorylation analysis of primary cells cultured on collagen gels, and quantified signaling pathways over the first 48 hours of treatment with vascular endothelial growth factor in the presence or absence of platelet factor 4. By observing early and late signaling dynamics in tandem with correlation network modeling, we found that platelet factor 4 has significant crosstalk with vascular endothelial growth factor by modulating cell migration and polarization pathways, centered around P38α MAPK, Src family kinases Fyn and Lyn, along with FAK. Interestingly, we found EphA2 correlational topology to strongly involve key migration-related signaling nodes after introduction of platelet factor 4, indicating an influence of the angiostatic factor on this ambiguous but generally angiogenic signal in this complex environment.

2014-04-15 | PXD000462 | Pride

ANKRD1 promotes cell migration by suppressing ELN production during early senescence

Project description:Cellular senescence is a complex biological process that contributes to wound healing, carcinogenesis, and age-related disease. Although the molecular mechanisms whereby senescence promotes wound repair are not well understood, the protein ANKRD1, which promoted wound healing in mice, was found to increase in senescent cells. We hypothesized that ANKRD1 may play a role in senescence-mediated wound healing. Conditioned medium (CM) from senescent WI-38 human diploid fibroblasts hastened cell migration of human HaCaT keratinocytes. Interestingly, silencing ANKRD1 in WI-38 cells reduced the effect of CM on cell migration, while overexpressing ANKRD1 accelerated it. Further proteomic analysis revealed that ANKRD1 associates with YBOX1, a multifunctional protein that modulates transcription of the ELN gene and reduces ELN mRNA production. The product of the ELN gene, the protein ELN or tropoelastin (a subunit of elastin), is a secreted factor that reduces motility. Thus, we propose that a rise in ANKRD1 during early senescence transiently limits the YBOX1-dependent transcriptional increase in ELN production, and thereby enables cell motility in early phases of senescence.

2023-06-01 | MSV000092079 | MassIVE

Assessment of the Diagnostic Role of Serum Insulin-like Growth Factor Binding Protein-3 as a Potential Biomarker for Colorectal Cancer (CRC) in Egypt

Project description:1. evaluation of diagnostic importance of insulin like growth factor binding protein3 in patient with recently diagnosed as Colorectal cancer 2. correlation between the diagnostic efficacy of insulin like growth factor binding protein 3 with routine marker carcinoembryonic antigen.

| 59449 | ecrin-mdr-crc

Role of IMP3 Expression in Colorectal Carcinoma: An Immunohistochemical Study

Project description:Colorectal carcinoma (CRC) is the third most common malignancy worldwide. In Egypt, the relative frequency of CRC is about 9-12% with high male predominance 3:1. The high mortality rates associated with CRC is reflective of several factors including: the lack of apparent symptoms in the early stages and the absence of cancer prevention strategies in developing countries. Insulin-like growth factor II m-RNA-binding protein 3 (IMP3) is a member of the IMP family which plays a key role in the transfer and stabilization of mRNA, cell growth, and migration during embryogenesis. IMP3 has gained considerable interest as a cancer-associated protein. Previous studies strongly suggest that IMP3 may represent a valuable prognostic marker in human cancer. Its overexpression has been reported in a variety of human types of cancer, including lung cancer, colon cancer, pancreatic cancer, gastric cancer, liver cancer, and breast cancer

| 2753051 | ecrin-mdr-crc

JAK/STAT coordinates cell proliferation during disc regeneration with Dilp8-mediated developmental delay in Drosophila melanogaster

2015-04-10 | GSE54868 | GEO

JAK/STAT coordinates cell proliferation during disc regeneration with Dilp8-mediated developmental delay in Drosophila melanogaster

Project description:Regeneration of fragmented Drosophila imaginal discs occurs in an epimorphic manner, involving local cell proliferation at the wound site. Following disc fragmentation, cells at the wound site activate a restoration program through wound healing, regenerative cell proliferation and repatterning of the tissue. However, the interplay of signaling cascades, driving these early reprogramming steps, is not well understood. Here we profiled the transcriptome of regenerating cells in the early phase within twenty-four hours after wounding. We found that JAK/STAT signaling becomes activated at the wound site and promotes regenerative cell proliferation in cooperation with Wingless (Wg) signaling. In addition, we demonstrated that the expression of Drosophila insulin-like peptide 8 (dilp8), which encodes a paracrine peptide to delay the onset of pupariation, is controlled by JAK/STAT signaling in early regenerating discs. Our findings suggest that JAK/STAT signaling plays a pivotal role in coordinating regenerative disc growth with organismal developmental timing. In order to analyze transcriptome change in early regenerating imaginal disc, Drosophila prothorasic leg discs were fragmented (to anterior one-quarter or posterior three-quarters) and cultured ex vivo in adult fly abdomen. Regenerating cells in early regeneration phase (at 12 or 24 hours after wounding) were subjected to transcriptome profiling with Affymetrix microarrays. For control samples, the corresponding regions of uncut-cultured discs and uncut-uncultured discs were used.

2015-04-10 | E-GEOD-54868 | biostudies-arrayexpress

Identification of phosphorylation sites in the IGF-1 Receptor

Project description:Although Insulin-like Growth Factor (IGF-1) signaling promotes tumor growth and cancer progression, IGF-1 Receptor-targeted therapies have shown poor clinical efficacy. The mechanistic basis for this is unclear as is our understanding of what distinguishes IGF-1R signaling from the closely related Insulin receptor (IR) signaling. This study illuminates both issues. A site in the IGF-1R C-terminal tail incorporating two tyrosines that are not present in the Insulin receptor (IR) was previously shown to be essential for IGF-1-mediated cancer cell survival, migration and tumorigenic growth. Here, we establish that the Y1250/Y1251 site is autophosphorylated in a cell adhesion-dependent manner.

2020-05-15 | PXD017644 | Pride

MicroRNA-198 an inhibitor of keratinocyte migration

Project description:This study identifies miR-198 as a potential inhibitor of keratinocyte migration in skin This study identifies genes differentially expressed during the early phases of wound healing using an ex vivo organ culture model of human skin

2013-03-02 | GSE37967 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data