Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA283140 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To characterize the global transcriptome of human keratinocyte stem cells (KSC) and keratinocyte progenitors (KP), primary basal keratinocyte subpopulations enriched in quiescent stem cells [Itg-α6bright / Trf-Rdim] or in cycling progenitors [Itg-α6bright / Trf-Rbright] were purified by flow cytometry from human skin samples. Sorted keratinocytes were then seeded in culture plates and maintained in culture medium overnight (15 hours), and genome-wide transcriptome analysis of these two subpopulations was directly performed, in order to globally maintain the initial phenotypes. After RNA preparation, gene profiling was performed using oligonucleotide microarrays (26068 probes). LOWESS normalisation was applied. Keywords: epidermis, keratinocyte stem cells, progenitors, transcriptome, stemness
2015-05-06 | GSE68583 | GEO
Project description:To characterize the global transcriptome of human keratinocyte stem cells (KSC) and keratinocyte progenitors (KP), primary basal keratinocyte subpopulations enriched in quiescent stem cells [Itg-?6bright / Trf-Rdim] or in cycling progenitors [Itg-?6bright / Trf-Rbright] were purified by flow cytometry from human skin samples. Sorted keratinocytes were then seeded in culture plates and maintained in culture medium overnight (15 hours), and genome-wide transcriptome analysis of these two subpopulations was directly performed, in order to globally maintain the initial phenotypes. After RNA preparation, gene profiling was performed using oligonucleotide microarrays (26068 probes). LOWESS normalisation was applied. Keywords: epidermis, keratinocyte stem cells, progenitors, transcriptome, stemness Dye-swap hybridization were performed. Slides were scanned with a Genepix 4000 microarray scanner (Axon Instruments, Molecular devices, Sunnyvale, CA). For each hybridized spot, the Cy3 and Cy5 fluorescence values were obtained by using Genepix Pro 4.0 software (Axon Instruments) and were saved as a result file
2015-05-06 | E-GEOD-68583 | biostudies-arrayexpress
Project description:Characterization at the global transcriptome level of the gene networks ensuring the regulation of the immature status of cutaneous stem- and precursor-cells is a necessary step to further understand the concept of ‘stemness’ in this tissue. Moreover, considering possible clinical applications, the search for molecular targets to control stem cell characteristics and regenerative capacity is a necessary step to improve therapeutic approaches. Cutaneous cell therapy is concerned by this objective, as skin graft bioengineering requires a phase of ex vivo expansion of keratinocytes from donors, during which the preservation of a sufficient stem cell pool is critical for graft take and long-term skin regeneration. We have investigated the role of transcription factor MXD4/MAD4 in native keratinocyte precursors from adult human skin. A stable lentiviral-based shRNA-mediated MXD4 knock‑down (KD) approach was developed and used to study the properties of MXD4-deficient [MXD4KD] versus control [MXD4WT] native keratinocyte precursors. Using long-term cultures and clonal assays, we found that decreased MXD4 expression increased keratinocyte precursor immaturity and clonogenic potential, thus promoting self-renewal. Importantly, [MXD4KD] keratinocyte precursors exhibited an improved capacity for three-dimensional epidermis reconstruction, which was preserved at a late ex vivo expansion stage where this potential was lost in [MXD4WT] keratinocytes. To analyze the biological impact of MXD4 knock‑down at the molecular level, comparative transcriptome profiling of [MXD4WT] and [MXD4KD] cells was performed using next-generation RNA sequencing (RNA-seq). This set of data provides a material that permits the dissection of genetic networks modulated by MXD4 in human keratinocyte precursor cells, and controlling their immature status and epidermis regeneration capacity.
2022-08-02 | GSE202700 | GEO
Project description:Gene expression comparison between human colonic epithelial cells cultured with Klebsiella pneumoniae (KP) derived from PSC patients versus KP JCM1662.
| EGAD00001004465 | EGA
Project description:Characterization at the global transcriptome level of the gene networks ensuring the regulation of the immature status of cutaneous stem- and precursor-cells is a necessary step to further understand the concept of ‘stemness’ in this tissue. Moreover, considering possible clinical applications, the search for molecular targets to control stem cell characteristics and regenerative capacity is a necessary step to improve therapeutic approaches. Cutaneous cell therapy is concerned by this objective, as skin graft bioengineering requires a phase of ex vivo expansion of keratinocytes from donors, during which the preservation of a sufficient stem cell pool is critical for graft take and long-term skin regeneration. We have investigated the role of transcription factor KLF4 in native keratinocyte precursors from adult human skin. A stable lentiviral-based shRNA-mediated KLF4 knock‑down (KD) approach was developed and used to study the properties of KLF4-deficient [KLF4KD] versus control [KLF4WT] native keratinocyte precursors. Using long-term cultures and clonal assays, we found that decreased KLF4 expression increased keratinocyte precursor immaturity and clonogenic potential, thus promoting self-renewal. Importantly, [KLF4KD] keratinocyte precursors exhibited an improved grafting capacity in an in vivo skin xenograft model and in serial grafting. To analyze the biological impact of KLF4 knock‑down at the molecular level, comparative transcriptome profiling of [KLF4WT] and [KLF4KD] cells was performed using next-generation RNA sequencing (RNA-seq). This set of data provides a material that permits the dissection of genetic networks modulated by KLF4 in human keratinocyte precursor cells, and controlling their immature status and epidermis regeneration capacity.
2019-01-01 | GSE111786 | GEO
Project description:<p>The human neocortex is created from diverse intermixed progenitors in the prenatal germinal zones. These progenitors have been difficult to characterize since progenitors - particularly radial glia (RG) - are rare, and are defined by a combination of intracellular markers, position and morphology. To circumvent these problems we developed a method called FRISCR (Fixed and Recovered Intact Single Cell RNA) for transcriptome profiling of individual fixed, stained and sorted cells. We developed and validated FRISCR on human embryonic stem cells. We then profiled primary human RG (96 - 132 days post conception) that constitute only 1% of the mid-gestation cortex. These RG could be classified into ventricular zone-enriched RG (vRG) that express ANXA1 and CRYAB, and outer subventricular zone-localized RG (oRG) that express HOPX. Our study identifies the first markers and molecular profiles of vRG and oRG cells, and provides an essential step for understanding molecular networks driving the lineage of human neocortical progenitors.</p> <p><i>Reprinted from Thomsen et. al. Nature Methods (2015), with permission from Nature Publishing.</i></p> <p>Human embryonic stem cell data may be obtained through NCBI's GEO database, using accession number <a href="http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE71858">GSE71858</a>. Raw data from one human sample that was not consented to be released to dbGaP may be obtained directly from the authors of Thomsen et. al., 2015.</p>
| phs001016 | dbGaP
Project description:The cell transition from an inflammatory phase to a subsequent proliferative phase is crucial for wound healing, yet the driving mechanism remains unclear. By profiling lncRNA expression changes during human skin wound healing and screening lncRNA functions, we identified SNHG26 as a pivotal regulator in keratinocyte progenitors underpinning this phase transition. To study the proteins interact with SNHG26, we performed RNA pull-down assay in human keratinocyte progenitors. The mass spectrometry (MS) analysis was performed to identify the proteins interacted with SNHG26.
2024-08-28 | PXD055231 | Pride
Project description:By profiling lncRNA expression changes during human skin wound healing and screening lncRNA functions, we identified SNHG26 as a pivotal regulator in keratinocyte progenitors underpinning this phase transition. we performed RNA pull-down assay in human keratinocyte progenitors and found SNHG26 interact with ILF2. ILF2, or the nuclear condensates it forms, is crucial for maintaining the stability of SNHG26. To identify other protein components within these condensates, we employed a proximity-dependent biotin identification (BioID) assay, which label proteins in close proximity to ILF2 that fused to BioID2, and subsequently identifying them through mass spectrometry (MS).
2024-08-28 | PXD055235 | Pride
Project description:Even though cutaneous atrophy is the major adverse effect of topical glucocorticoids, its molecular mechanisms are poorly understood. We found that glucocorticoids strongly increased the expression of REDD1 (regulated in development and DNA damage response 1), a stress-inducible inhibitor of mTOR, in mouse and human epidermis. We found that REDD1 knockout animals are partially resistant to glucocorticoid-induced epidermal and subcutaneous adipose atrophy which correlated with the protection of CD34+ follicular epithelial stem cells as well as p63+ keratinocyte progenitors in REDD1 knockout epidermis during chronic steroid treatment. At the same time, REDD1 knockout did not affect anti- inflammatory effect of glucocorticoids, as evaluated by ear edema test. Expression profiling revealed that ~ 50% of the glucocorticoid receptor (GR) target genes were not activated in epidermis of REDD1 knockouts, however, the negative effect of glucocorticoids on gene expression was similar to that in w.t. animals. Overall, our findings reveal a novel pathway in GR activation by its target gene/protein REDD1; and indicate an important role of REDD1 in glucocorticoid-induced skin atrophy, and maintenance of the epidermis and subcutaneous adipose. In addition, our findings form the foundation for the development of safer topical glucocorticoid treatment regimens by combining this therapy with REDD1 inhibitors.
2014-08-01 | GSE59151 | GEO
Project description:SAGE libraries from cultured, differentiated keratinocytes and human epidermis, both normal and affected by actinic keratosis Keywords = Keratinocyte, Epidermis, Homo sapiens, Actinic Keratosis, TNF alpha
2002-02-22 | GSE31 | GEO