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Expression data from squamous cell carcinoma stem cells, epidermal progenitor cells and hair follicle bulge stem cells

ABSTRACT: We used microarrays to assess the global gene expression profiles of cancer stem cells which were isolated from cutaneous squamous cell carcinomas which developed when WT, TGF beta receptor II ko, FAK KO, and TGF beta receptor II/FAK double KO were subjected to continuous DMBA treatment. Squamous cell carcinoma stem cells were compared to epidermal progenitor cells (CD49fhighCD34low) and hair follicle bulge stem cells (CD49fhighCD34high).

ORGANISM(S): Mus musculus

PROVIDER: GSE29328 | GEO | 2011/12/30

SECONDARY ACCESSION(S): PRJNA140125

REPOSITORIES: GEO

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Expression data from squamous cell carcinoma stem cells, epidermal progenitor cells and hair follicle bulge stem cells

Project description:We used microarrays to assess the global gene expression profiles of cancer stem cells which were isolated from cutaneous squamous cell carcinomas which developed when WT, TGF beta receptor II ko, FAK KO, and TGF beta receptor II/FAK double KO were subjected to continuous DMBA treatment. Squamous cell carcinoma stem cells were compared to epidermal progenitor cells (CD49fhighCD34low) and hair follicle bulge stem cells (CD49fhighCD34high). Squamous cell carcinoma was initiated by continuous DMBA treatment (complete carcinogenesis). Cancer cells were sorted based on high CD29 and CD49f expression, infected with a retrovirus expressing a triple modality reporter (luciferase, RFP, thymidine kinase) and grafted onto nude recipient mice. RFP positive lineage was separated into CD29 high, CD49f high and CD34 low; or CD29high, CD49f high and CD34high squamous cell carcinoma initiating cells.

2011-12-30 | E-GEOD-29328 | biostudies-arrayexpress

Integrin α3β1-dependent mRNA expression profile of hair bulge keratinocytes and their progeny during DMBA/TPA-mediated skin tumorigenesis

Project description:Integrin α3β1 in hair bulge population affects the tumor formation following DMBA/TPA carcinogenesis protocol, however linage tracing showed that hair bulge cells do not largely contributre to tumor mass. To investigate whether α3β1 might affect tumor promoting environment and to better understand its role in hair bulge population during skin tumorigenesis, we determined the expresison profile of hair bulge-originating keratinocytes isolted from α3β1KO and WT mice during initiation of tumorigenesis.

2020-05-14 | GSE135983 | GEO

Gene expression changes by 2,4-dinitrochlorobenzene in human bulge-derived keratinocytes

Project description:In the epidermis, keratinocytes are involved in physical and first-line immune protection of the host. In this work, we analyzed molecular responses after the addition of contact sensitizers, 2,4-dinitrochlorobenzene (DNCB) using cultured human keratinocytes from the bulge region of a plucked hair follicle (bulge-derived keratinocytes; BDKs) in comparison with neonatal human epidermal keratinocytes NHEK and human monocytic leukemia THP-1. The changes in gene expression by the treatment of DNCB in BDKs were different from those in THP-1. Many genes orchestrating keratinocyte differentiation, which interact TGF-β and BMP signaling pathway, were significantly up-regulated in response to DNCB. Keywords: Comparison analysis of gene expression changes by the treatment of DNCB

2009-09-30 | GSE14838 | GEO

Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [10wk skin]

Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=4 WT and KO (each sample contain RNA from one mouse)

2014-01-01 | E-GEOD-50671 | biostudies-arrayexpress

Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [skin wound]

Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)

2014-01-01 | E-GEOD-50670 | biostudies-arrayexpress

Ablation of coactivator Med1 regulates bulge keratinocyte stem cells and accelerates epidermal regeneration after injury [10wk keratinocyte]

Project description:Transcriptional coactivator Mediator complex facilitates transcription of various transcription factors. Previously, we have generated Med1 conditional null mice, where a critical subunit of Mediator, Med1, is removed from keratinocytes. Here we present evidence that ablation of Med1 accelerated epidermal regeneration after injury. As bulge keratinocyte stem cells are important contributors to regenerate epidermis, we first analyzed properties of stem cells in Med1 null mice. BrdU long retaining analysis revealed that deletion of Med1 still maintained quiescence of bulge keratinocyte stem cells, despite of general hyperplasia observed in Med1 deficient keratinocytes. Gene expression analysis demonstrated that a series of niche matrix proteins decreased in Med1 deficient keratinocytes. In contrast, the expression of stem cell marker Sox9 was not altered, suggesting stem cells are present but activated because of abnormal niche surrounding stem cells. In addition, Med1 deletion suppressed injury induced inflammatory reaction, which indirectly regulates epidermal regeneration. We also indicated that TGFβ1 significantly decreased in both bulge and epidermal keratinocytes upon Med1 deletion. Our study demonstrates that coactivator Med1 has a critical role to maintain bulge stem cells and epidermal regeneration presumably through regulation in TGFβ signaling. n=3 WT and KO (each group contains keratinocytes isolated from adult skins excised from 2 mice)

2014-01-01 | E-GEOD-50672 | biostudies-arrayexpress

Characterization and isolation of stem cell enriched human hair follicle bulge cells

Project description:The human hair follicle bulge is an important niche for keratinocyte stem cells (KSC). Elucidation of human bulge cell biology could be facilitated by analysis of global gene expression profiles and identification of unique cell surface markers. The lack of distinctive bulge morphology in human hair follicles has hampered studies of bulge cells and KSC. In this study, we determined the distribution of label-retaining cells to carefully define the human anagen bulge. Using navigated-laser capture microdissection, bulge cells and outer root sheath cells from other follicle regions were obtained and analyzed with cDNA microarrays. Gene transcripts encoding inhibitors of WNT and Activin/BMP signaling were over-represented in the bulge while genes responsible for cell proliferation were under-represented, consistent with quiescent non-cycling KSC in anagen follicles. Positive markers for bulge cells included CD200, PHLDA1, follistatin, and frizzled homolog 1 while CD24, 34, 71 and 146 were preferentially expressed by non-bulge keratinocytes. Importantly, CD200+ cells (CD200hi24lo34lo71lo146lo) obtained from hair follicle suspensions demonstrated high colony forming efficiency in clonogenic assays, indicating successful enrichment of living human bulge stem cells. Keywords: Affymetrix micrarray analysis of human hair follicles

2005-12-06 | GSE3419 | GEO

Transcription profiling of human stem cells enriched for hair follicle bulge cells

Project description:The human hair follicle bulge is an important niche for keratinocyte stem cells (KSCs). Elucidation of human bulge cell biology could be facilitated by analysis of global gene expression profiles and identification of unique cell-surface markers. The lack of distinctive bulge morphology in human hair follicles has hampered studies of bulge cells and KSCs. In this study, we determined the distribution of label-retaining cells to define the human anagen bulge. Using navigated laser capture microdissection, bulge cells and outer root sheath cells from other follicle regions were obtained and analyzed with cDNA microarrays. Gene transcripts encoding inhibitors of WNT and activin/bone morphogenic protein signaling were overrepresented in the bulge, while genes responsible for cell proliferation were underrepresented, consistent with the existence of quiescent noncycling KSCs in anagen follicles. Positive markers for bulge cells included CD200, PHLDA1, follistatin, and frizzled homolog 1, while CD24, CD34, CD71, and CD146 were preferentially expressed by non-bulge keratinocytes. Importantly, CD200+ cells (CD200hiCD24loCD34loCD71loCD146lo) obtained from hair follicle suspensions demonstrated high colony-forming efficiency in clonogenic assays, indicating successful enrichment of living human bulge stem cells. The stem cell behavior of enriched bulge cells and their utility for gene therapy and hair regeneration will need to be assessed in in vivo assays.

2007-11-08 | E-GEOD-3419 | biostudies-arrayexpress

RNA sequencing of ILK-deficient hair follicle bulge stem cells

Project description:We sequenced mRNA from FACS purified hair follicle bulge stem cells from 21 d old control and ILK-deficient mice, 3 biological replicates each Examination of mRNA levels in control and ILK-deficient hair follicle bulge stem cells

2015-09-01 | E-GEOD-68846 | biostudies-arrayexpress

RNA sequencing of ILK-deficient hair follicle bulge stem cells

Project description:We sequenced mRNA from FACS purified hair follicle bulge stem cells from 21 d old control and ILK-deficient mice, 3 biological replicates each

2015-09-01 | GSE68846 | GEO

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