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Epidermal differentiation: basal vs. suprabasal keratinocytes

ABSTRACT: In epidermal differentiation basal keratinocytes detach from the basement membrane, stop proliferating, and express a new set of structural proteins and enzymes, which results in an impermeable protein/lipid barrier that protects us. To define the transcriptional changes essential for this process, we purified large quantities of basal and suprabasal cells from human epidermis, using the expression of b4 integrin as the discriminating factor. The expected expression differences in cytoskeletal, cell cycle and adhesion genes confirmed the effective separation of the cell populations. Using DNA microarray chips, we comprehensively identify the differences in genes expressed in basal and differentiating layers of the epidermis, including the ECM components produced by the basal cells, the proteases in both the basal and suprabasal cells, and the lipid and steroid metabolism enzymes in suprabasal cells responsible for the permeability barrier. We identified the signaling pathways specific for the two populations, and found two previously unknown paracrine and one juxtacrine signaling pathway operating between the basal and suprabasal cells. Furthermore, using specific expression signatures, we identified a new set of late differentiation markers and mapped their chromosomal loci, as well as a new set of melanocyte-specific markers. The data represent a quantum jump in understanding the mechanisms of epidermal differentiation. Basal keratinocytes are defined as integrin b4-positive. Suprabasal sample contains all melanocytes as well.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26059 | GEO | 2010/12/15

SECONDARY ACCESSION(S): PRJNA135569

REPOSITORIES: GEO

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Epidermal differentiation: basal vs. suprabasal keratinocytes

Project description:In epidermal differentiation basal keratinocytes detach from the basement membrane, stop proliferating, and express a new set of structural proteins and enzymes, which results in an impermeable protein/lipid barrier that protects us. To define the transcriptional changes essential for this process, we purified large quantities of basal and suprabasal cells from human epidermis, using the expression of b4 integrin as the discriminating factor. The expected expression differences in cytoskeletal, cell cycle and adhesion genes confirmed the effective separation of the cell populations. Using DNA microarray chips, we comprehensively identify the differences in genes expressed in basal and differentiating layers of the epidermis, including the ECM components produced by the basal cells, the proteases in both the basal and suprabasal cells, and the lipid and steroid metabolism enzymes in suprabasal cells responsible for the permeability barrier. We identified the signaling pathways specific for the two populations, and found two previously unknown paracrine and one juxtacrine signaling pathway operating between the basal and suprabasal cells. Furthermore, using specific expression signatures, we identified a new set of late differentiation markers and mapped their chromosomal loci, as well as a new set of melanocyte-specific markers. The data represent a quantum jump in understanding the mechanisms of epidermal differentiation. Basal keratinocytes are defined as integrin b4-positive. Suprabasal sample contains all melanocytes as well. Basal (integrin b4+), suprabasal (b4-) and total epidermal keratinocytes. In duplicate, from 2 independent donors, breast reduction surgery.

2010-12-15 | E-GEOD-26059 | biostudies-arrayexpress

Homo sapiens

Project description:Epidermal differentiation: basal vs. suprabasal keratinocytes

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Grhl3 is essential for epidermal barrier repair from both physical and immune injury, relevance to lesional skin disease

Project description:Epidermal barrier repair mechanisms activated in psoriasis lesions are likely involved in limiting the severity of this disease. We show that loss of grainyhead-like 3 (Grhl3), a pro-terminal differentiation factor in the epidermis, is sufficient to trigger greater sensitivity to and delayed resolution of epidermal lesions resulting from either physical or immune mediated barrier injury. After stimulation of Toll like receptors, the loss of Grhl3 resulted in increased epidermal damage with a striking increase in basal cell proliferation, hyperplasia of partially differentiated suprabasal layers, and a transcriptional profile highlighted by the overexpression of epidermal wound response and alarmin genes. This study reveals an important role for the epidermis in the initiation and recovery from immune-mediated lesions, and indicated that the epidermal regulator Grhl3 acts to both suppress disease initiation and resolve existing lesions. This work suggests that treatments focused on improving barrier function could be used preventatively and therapeutically in psoriasis. Whole skin was collected from E16.5 mouse backskins for Grhl3 ChIP. Adult epidermis for depilation and imiquimod experiments was seperated from dermis using dispase prior to Grhl3 ChIP.

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Genome-wide analysis of gene expression in Krt1+/+ versus Krt1-/- epidermis and full-thickness skin.

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Grhl3 is essential for epidermal barrier repair from both physical and immune injury, relevance to lesional skin disease

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Creation of differentiation-specific genomic maps of human epidermis through laser capture microdissection

Project description:We sought to understand the differences between the basal and suprabasal layers of normal human skin epidermis. Comparison of transcriptomes among basal epidermis, suprabasal epidermis, whole epidermis, and reticular dermis

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Key roles for SRF in embryonic epidermal differentiation

Project description:During development, a polarized sheet of epidermal cells undergoes stratification and differentiation to produce the skin barrier. Through mechanisms poorly understood, the process involves adhesion and Notch signaling. To elucidate how epidermal embryogenesis is governed, we conditionally targeted transcription factor serum response factor (SRF), which has been shown to be essential for proper epidermal differentiation in vitro and in vivo. Seeking mechanism, we identified actomyosin-related genes as well-known SRF targets downregulated shortly after ablation. We show that this results in a diminished cortical actomyosin network which fails to regulate the transition of cells from the basal proliferative layer to the suprabasal differentiating layer resulting in an inability of cells to properly execute stratification and differentiation. FACS purification of basal epidermal cells from E16.5 SRF fl/fl ROSA26 YFP fl/fl K14-Cre (cKO) or SRF fl/+ ROSA26 YFP fl/fl K14-Cre (WT) was performed on a FACS Vantage SE system equipped with FACS DiVa software (BD Biosciences). Cells were gated for single events and viability and then sorted according to α6 integrin-PE expression and YFP.

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