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Alteration of keratinocyte gene expression as a result of Flg deficiency

ABSTRACT: Alteration of keratinocyte gene expression as a result of Flg deficiency

PROVIDER: PRJNA663791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12650415.fastq.gz	Fastqsanger.gz
	SRR12650416.fastq.gz	Fastqsanger.gz
	SRR12650417.fastq.gz	Fastqsanger.gz
	SRR12650418.fastq.gz	Fastqsanger.gz
	SRR12650419.fastq.gz	Fastqsanger.gz

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Alteration of keratinocyte gene expression as a result of Flg deficiency

Project description:Defects of filaggrin (FLG) compromise epidermal barrier function and represent an important known genetic risk factor for atopic dermatitis (AD), but also for systemic atopy, including allergic sensitization and asthma. A loss of epidermal barrier integrity can provide a significant stress for the keratinocytes in the skin, either due to the increased moisture evaporation from the skin or increased penetration of the antigens and microflora into the lower epidermal layers. To understand the effect of this loss of barrier integrity on keratinocyte function our aim is to analyze the alterations in the transcriptional profile of keratinocytes from Flg-deficient mice.

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Alteration of the whole skin gene expression as a result of Flg deficiency

Project description:Alteration of the whole skin gene expression as a result of Flg deficiency

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Alteration of the whole skin gene expression as a result of Flg deficiency

Project description:Defects of filaggrin (FLG) compromise epidermal barrier function and represent an important known genetic risk factor for atopic dermatitis (AD), but also for systemic atopy, including allergic sensitization and asthma. A loss of epidermal barrier integrity can provide a significant stress for the cells in both the epidermis as well as the underlying dermal layer of the skin, either due to the increased moisture evaporation from the skin or increased penetration of the antigens and microflora into the lower layers. This analysis was therefore designed to understand the effect of this loss of barrier integrity on the total skin transcriptional profile.

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Depletion of ZNF185 causes delay of keratinocyte differentiation

Project description:Development of epidermis includes a complicated program of keratinocyte differentiation. Here we study a new membrane LIM-domain containing Zn-finger protein ZNF185 which is expressed in upper layers of human skin and is up-regulated during keratinocyte differentiation in vitro. Interestingly, depletion of ZNF185 causes delay of keratinocyte differentiation with decreased levels of FLG, LOR, LCEs expression.

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ZNF750 in late keratinocyte differentiation

Project description:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demostrated that a dominante mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrehic dermatitis. We defined ZNF750 as a nuclear effector that is atrongly activated in and essiential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differnetiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier Gene expression analysis: To determine the differentaition signature for HaCaT keratinocytes, with ZNF750 gene silencing, total RNA was isolated in biologic triplicates from cells induced to differentiate for twelve days and hybridized to Affymerix Human Gene 1.0 ST arrays.

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ZNF750 in late keratinocyte differentiation

Project description:Disrupted skin barrier due to altered keratinocyte differentiation is common in pathologic conditions such as atopic dermatitis, ichthyosis and psoriasis. However, the molecular cascades governing keratinocyte terminal differentiation are still poorly understood. We have previously demonstrated that a dominant mutation in ZNF750 leads to a clinical phenotype that reminiscent of psoriasis and seborrheic dermatitis. We defined ZNF750 as a nuclear effector that is strongly activated in and essential for keratinocyte terminal differentiation. ZNF750 knockdown in HaCaT keratinocytes markedly reduced the expression of epidermal late differentiation markers, including gene subsets of epidermal differentiation complex and skin barrier formation such as FLG, LOR, SPINK5, ALOX12B and DSG1, known to be mutated in various human skin diseases. Furthermore, ZNF750 over-expression in undifferentiated cells induced terminal differentiation genes. Thus, ZNF750 is a regulator of keratinocyte terminal differentiation, and with its downstream targets can serve in future elucidation of therapeutics for common disease of skin barrier

2012-09-24 | GSE38039 | GEO

Different response of WT and Ts keratinocyte to TPA treatment

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Different response of WT and Ts keratinocyte to TPA treatment

Project description:Ts keratinocyte has increased proliferation compare to WT keratinocyte upon TPA treatment. This result showed the different transcription regulation in Ts and WT keratinocyte upon TPA treatment. Total RNA extracted from WT or Ts keratinocytes, not treated or treated with TPA for 12 hours.

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