Keratinocyte-derived circulating exosomal miRNAs as a novel biomarker of disease severity in psoriasis
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ABSTRACT:
PROVIDER: PRJNA888960 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21850582.fastq.gz | Fastqsanger.gz | |||
| SRR21850583.fastq.gz | Fastqsanger.gz | |||
| SRR21850584.fastq.gz | Fastqsanger.gz | |||
| SRR21850585.fastq.gz | Fastqsanger.gz | |||
| SRR21850586.fastq.gz | Fastqsanger.gz |
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Project description:We report the high-throughput profiling of human primary keratinocytes transfected with either miR-378 mimic or miR-378 inhibitor at 24 or 48 hours. Our study focused on the dysregulation of microRNAs that might partially be a fundamental mechanism leading to psoriasis development. We knock-in and knock-out a specific miR-378 and see the cellular responses. As expected, overexpression of miR-378a inhibited the proliferation, enhanced the apoptosis and disturbed the cell cycle. Regarding to the confirm experiment, our results suggested that the expression of miR-378a associated with the psoriasis pathogenesis enhancing the severity of psoriatic lesion, and might useful for further development of therapeutic strategy for psoriasis.
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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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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
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