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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

ABSTRACT: Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

PROVIDER: PRJNA407977 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6051650.fastq.gz	Fastqsanger.gz
	SRR6051660.fastq.gz	Fastqsanger.gz
	SRR6051641.fastq.gz	Fastqsanger.gz
	SRR6051651.fastq.gz	Fastqsanger.gz
	SRR6051661.fastq.gz	Fastqsanger.gz

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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

Project description:DLX3 is a homeodomain transcription factor involved in epidermal and hair follicle differentiation. Epidermal specific deletion of DLX3 leads to IL17 related inflammation. However, the downstream signals from DLX3-deficient keratinocytes that initiates IL17 associated inflammation is not well-characterized. Therefore we performed acute Dlx3 deletion to identify the initial molecular changes causing the skin inflammatory reponse and tried to rescue the immune phenotype by STAT3 inhibitor treatment (Cryptotanshinone). In this study, we compared the epidermal and dermal transcriptome from Dlx3 wild-type (WT) and K14CreERT;DLX3 fl/fl (icKO).

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Project description:Transcriptional profiling of SOX11-expressing mouse epidermis (K14-rtTA;TRE-Sox11-FLAG) compared to control (K14-rtTA) epidermis at postnatal day 4 (P4). The littermate pairs were injected with Dox for 12 h before their epidermis was harvested. Goal was to identify the gene expression profile of postnatal epidermis changed by SOX11 induced expression.

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Global microarray analysis of changes of gene expression in the epidermis of K14-caSmad1 mice

Project description:Bone morphogenetic protein (BMP) signalling plays a key role in the control of skin development and postnatal remodelling by regulating keratinocyte proliferation, differentiation and apoptosis. To study the role of BMPs in wound-induced epidermal repair, we used transgenic mice overexpressing the BMP downstream component Smad1 under the control of a K14 promoter as an in vivo model, as well as ex vivo and in vitro assays. K14-caSmad1 mice exhibited retarded wound healing associated with significant inhibition of proliferation and increased apoptosis in healing wound epithelium. Furthermore, microarray and qRT-PCR analyses revealed decreased expression of a number of cytoskeletal/cell motility-associated genes including wound-associated keratins (Krt16, Krt17) and Myo5a, in the epidermis of K14- caSmad1 mice versus wild-type controls during wound healing. BMP treatment significantly inhibited keratinocyte migration ex vivo, and primary keratinocytes of K14-caSmad1 mice showed retarded migration compared to wild-type controls. Finally, siRNA-mediated silencing of Bmpr-1B in primary mouse keratinocytes accelerated cell migration and was associated with increased expression of Krt16, Krt17 and Myo5a compared to controls. Thus, this study demonstrates that BMPs inhibit keratinocyte proliferation, cytoskeletal organization and migration in regenerating skin epithelium during wound healing, and raises a possibility for using BMP antagonists for the management of chronic wounds.

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Global microarray analysis of changes of gene expression in the epidermis of K14-caSmad1 mice

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Molecular consequences of Dlx3 deletion in mouse enamel organ as determined by RNASeq analysis

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Expression data from murine skin of tamoxifen-induced Ugcgfl/fl K14CreERT2 vs. Ugcgfl/fl

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