Project description:To obtain insights into the global changes of gene expression in the mouse skin in response to epidermal YAP activity, we performed whole transcriptome sequencing of skin tissue of YAP2-5SA-∆C transgenic mice.
Project description:The peripheral nervous system plays important roles in orchestrating tissue function in health and disease. In this work, we perform single nuclei RNAseq of skin sensory neuron DRGs in a mouse model of psoriasis to interrogate the impact of skin inflammation on the function and transcriptome of skin sensory neurons.
Project description:We investigate and define here the in vivo biological effects of shikonin, at the transcriptome and microRNA levels, in mouse skin tissues. Through cross-examination between total RNA transcripts and microRNA data sets, we predicted that shikonin treatment may affect the epithelial–mesenchymal transition (EMT) process and the expression of related microRNAs, including 200a, 200b, 200c, 141, 205 and 429 microRNAs, in test skin tissue. Indeed, further in vivo tests on mouse abdominal skin tissue confirmed the stimulatory effect of shikonin on regulatory molecules of the EMT process in epidermal tissue. In addition, RT-PCR analyses confirmed the downregulating effects of shikonin on the expression of microRNA 205 and members of the microRNA 200 family, which are known to be involved in the EMT process. Gene expression of two RNA targets of the microRNA 200 family in EMT regulation, namely Sip1 (Zeb2) and Tcf8 (Zeb1), were consistently upregulated by shikonin treatment. We demonstrate here that shikonin can confer a potent stimulatory effect on the EMT process and suppress the associated-microRNAs expression in vivo in skin tissues.
Project description:TREX2 is a keratinocyte specific 3â-deoxyribonuclease that participates in the maintenance of skin homeostasis upon damage. This transcriptome analysis identified multiple genes and pathways deregulated by TREX2 loss in the IMQ-induced psoriasis-like model in mouse skin. mRNA sequencing of 5 biological replicates of skin from wild-type mice treated with Imiquimod and 6 of Trex2 knockout mice treated with Imiquimod
