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The function of DP cells during the development of hair follicles in cashmere goats

ABSTRACT: OBJECTIVE: To study the function of DP cells during the development of hair follicles in cashmere goats, we used single-cell sequencing to perform transcriptome sequencing of skin samples from different periods. Method: Single cell barcoding and library preparation were performed based on 10x Genomics single-cell RNA sequencing platform, CellRanger (v2.2.0) software was used for analyzing raw sequencing data, the quality control (QC) and cell clustering were analyzed with single- Cell RNA seq Seurat software (v2.3.0) based on R environment, Monocle (v 2.4.0) was used to order single cells along pseudotime according, Metascape (http://metascape.org/gp/index.html#/main /step1) was used to perform gene ontology (GO) analysis Conclusion: we show the function of four different intermediate DP cells: Intermediate cells 10 show important functions in the growth of villi and maintenance of villus attachment to the skin, and intermediate cell 1 shows important functions in the process of apoptosis and villous shedding of hair Follicles, intermediate cell 0 initiates a new follicular cycle, completes the migration of hair follicles and the occurrence of villi, and intermediate cell 15 maybe DP progenitor cells, In addition, we speculated the apoptotic order of different bulge cells. More importantly, we provided a molecular landscape for the mechanism of DP cells in the process of hair follicle cycle initiation. Skin samples from telogen, anagen, and catagen were used to sequence single-cell transcriptomes, revealing the function and evolution of DP cells.

ORGANISM(S): Capra hircus

PROVIDER: GSE141284 | GEO | 2020/01/15

REPOSITORIES: GEO

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Project description:The vitamin D receptor (VDR) regulates cell proliferation and differentiation including epidermal keratinocytes by modulating transcription of its target genes. We are investigating the role of VDR in epidermal stem cells and their progenies in the regeneration process of epidermis and hair in the skin. VDR null mice are utilized in which VDR is specifically deleted in keratin 14 (K14) expressing keratinocytes by Cre-lox strategy. The impact of VDR deletion was evaluated by comparison of VDR null mice with no cre littermate control mice. The VDR was abundantly expressed in potential epidermal stem cells including basal cells in interfollicular epidermis (IFE), and in CD34 expressing bulge keratinocytes in hair follicles. Gene expression profiles and subsequent pathway analysis of stem cell enriched keratinocyte populations revealed that the VDR deletion significantly suppressed β-catenin signaling as well as VDR signaling. The role of VDR in epidermal stem cells was studied during hair follicle cycling and wound healing processes. The epidermal stem cells were not appropriately stimulated by hair depilation, and did not reinitiate anagen in the hair follicles resulting in a failure of hair regrowth. In addition, the stem cells were not fully activated after full thickness wounds were generated in VDR null skin under a low calcium diet to suppress compensation pathways. Cell proliferation was not fully induced in potential stem cells located in both IFE and hair follicles near the wounding edges, and re-epithelialization rate was delayed in VDR null skin. Gene expression profiling of the wounded skin (3 days after injury) indicated that β-catenin signaling was not fully induced in VDR null skin comparable to that observed in β-catenin null mice. The β-catenin target genes including Axin2 and cell cycle regulators involved in epidermal stem cell function were not induced in the edges of the wound of VDR null skin. These results demonstrated that VDR plays an essential role in hair cycling and wound healing processes through regulation of β-catenin signaling in epidermal stem cells and their progenies. n=3 CON and KO (each sample contain RNA isolated from wounded or nonwounded skins excised from 3 mice)

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The function of DP cells during the development of hair follicles in cashmere goats

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