Dataset Information

Gene expression in mouse whole proliferative phase wounds in response to alterations in β-Catenin levels [induced post-injury].

ABSTRACT: β-Catenin is a regulator of cutaneous wound repair. The expression of genes that are modulated in response to changes in β-Catenin levels (stabilization and downregulation) in cutaneous mouse wounds, post injury, during the proliferative phase of repair, was investigated. We are particularly interested in genes that are modulated (in opposite directions) in response to both the induction (stabilization) versus downregulation of β-Catenin. To investigate this, conditional β-Catenin stabilized (Harada, N., et al. EMBO J. 1999 Nov 1;18(21):5931-42) mice were injected with either a Cre-expressing adenovirus, or a GFP-expressing control virus, three days following injury, and wounds were harvested eight days post injury. For conditional knockdown of β-Catenin, mice generated from a cross between conditional β-Catenin knockdown mice (Brault, V. et al., Development. 2001 Apr;128(8):1253-64), and mice that express a tamoxifen-inducible form of Cre (Hayashi, S., and McMahon, A.P., Dev Biol. 2002 Apr 15;244(2):305-18), were treated with Tamoxifen for five days, beginning at the third day after injury. Wounds were harvested eight days after wounding. This provides insight into the identities of genes modulated in response to changes in β-Catenin levels during the proliferative stage of cutaneous wound repair.

ORGANISM(S): Mus musculus

PROVIDER: GSE50153 | GEO | 2018/12/31

REPOSITORIES: GEO

ACCESS DATA

Similar Datasets

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)

Dataset Information

Gene expression in mouse whole proliferative phase wounds in response to alterations in β-Catenin levels [induced post-injury].

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure