Troy/Tnfrsf19 marks epidermal cells that govern interfollicular epidermal renewal and cornification
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE165379 | GEO | 2021/08/05
REPOSITORIES: GEO
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Project description:There are multiple stem cells in adult mammalian epidermis, but the mechanisms controlling lineage specification are poorly understood. To identify gene expression signatures of the three major epidermal differentiation compartments we micro-dissected individual SG, IFE and HF from adult epidermis. The RNA was isolated from age and sex matched wild-type mice and performed transcriptome analysis with Affymetrix Exon microarrays We micro-dissected individual interfollicular epidermis (IFE), hair follicle (HF) and sebaceous gland (SG) from adult tail epidermis. The RNA was isolated from age and sex matched wild-type mice. Three biological replicates for each epidermal differentiation compartment were analyzed.
2017-05-16 | E-GEOD-62604 | biostudies-arrayexpress
Project description:Troy/Tnfrsf19 marks epidermal cells that govern interfollicular epidermal renewal and cornification
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Project description:We report global transcriptional profiles of epidermal basal cells from plantar skin of control mice, high fat diet-fed (HFD) mice and aged mice. By RNA-sequencing of FACS-isolated interfollicular epidermal (IFE) basal cells, we revealed that calcium signal-associated genes, which regulate differentiatin of keratinocytes,were enriched in the plantar skin of HFD and aged mice.
2022-05-15 | GSE171035 | GEO
Project description:Purpose: To unravel the molecular heterogeneity of distinct epidermal populations in interfollicular epidermis (IFE) in vivo Methods: We performed bulk RNA sequencing of FACS purified basal (Sca1+/alpha6-integrin+) IFE cells enriched in Slc1a3/Dlx1/Aspm CreER marked lineages. We used >10000 tdTomato+/Sca1+/α6-int+ (basal) cells from both back and tail skin at 2-weeks post TM induction from each of four CreER mouse lines and normalized them to Sca1+/α6-int+ sorted from the same mouse. Extracted RNA of high quality and low input was processed for library preparation followed by Illumina seq on HiSeq4000. The raw sample-specific FASTQ files were trimmed and mapped to the reference genome/transcriptome (mouse/mm10) and DESeq2 v1.26.0 were used to generate normalized counts and statistical analysis of differential gene expression.
2022-07-05 | GSE205744 | GEO
Project description:Although interfollicular epidermal (IFE) differentiation is thought to be stepwise as reflected in sharp boundaries between the basal, spinous, granular and cornified layers, this prediction has not been studied at a single cell resolution. We used single cell RNA-seq to show that IFE differentiation is best described as a single step gradualistic process with a large number of transition cells between the basal and spinous layer. RNA-velocity analysis identifies a commitment point that separates the plastic basal and transition cell state from the unidirectionally differentiating cells. We also show that GRHL3, best known for promoting IFE terminal differentiation, has a major function in suppressing epidermal stem cell expansion and the emergence of an abnormal stem cell state by suppressing Wnt signaling in stem cells.
2020-09-01 | GSE154579 | GEO
Project description:The epidermis and associated appendages ensure a number of critical functions necessary for survival and social interactions. Perturbations of epidermal stem cell homeostasis lead to a variety of skin diseases affecting humans and dogs. Therefore, the establishment of an in vitro system to investigate canine epidermal stem cells, representing a model for human diseases, is essential. Here we report the establishment and characterization of organoids derived from microdissected canine hair follicles (HFs) and interfollicular epidermal (IFE). Gene and protein expression analysis revealed high mRNA and protein levels of keratin 5 and 14, IFE differentiation markers and intercellular molecules (e.g., keratin 10 and desmoglein), indicating a strong basal cell signature as well as differentiation towards mature epidermis. Key markers of HF stem cells were lacking. This suggests that, independently of the tissue of origin, both organoid lines develop into the same cell type (basal IFE-like keratinocytes). Signaling pathways members important for regulation of HF growth and cycling (such as Wnt, Hh, BMP and Notch) were present in both HF and IFE organoids at low levels. Withdrawal of growth factors (Noggin, R-spondin and FGFs) resulted in upregulation of markers such as KRT16, IVL, KRT17 and SOX9, showing the potential of the organoids to develop towards more differentiated tissue. However, for induction of HF signatures or hair growth, addition of different growth factors or dermal papilla co-culture might be required. Taken together, our in vitro culture system can provide the basis to address hair growth and explore epidermal function/regeneration, allowing us to further investigate pathomechanisms of cutaneous disorders in dogs and potentially human patients.
2018-07-02 | GSE104622 | GEO
Project description:The skin interfollicular epidermis (IFE) is the first barrier against the external environment and its maintenance is critical for survival. Two seemingly opposite theories have been proposed to explain IFE homeostasis. One posits that IFE is maintained by a long-lived slow-cycling stem cell (SC) population that give rise to short-lived transit-amplifying (TA) cell progeny, while the other suggests that homeostasis is achieved by a single committed progenitor (CP) that balances stochastic fate. Here, we probed the cellular heterogeneity within the IFE using two different inducible CREER targeting IFE progenitors. Quantitative analysis of clonal fate data and proliferation dynamics demonstrate the existence of two distinct proliferative cell compartments composed of slow-cycling SC and CP, both of which undergo population asymmetric self-renewal. However, following wounding, only SCs contribute substantially to the repair and long-term regeneration of the tissue, while CP cells make a minimal and transient contribution. Transcriptional profile of InvCREER/RosaYFP and K14CREER/RosaYFP targeted FACS-isolated alpha6 integrin-high CD34-neg basal cells from mouse tail epidermis. Skin epidermis was removed from tail bone and incubated overnight in HBSS (Gibco) 0.25% trypsin (Gibco) at 4M-BM-0C. Epidermis was separated from the dermis and incubated on a rocking plate (100 rpm) at room temperature for 5 min. Basal cells were mechanically separated from the epidermis by flushing 10 times under the epidermis. Tissues were then cut in pieces of 1 mm2 with scalpel, and trypsin was neutralized by adding DMEM medium (Gibco) supplemented with 2% Chelex Fetal Calf Serum (FCS). Samples were filtrated on 70 and 40M-BM-5m filter (Falcon). Immunostaining was performed using biotin-conjugated anti-CD34 (clone RAM34; BD Biosciences) PE-conjugated anti-M-NM-16-integrin (clone GoH3; BD biosciences). Primary antibodies were washed with 2% FCS/PBS and cells were incubated for 30 min in APC conjugated streptavidin (BD Biosciences) secondary antibodies, on ice, with shaking every 10 min. Living K14- and involucrin-expressing epidermal cells were gated by forward scatter, side scatter, negative staining for Hoechst dye and by following the YFP signal. Basal cells from the interfollicular epidermis were targeted using CD34 negative alpha 6 high gating. Fluorescence-activated cell sorting analysis was performed using FACSAria I at high pressure (70 psi) and FACSDiva software (BD Biosciences). Sorted cells were harvested directly in the lysis buffer provided by the RNeasy microkit (QIAGEN) supplemented with 1M-BM-5l of beta-mercaptoethanol for every 100M-BM-5l of lysis buffer. RNA extraction was performed on freshly sorted cells according to the manufacturerM-bM-^@M-^Ys protocol.
2012-09-07 | E-GEOD-36688 | biostudies-arrayexpress
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 skins excised from 3 mice)
2015-07-31 | E-GEOD-68728 | biostudies-arrayexpress
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 extracted from keratinocytes, which is isolated from VDR KO and littermate control skins excised from 3 mice)
2015-07-31 | E-GEOD-68729 | biostudies-arrayexpress
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)
2015-07-31 | E-GEOD-68727 | biostudies-arrayexpress