E-MTAB-9362
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9362 | ExpressionAtlas | 2025-01-23
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:LXR mediated-signalling protects human hair follicles against doxorubicin-induced toxicity ex vivo
| PRJEB39421 | ENA
Project description:Although chemotherapy-induced alopecia (CIA) is one of the most distressing adverse effects of cancer treatment, there are still no pharmacological interventions available and there remains an urgent unmet need to identify novel targets for therapy. We hypothesized that selected compounds which enhance ABC transporter activity and thus drug efflux from CIA-affected hair follicle (HF) epithelium may award relative protection from chemotherapy-induced HF toxicity. We found that the LXR agonist T0901317 significantly increased cell survival, attenuated LDH release, caspase-3 activity and DNA double strand breaks (DSBs) in doxorubicin (DOX)-treated outer root sheath keratinocytes (ORS-KCs) in vitro and protected human HFs from DOX-induced apoptosis ex vivo. RNA sequencing was performed to investigate the potential mechanism(s) by which T0901317 may protect against DOX-induced cell survival and apoptosis of ORS-KC.
2021-02-19 | E-MTAB-9362 | biostudies-arrayexpress
Project description:RNA sequencing of native and ex vivo cultured murine tail tendon fascicles
2021-01-19 | E-MTAB-9540 | ExpressionAtlas
Project description:Transcription profiling by array to investigate doxorubicin-induced toxicity in human cardiomyocytes derived from embryonic stem cell line SA121
2025-01-23 | E-MTAB-6045 | ExpressionAtlas
Project description:3-Seq of ex vivo isolated mouse multipotent steady state hematopoietic stem cells (sHSC) and proliferating HSCs
2019-01-16 | E-MTAB-7390 | ExpressionAtlas
Project description:Expression data from normal and MDS erythroids cell cutlures ex vivo
2025-01-24 | E-GEOD-34268 | ExpressionAtlas
Project description:Olfactory receptors (OR) regulate physiological cell functions beyond olfaction. Here, we show that human hair follicle (HF) epithelium engages in chemosensation: it expresses OR2AT4, whose stimulation by a synthetic sandalwood odorant (prolongs hair growth (anagen) ex vivo via increased IGF-1 production. Instead, OR2AT4-silencing inhibits hair growth. Thus, human HFs can “smell” and require OR2AT4-mediated signaling to sustain their growth, inviting novel therapeutic hair growth regulation by targeting HF chemosensation.
2017-08-29 | GSE102887 | GEO
Project description:The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signalling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients indicated active STAT1 signalling and interferon target expression. Notably, a case study of folliculitis decalvans, characterized by progressive hair loss, scaling and perifollicular erythema, demonstrated successful treatment with JAK1/2 inhibition. Our findings offer molecular insights and present a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.
2024-07-31 | GSE273572 | GEO
Project description:The hair follicle stem cell niche is an immune-privileged microenvironment, characterized by reduced antigen presentation, thus shielding against permanent immune-mediated tissue damage. In this study, we demonstrated the protective role of hair follicle-specific epidermal growth factor receptor (EGFR) against scarring hair follicle destruction. Mechanistically, disruption of EGFR signalling generated a cell-intrinsic hypersensitivity within the JAK-STAT1 pathway, which, synergistically with interferon gamma expressing CD8 T-cell and NK-cell-mediated inflammation, compromised the stem cell niche. Hair follicle-specific genetic depletion of either JAK1/2 or STAT1 or therapeutic inhibition of JAK1/2 ameliorated the inflammation, restored skin barrier function and activated the residual stem cells to resume hair growth in mouse models of epidermal and hair follicle-specific EGFR deletion. Skin biopsies from EGFR inhibitor-treated and cicatricial alopecia patients indicated active STAT1 signalling and interferon target expression. Notably, a case study of folliculitis decalvans, characterized by progressive hair loss, scaling and perifollicular erythema, demonstrated successful treatment with JAK1/2 inhibition. Our findings offer molecular insights and present a mechanism-based therapeutic strategy for addressing chronic folliculitis associated with EGFR-inhibitor anti-cancer therapy and cicatricial alopecia.
2024-07-31 | GSE273571 | GEO
Project description:mRNA-Seq of zebrafish embryos (96hpf) exposed to different concentrations of Chlorpyrifos below acute toxicity levels against untreated control groups
2023-06-16 | E-MTAB-9853 | ExpressionAtlas