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E-MTAB-9362

ABSTRACT: LXR mediated-signalling protects human hair follicles against doxorubicin-induced toxicity ex vivo

PROVIDER: E-MTAB-9362 | ExpressionAtlas | 2025-01-23

REPOSITORIES: ExpressionAtlas

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LXR mediated-signalling protects human hair follicles against doxorubicin-induced toxicity ex vivo

Project description:LXR mediated-signalling protects human hair follicles against doxorubicin-induced toxicity ex vivo

| PRJEB39421 | ENA

LXR mediated-signalling protects human hair follicles against doxorubicin-induced toxicity ex vivo

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

Hair follicles engage in chemosensation: Olfactory receptor OR2AT4 regulates human hair growth

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:Cardiac toxicity induced by doxorubicin

| PRJNA1035242 | ENA

Gene expression analysis of the p53 response in PHA-stimulated human T-lymphocytes

Project description:Gene expression analysis of the p53 response in PHA-stimulated human T-lymphocytes treated ex vivo with either Doxorubicin, Nutlin-3, or DMSO

2018-07-24 | GSE110369 | GEO

CRISPRi/a screen of doxorubicin induced cardiotoxicity

Project description:Druggable genome of CRISPRi/a sgRNA libraries for druggable genes protecting doxorubicin induced cardiomyocyte toxicity using human induced pluripotent stem cell (iPSC) derived cardiomyocytes.

2024-09-01 | GSE276161 | GEO

Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description:Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

| PRJNA1203896 | ENA

Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description:Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

| PRJNA994158 | ENA

Effect of Annona Muricata Leaves on Colorectal Cancer Patients and Colorectal Cancer Cells

Project description:Annona muricata L., include the leaves, is found to contain biologically active Annonaceous acetogenins and plant polyphenols that are important components of human diet and a number of them are considered to have chemopreventive and therapeutic properties against cancer. To confirm previous findings in in vitro, animal study and traditionally use, a human, ex vivo and in vitro studies were conducted to evaluate the effects of consecutive ingestion of A. muricata leaves extract for eight weeks.

| 2189667 | ecrin-mdr-crc

JAK-STAT1 as therapeutic target for EGFR deficiency-associated inflammation and scarring alopecia (scRNA-seq)

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

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