RNA sequencing of hydrogen peroxide (H2O2)-treated melanocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE216447 | GEO | 2023/07/28
REPOSITORIES: GEO
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Project description:RNA sequencing of hydrogen peroxide (H2O2)-treated melanocytes
| PRJNA893636 | ENA
Project description:Purpose: Determine the mechanism of particulate matter-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with particulate matter (5 μg/cm2) and incubated for 24 h. Total RNA (1 ug) from melanocytes were extracted and subjected to library synthesis. Results: Particulate matter-treated melanocytes exhibited upregulation of ER stress, unfolded protein response, and melanogenesis-related molecules. Conclusion: Particulate matter-induced melanocyte signaling was well evaluated using RNA sequencing.
2021-08-19 | GSE165333 | GEO
Project description:Purpose: Determine the mechanism of high mobility group box 1 (HMGB1)-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with HMGB1 (1 μg/ml) and incubated for 24 h. Total RNA (500 ng) from melanocytes were extracted and subjected to library synthesis. Results: HMGB1-treated melanocytes exhibited upregulation of cell death and type 1 interferon-related genes. Conclusion: HMGB1-induced melanocyte signaling was well evaluated using RNA sequencing.
2023-07-28 | GSE216423 | GEO
Project description:Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Melanocyte dysfunction leads to pigmentation defects including albinism, vitiligo, and piebaldism and is a key feature of systemic pathologies such as Hermansky-Pudlak (HP) and Chediak-Higashi (CH) Syndromes. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Surprisingly, suppression of BMP signaling does reduce neural crest yield. Subsequent differentiation of hESC-derived melanocyte precursors under defined conditions yields pure populations of pigmented cells matching the molecular and functional properties of adult melanocytes. Melanocytes from patient-specific iPSCs faithfully reproduce the ultrastructural features of the HP- and CH-specific pigmentation defects with minimal variability across lines. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders. Total RNA obtained from embryonic stem cells (ESCs), ESC-derived melanocyte progenitors, ESC-derived mature melanocytes, primary melanocytes, and disease-specific induced pluripotent stem cell-derived melanocytes.
2013-06-01 | E-GEOD-45226 | biostudies-arrayexpress
Project description:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target. Biologic replicates of UVA- and UVB-treated mouse melanocytes, as well as untreated mouse melanocytes and mouse keratinocytes, were used to define melanocyte expression signatures associated with UV treatment.
2011-01-01 | E-GEOD-25164 | biostudies-arrayexpress
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived H2O2-treated HCC transcriptome profiling (RNA-seq) to NGS-derived mock-treated HCC transcriptome profiling. Methods: HCC mRNA profiles of mock-treated Huh7 cells and H2O2-treated Huh7 cells were generated by deep sequencing, in duplicate, using Illumina Pipeline (CASAVA) v1.8.2. The sequence reads that passed quality filters were analyzed at the transcript isoform level with TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: RNA-seq data validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.90. Conclusions: We conclude that our study represents the first detailed analysis of H2O2-treated HCC cells transcriptomes compared to mocke-treated HCC cells, with biologic replicates, generated by RNA-seq technology.
2021-01-30 | GSE109915 | GEO
Project description:Nrf2-Keap1 signaling pathway protects cells against photo-oxidative stress. Yet in recent works, its role in melanogenesis together with cell protection functions against oxidative stress has been gaining interest. However, its effect on melanogenesis still has contradictory results from different studies. The aims of our study were to investigate the effect of Keap1 silencing in melanocyte on melanogenesis and its associated mechanism. Primary human epidermal melanocytes and melan-a cell line were used for this experiment. RNA sequencing was done to identify genes involved in melanocyte biology using Keap1 knockdown through siRNA techniques. And melanogenesis and the expression of melanogenesis-associated molecules were evaluated in Keap1 silenced melanocyte to examine the effects of Keap1 on melanogenesis, melanocyte growth, and related pathways. RNA-sequencing data revealed that Keap1 knockdown in primary human epidermal melanocytes (PHEMs) induced cell survival-related gene expression. Additionally, siRNA-mediated inhibition of Keap1 led to upregulation of MITF and melanogenesis-associated molecules along with Nrf2 activation in PHEMs. HO-1, a major gene that is upregulated in RNA-sequencing using Keap1-silenced PHEMs, protected melanocytes against H2O2-induced cell death and upregulated MITF and β-catenin expression. Further, increased expression of melanogenesis-associated molecules after Keap1 silencing was validated to occur through HO-1-associated β-catenin activation in a Keap1 and HO-1 double knockdown experiment. This work suggests that Keap1 silencing in melanocytes induced melanogenesis and the expression of melanogenesis-associated molecules through HO-1-associated β-catenin activation. Keap1 downregulation in melanocytes is important for cell proliferation and survival.
2018-01-20 | GSE93895 | GEO
Project description:Melanocytes are pigment-producing cells of neural crest origin responsible for protecting the skin against UV-irradiation. Melanocyte dysfunction leads to pigmentation defects including albinism, vitiligo, and piebaldism and is a key feature of systemic pathologies such as Hermansky-Pudlak (HP) and Chediak-Higashi (CH) Syndromes. Pluripotent stem cell technology offers a novel approach for studying human melanocyte development and disease. Here we report that timed exposure to activators of WNT, BMP and EDN3 signaling triggers the sequential induction of neural crest and melanocyte precursor fates under dual-SMAD inhibition conditions. Using a SOX10::GFP hESC reporter line, we demonstrate that the temporal onset of WNT activation is particularly critical for human neural crest induction. Surprisingly, suppression of BMP signaling does reduce neural crest yield. Subsequent differentiation of hESC-derived melanocyte precursors under defined conditions yields pure populations of pigmented cells matching the molecular and functional properties of adult melanocytes. Melanocytes from patient-specific iPSCs faithfully reproduce the ultrastructural features of the HP- and CH-specific pigmentation defects with minimal variability across lines. Our data define a highly specific requirement for WNT signaling during neural crest induction and enable the generation of pure populations of hiPSC-derived melanocytes for faithful modeling of human pigmentation disorders.
2013-06-01 | GSE45226 | GEO
Project description:Adaptation to hydrogen peroxide in Saccharomyces cerevisiae is profiled with expression arrays. Adaptation describes the process in which a mild dose of toxin (in this case, hydrogen peroxide) is able to protect against a later acute dose. Here, we study two adaptive protocols (0.1 mM H2O2 and 0.1 + 0.4 mM H2O2) and one acute protocol (0.4 mM H2O2) to identify processes uniquely involved in adaptation. Predictions from these studies are validated in expression profiling of deletion mutants of the transcription factors Yap1, Mga2, and Rox1.
2009-04-23 | GSE12602 | GEO
Project description:Little is known about the mechanisms underlying the localization of human melanocytes during embryogenesis, and how the characteristics of melanocytes differ in various body sites. Immunohistochemical studies of biopsy tissue obtained from four different anatomic sites (scalp, back, abdomen, and sole) of 31 aborted fetuses following the approval of the ethics committee for the study of human gene analysis revealed that the melanocyte-associated marker gp100 was expressed earlier in embryogenesis than other melanocyte markers. Human fetal melanocytes are initially localized in the epidermis, and then migrate to the hair buds from the epidermis but not the dermis. In the sole, melanocytes localize in eccrine sweat gland ducts. Cultured fetal melanocytes did not stain positively for any melanocyte markers other than MITF and nestin. When co-cultured with normal human keratinocytes and fibroblasts, fetal melanocytes stained positively for gp100. Gene expression studies indicated that fetal melanocytes were topographically diverse, especially sole-derived melanocytes compared with other melanocytes. Expression of several genes, including CHI3L1 and FGF7, was higher in sole-derived melanocytes. These findings suggest that human fetal melanocytes derived from the sole have different profiles both in vivo and in vitro compared with melanocytes from other sites. In this study, microarray analyses were performed using cultured fetal melanocytes from 4 different sites (scalp, back, abdomen and sole) obtained at 19 WOG, and newborn normal epidermal melanocyte as a control. RNA purification was performed using an RNeasy Mini kit (Qiagen, Germany) and those 5 samples, were analyzed using GeneChip 1.0 ST Array (Affymetrix, CA, USA).
2011-04-30 | E-GEOD-24041 | biostudies-arrayexpress