Effect of enhanced melanin synthesis on the production of extracellular vesicles in melanocytes and communication with keratinocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA818167 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18395817.fastq.gz | Fastqsanger.gz | |||
| SRR18395818.fastq.gz | Fastqsanger.gz | |||
| SRR18395819.fastq.gz | Fastqsanger.gz | |||
| SRR18395820.fastq.gz | Fastqsanger.gz | |||
| SRR18395821.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Extracellular vesicle(EV) secretion and capture is an important method of communication between cells. Melanocytes and their surrounding keratinocytes form epidermal melanin units in the thin, outermost layer of the skin to protect the skin from ultraviolet radiation damage. It is important to understand the mechanisms by which changes in melanocyte EV signal transduction influence pigmentation. Mouse melanocytes (melan-α cell) overexpressing MITF and CD63-GFP were used to to investigate the effect on vesicle formation by WB and SEM. Coculturing of melanocyte with keratinocyte(PAM212) was used to explore the polarization of vesicles and transfer between cells by immunofluorescence, flow cytometry. EVs from melanocytes were extracted and used to investigate changes in the miRNA profile of EVs, and the effect of exosomal miR-28 on keratinocyte growth and transcriptomics was analyzed by flow cytometry, TEM, particle size analysis, WB, the iCELLigence system and RNA-seq analysis.Our results indicate that melanocytes in the skin affected vesicle synthesis under the condition of enhanced melanin synthesis function: the expression of CD81, VPS37, VPS36B and Rab27b (melanosome and vesicle transport protein during ESCRT machinery) increased. Keratinocytes can cause the polarization of vesicles in melanocytes and capture EVs from melanocytes via plasmalemma fusion. Analysis of the miRNA profile derived from melanocyte EVs showed that the expression levels of miR-125, miR-130, miR-211, miR-127, miR-692 and miR-709 were increased, while the expression levels of miR-28, miR-744, let-7g and miR-6240 were decreased. The content of miR-28 in EVs may be reduced to induce keratinocytes to prevent carcinogenesis, resist infection and prevent premature apoptosis.
2022-03-23 | GSE199035 | GEO
Project description:Extracellular vesicle(EV) secretion and capture is an important method of communication between cells. Melanocytes and their surrounding keratinocytes form epidermal melanin units in the thin, outermost layer of the skin to protect the skin from ultraviolet radiation damage. It is important to understand the mechanisms by which changes in melanocyte EV signal transduction influence pigmentation. EVs from melanocytes were extracted and used to investigate changes in the miRNA profile of EVs, and the effect of exosomal miR-28-3p on keratinocyte with transcriptomics was analyzed by RNA-seq analysis.Our results indicate that the content of miR-28 in EVs may be reduced to induce keratinocytes to prevent carcinogenesis, resist infection and prevent premature apoptosis.
2022-03-28 | GSE199220 | GEO
Project description:Melanoma arises from transformation of melanocytes in the basal layer of the epidermis where they are surrounded by keratinocytes, with which they interact through cell contact and paracrine communication. Although research focuses on how the accumulation of oncogene and tumor suppressor gene mutations in melanocytes drive melanoma development, how alterations in keratinocytes serve as extrinsic drivers of melanoma initiation and progression is poorly understood. We recently identified keratinocyte desmoglein 1 (Dsg1) as an important mediator of keratinocyte:melanoma crosstalk. Here we address the extent to which Dsg1 loss, which occurs in response to acute environmental stress such as ultraviolet radiation, affects early steps in melanomagenesis. RNA-Seq analysis revealed that paracrine signals from Dsg1-deficient keratinocytes mediate a transcriptional switch from a differentiated to undifferentiated cell state in melanocytes expressing BRAFV600E. Of 221 differentially expressed genes in BRAFV600E cells treated with Dsg1-deficient conditioned media (CM), the laminin superfamily member NTN4/Netrin-4, which inhibits senescence in endothelial cells, stood out. Indeed, while BRAFV600E melanocytes treated with Dsg1-deficient CM showed signs of senescence bypass, knockdown of NTN4 reversed these effects. These results suggest that Dsg1 loss in keratinocytes provides an extrinsic signal to push melanocytes towards oncogenic transformation once an initial mutation has been introduced.
2024-11-18 | GSE255546 | GEO
Project description:Transcriptome profiling (mRNA-seq) of Fibroblasts, keratinocytes, melanocytes and melanocytes irradiated with UVB
2020-02-08 | GSE110375 | GEO
Project description:We used whole transcriptome sequencing (RNA-Seq) to assess differential gene expression of normal human melanocytes with respect to keratinocytes, fibroblasts and whole skin. We have identified a number of genes and pathways, which are characteristic or unique for MC compared to KC and FB. We also demonstrated the extent of the difference between genes detectable in MC culture and the whole skin. The present results reveal melanocytes as highly proliferative cells with stem cell-like properties.
2017-02-09 | GSE94655 | GEO
Project description:Dickkopf 1 (DKK1), which is expressed at high mRNA levels by fibroblasts in the dermis of human skin on the palms and soles, inhibits the function and proliferation of melanocytes in the epidermis of those areas via the suppression of beta-catenin and microphthalmia-associated transcriptor factor (MITF). In this study, we report that treatment of keratinocytes with DKK1 increases their proliferation and decreases their uptake of melanin, and that treatment of reconstructed skin with DKK1 induces a thicker and less pigmented epidermis. We investigated the effects of DKK1 on keratinocytes using DNA microarray technology. Keywords: compound treatment design
2007-12-31 | GSE9211 | GEO
Project description:The function and survival of melanocytes is regulated by an elaborate network of paracrine factors synthesized mainly by epidermal keratinocytes. Keratinocytes and melanocytes respond to UV exposure by eliciting a tanning response. However, how keratinocytes and melanocytes interact in the absence of UV exposure is unknown. Here, we demonstrate that after Spry1 knockout in epidermal keratinocytes, melanocyte stem cells (McSCs) in the hair follicle exit the stem cell niche without depleting the pool of these cells. We also found that McSCs migrate to the epidermis in a Scf/C-kit-dependent manner induced by a tanning-like response resulting from Spry1 loss in epidermal keratinocytes. Once there, these cells differentiate into functional melanocytes. These findings show the potential for developing therapies for skin pigmentation disorders by manipulating McSCs.
2024-02-21 | GSE252889 | GEO
Project description:Melanoma is an aggressive cancer typically arising from transformation of melanocytes residing in the basal layer of the epidermis, where they are in direct contact with surrounding keratinocytes. The role of keratinocytes in shaping the melanoma tumor microenvironment remains understudied. We previously showed that temporary loss of the keratinocyte-specific cadherin, Desmoglein 1 (Dsg1) controls paracrine signaling between normal melanocytes and keratinocytes to stimulate the protective tanning response. Here, we provide evidence that melanoma cells hijack this intercellular communication by secreting factors that keep Dsg1 expression low in surrounding keratinocytes, which in turn generate their own paracrine signals that enhance melanoma spread through CXCL1/CXCR2 signaling. Evidence suggests a model whereby paracrine signaling from melanoma cells increases levels of the transcriptional repressor Slug, and consequently decreases expression of the Dsg1 transcriptional activator Grhl1. Together, these data support the idea that paracrine crosstalk between melanoma cells and keratinocytes resulting in chronic keratinocyte Dsg1 reduction contributes to melanoma cell movement associated with tumor progression.
2023-09-11 | GSE239634 | GEO
Project description:Immortalized, amelanotic melanocytes isolted from skin of Balb/c express enzymatically-inactive tyrosinase due to a homozygous point mutation (TGT->TCT) in tyrosinase gene, resulting in a lack of melanin . To serve as a control cell line, pigmentation was restored in these cells by correcting the point mutation using an RNA-DNA oligonucleotide (kingly gift from Dr. Alexeev Y. Vitali). We used microarray to detail the effect of tyrosinase mutation on gene expression in normal versus mutant melanocytes. Pigmented and non-pigmented melanocytes were grown for RNA extraction and hybridization on Affymetrix microarrays. We used both normal and mutant melanocyte in order to obtain expression profiles. We then examined variances in gene expression between the two cell lines.
2013-09-21 | E-GEOD-51073 | biostudies-arrayexpress
Project description:Cell-cell communication between keratinocytes and fibroblasts is essential for skin homeostasis, regulation and regeneration. How extracellular cytokine signaling, intra-cellular protein signaling and transcriptional regulation initiate and maintain this communication is still largely unknown. Here, we study in vitro the secretome and transcriptome dynamics that establish double paracrine cell-cell communication between primary human keratinocytes and fibroblasts. We find that keratinocyte-derived interleukin 1α initiates the cell communication, eliciting a constitutive NF-κB-mediated inflammation response in the fibroblasts. Their resulting transcriptome response over at least 12 hours induces a fibroblast secretome capable of enhancing keratinocyte migration. Applying partial least square regression to secretome perturbation experiments using recombinant proteins or antibodies demonstrates the synergistic interaction of early and late secreted inflammatory CC and CXC chemokines as well as IL6, whose relative composition directly controls keratinocyte migration. Conversely, inhibiting individual cytokines during cell-communication abrogates the keratinocyte phenotype. Hence, only the simultaneous activity of multiple inflammatory cytokines together with prolonged inflammatory response in the fibroblasts lead to increased keratinocyte migration after double paracrine cell communication, putatively serving as safeguard mechanisms for proper skin regeneration.
2019-10-22 | GSE53037 | GEO