Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A novel butyrate derivative, zinc dibutyroyllysinate, blunts MITF expression and up-regulates retinol and differentiation pathway mRNAs in a full-thickness human skin model

ABSTRACT: Lysine, butyric acid and zinc play important roles in skin homeostasis that involve aging, inflam-mation and prevention of skin barrier disruption. This bioactivity spectrum is not replicated by any one topical compound currently in use. Our purpose in this study was to characterize a novel compound, zinc dibutyroyllysinate (ZDL), consisting of zinc with lysine and butyric acid moieties. We used RNA-seq to evaluate its effect on gene expression in a full-thickness skin model. We show that lysine alone has minimal effects on gene expression, whereas ZDL had greater transcriptional bioactivity. Effects of ZDL included increased expression of genes promoting epidermal differenti-ation and retinol metabolism, along with decreased expression of microphthalmia-associated transcription factor (MITF) and other melanogenesis genes. These effects were not replicated by an alternative salt compound (i.e., calcium dibutyroyllysinate). ZDL additionally led to a dose-dependent increase of extracellular matrix proteins in skin fibroblasts, including collagen I, collagen IV and prolidase. Loss of melanin secretion was also seen in ZDL-treated melanocytes. These results provide an initial characterization of ZDL as a novel topical agent. Our findings support a rationale for development of ZDL as a skincare ingredient, with potential applications for diverse conditions involving melanocyte hyperactivity, pigmentation, inflammation, or aging.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290668 | GEO | 2025/03/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE290668_Counts_all_samples.txt.gz	Txt

Items per page:

1 - 2 of 2

Similar Datasets

Effects of hydroquinone on whole-genome scale transcription of human epidermal keratinocytes.

Project description:Hydroquinone (HQ) is a well-known phenolic compound that causes chemical leukoderma. Hydroquinone was once used as photographic developers for films and papers, and it is widely used as a topical application in skin whitening to reduce the color of skin. Recently, the United States Food and Drug Administration (US FDA) banned all over-the-counter products with hydroquinone due to its potential toxicity. Topical cream with hydroquinone up to 4% should be prescribed and used with specific caution. In this study, to elucidate the toxicological role of keratinocyte in the pathogenesis of chemical leukoderma, we analyzed genome-wide transcriptional data of cultured human epidermal keratinocytes (HEKs) treated with sub-cytotoxic hydroquinone concentration.

2019-07-21 | GSE126721 | GEO

Gene expression data from atopic dermatitis induced NC/Nga mouse model skin

Project description:We identified zinc-alpha-2-glycoprotein (ZAG), a 41-kDa adipokine that regulates body weight, lipid, and mobilization, as a novel biomarker for AD. ZAG levels were consistently decreased in sera, T cells, and skin in human AD patients compared with healthy controls. We used microarrays to obtain the change of signaling molecules by topical treatment of recombinant ZAG using atopic dermatitis induced mouse model.

2019-01-03 | GSE124550 | GEO

Bakuchiol and ethyl (linoleate/oleate) synergistically modulate endocannabinoid tone in keratinocytes and repress inflammatory pathway mRNAs

Project description:The endocannabinoid (eCB) system plays an active role in epidermal homeostasis. Phytocannabinoids such as CBD modulate this system but also act through eCB-independent mechanisms. This study evaluated effects of CBD, bakuchiol (BAK) and ethyl (linoleate/oleate) (ELN) in keratinocytes (KCs) and reconstituted human epidermis (RHE). Molecular docking simulations showed that each compound binds the active site of the eCB carrier fatty-acid-binding protein 5 (FABP5). However, BAK and ethyl linoleate bound this site with highest affinity when combined 1:1 (w/w) and in vitro assays showed that BAK+ELN most effectively inhibited FABP5 and fatty acid amide hydrolase (FAAH). In TNF-stimulated KCs, BAK+ELN reversed TNF-induced expression shifts and uniquely down-regulated type I interferon genes and PTGS2 (COX-2). BAK+ELN also repressed expression of genes linked to KC differentiation but up-regulated those associated with proliferation. Finally, BAK+ELN inhibited cortisol secretion in RHE skin (not observed with CBD). These results support a model in which BAK and ELN synergistically interact to inhibit eCB degradation, favoring eCB mobilization and inhibition of downstream inflammatory mediators (e.g., TNF, COX-2, type I interferon). Topical combination of these ingredients may thus enhance cutaneous eCB tone or potentiate other modulators, suggesting new ways to modulate the eCB system for innovative skincare product development.

2022-11-23 | GSE216614 | GEO

Single cell RNA-seq for a mouse model of recessive dystrophic epidermolysis bullosa

Project description:Recessive dystrophic epidermolysis bullosa (RDEB), intractable skin genetic disease, is caused by mutations in COL7A1. Most RDEB patients have mutations in a compound heterozygous manner. We established an RDEB model mouse with patient type mutations in a compound heterozygous manner. We selected two mutations, c.5818delC and E2857X, which is recurrently identified in human RDEB cohort, and introduced the mutations at corresponding locations of the mouse genome. We analyzed the established mouse by single cell RNA-seq to clarify how loss of functional type VII collagen impact on the integrity of skin.

2022-03-16 | GSE181357 | GEO

Percutaneous Collagen Induction (PCI) in rat

Project description:The purpose of the present study is to determine the effect of Percutaneous Collagen Induction (PCI) on the epidermis and dermis, including the systemic inflammatory response on gene expression level using microarray analysis. PCI Therapy is an alternative for safely treating wrinkles and scars and smoothening the skin. Therefore animal experiments were performed using 31 male Sprague-Dawley rats (350–375 g), age 4 month, randomly assigned into three groups: group (A) (n=24: needling plus skin care), group (B) (n=6: skincare only, controls after 24 h) and group (C) (n=1: negative control). Rats were anesthetized, shaved, and received a 30% total body surface area (TBSA) scald needling (10min) to induce percutaneous collagen, using a medical needling instrument (Environ® Medical Roll-CITTM, Vivida SA cc, Cape Town, South Africa). After needling surgery, the rats were immediately prepared with high levels of vitamin A cream and vitamin C cream, applied topically after cleaning once per day. The control group (C) rats received no injury, no skin care, no treatment, no anesthesia, and no analgesia. Gene expression analyses were performed 1 h, 24 h, 2, 4, and 8 weeks after PCI surgery. To confirm RNA expression in rat skin, self developed microarrays including genes like cytokines, such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF 2), keratinocyte growth factor (KGF), epidermal growth factor (EGF), and transforming growth factors (TGF ß1, ß2, ß3) were used.

2008-05-31 | GSE11617 | GEO

Distinct activation of positive and negative regulatory immune genes during an evolving T cell response to diphencyprone (DPCP) in human skin

Project description:We sought to characterize delayed-type hypersensitivity (DTH) responses elicited by topical hapten DPCP in normal human skin Comparison of transcriptomes among DPCP- and placebo-treated skin at different time points

2014-03-29 | E-GEOD-52360 | biostudies-arrayexpress

Treatment of C3H/HeJ grafted mice with baricitinib [topical]

Project description:The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease. The efficacy of topical baricitinib at treating established alopecia in the C3H/HeJ grafted model was also assessed. Microarrays were performed on skin RNA at week 0 and week 12 after starting treatment in all models. Baricitinib was administered in topical form after disease establishement. Skin samples were taken at the start of treatment and after 12 weeks.

2015-05-01 | E-GEOD-61554 | biostudies-arrayexpress

Gene expression analysis of mouse ear samples treated with chemical allergen

Project description:Identification of chemical allergen inducible genes in mouse skin. Ear samples were isolated from CL57BL/6 mice 6 hours after topical application of a prototypic chemical allergen, a skin irritant or vehicle alone. Total RNA were extracted from ear skin samples treated with a chemical allergen, a skin irritant, or vehicle alone for 6 hours.

2011-03-10 | E-GEOD-20726 | biostudies-arrayexpress

Expression data from IMQ-induced psoriasis-like skin inflammation in miR-146a-/- and C57BL6J mice

Project description:miR-146a acts as a negative feedback regulator of inflammation. To investigate the role of miR-146a in psoriasis psoriasiform skin inflammation was indeuced in Mir-146a-/- and wild type mice (C57BL6J) by topical applciation of imiquimod (IMQ)-cream (Aldara). Gene expression profiling (Affymetrix) was used to identify transcriptomic changes associated with psoriasis-like skin inflammation in wild type vs. miR-146a -/-mice. A daily topical dose of 31.25 mg of Aldara cream (5% IMQ) was applied on the right ear of miR-146a -/- and C57BL/6 mice on three consecutive days to induce psorisis-like skin inflammation. Mice were sacrificed at day 4. Ear flaps were collected for total RNA extraction and hybridization on Affymatrix GeneTitan plate format Gene ST 2.1 (mouse).

2016-02-19 | E-GEOD-78057 | biostudies-arrayexpress

RNAseq changes in mouse wound with or without time course treatment by Vemurafenib

Project description:BRAF inhibitors are highly effective therapies for patients with BRAF V600 mutated metastatic melanoma. Patients who receive BRAF inhibitors develop a variety of hyper-proliferative skin conditions, whose pathogenic basis is the paradoxical activation of the mitogen-activated protein kinase (MAPK) pathway in BRAF wild-type cells. Most of these hyper-proliferative skin changes improve when a MEK inhibitor is co-administered, as a MEK inhibitor blocks paradoxical MAPK activation. We tested whether we could take advantage of the mechanistic understanding of the skin hyper-proliferative side effects of BRAF inhibitors to accelerate skin wound healing by inducing paradoxical MAPK activation. Here we show that the BRAF inhibitor vemurafenib accelerates human keratinocyte proliferation and migration by increasing ERK phosphorylation and cell cycle progression. Topical treatment with vemurafenib in two wound-healing models in mice accelerated cutaneous wound healing and improved the tensile strength of healing wounds through paradoxical MAPK activation; addition of a MEK inhibitor reversed the benefit of vemurafenib-accelerated wound healing. The same dosing regimen of topical BRAF inhibitor did not increase the incidence of cutaneous squamous cell carcinomas in mice even after the application of a carcinogen. Therefore, topical BRAF inhibitors may have clinical applications in accelerating the healing of skin wounds. Full depth incisional wound mice tissues with/without Vemurafenib treatment were sent for RNAseq analysis on day 2, 6 and 14

2016-07-29 | E-GEOD-74558 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data