Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparative expression data between the epidermis and dermis of wild-type (Pparb/d^fl/fl) and fibroblast-selective knockout Pparb/d (FSPCre-Pparb/d^fl/fl) mice

ABSTRACT: The role of PPARβ/δ in maintaining skin homeostasis during skin injury or inflammation has been widely studied. However, the majority of these reports based their studies in PPARβ/δ found in keratinocytes, which is the major cell type of the skin epidermis. The skin is mainy made up of the epidermis and dermis, and skin homeostasis is tightly regulated by complex crosstalks between epidermis and dermis. The dermis is predominantly made up of fibroblasts, and the predominant PPAR subtype in dermal fibroblasts is PPARβ/δ. Knowledge in the role of fibroblasts PPARβ/δ in skin homeostasis is lacking. To identify gene changes leading to phenotypical and biological functions alterations upon deletion of fibroblasts PPARβ/δ, we performed a comparative microarray gene expression analysis between Pparb/d^fl/fl and FSPCre-Pparb/d^fl/fl mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE71419 | GEO | 2018/04/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Vascular PPARb/d Promotes Tumor Angiogenesis and Progression

Project description:PPARβ/δ has been suggested to be involved in the regulation of the angiogenic switch in tumor progression. However, until now it is not clear to what extent the expression of PPARβ/δ in tumor endothelium influences tumor progression and metastasis formation. We addressed this question using transgenic mice with an inducible conditional vascular-specific overexpression of PPARβ/δ. Following specific over-expression of PPARβ/δ in endothelial cells, we induced syngenic tumors. We observed an enhanced tumor growth, a higher vessel density, and enhanced metastasis formation in the tumors of animals with vessel-specific overexpression of PPARβ/δ. In order to identify molecular downstream targets of PPARβ/δ in the tumor endothelium, we sorted endothelial cells from the tumors and performed RNA sequencing.We show here that PPARβ/δ activation, regardless of its action on different cancer cell types, leads to a higher tumor vascularization which favors tumor growth and metastasis formation.

2019-12-12 | GSE140513 | GEO

Genome-wide maps of Qki-5 and PPARb in mouse oligodendrocytes

Project description:We found that there is a big overlap between the Qki5- and PPARb-binding events by ChIP-seq. Interestingly, the genomic distribution analyses of Qki-5- and PPARβ-binding events showed significant enrichment at the regions of the promoter/transcription start site (TSS) which were indicated by Pol II-binding events. The strong preference of the promoter/TSS co-occupancy suggested that Qki-5 might play an important role in PPARβ-mediated transcriptional regulation of its downstream genes.

2020-01-05 | GSE126577 | GEO

Transcriptional and UV-response regulatory role of PPARb in Normal Human Keratinocytes

Project description:Solar radiation is the major source of human exposure to UV radiation, the major carcinogen in skin cancers, by triggering a number of cellular responses that can indirectly or directly induce DNA damage. Skin cells attempt to repair these damages by activating cascades of DNA Damage Response mechanisms to safeguard genome integrity, thereby preventing skin cancers. The role of PPARb - a druggable transcription factor, in the development of UV-dependent skin cancers is not mechanistically elucidated. We have shown previously that PPARb knockout mice are less prone to UV-induced skin cancers. Here, we report on our global transcriptomic analysis revealing that PPARb directly regulates gene expression programs associated with cell cycle and DNA repair pathways in normal human epidermal keratinocytes. We show that in these cells, as well as in malignant human keratinocytes and in human melanoma cells, PPARb controls cellular proliferation and cell cycle progression and its depletion leads to cell cycle arrest. We also show that PPARb controls the response of normal human epidermal keratinocytes to UV-induced DNA damage. PPARb depletion decreases the expression and/or activation of multiple effectors of DNA Damage Response (DDR) pathway and favours the apoptotic response of human keratinocytes to UV irradiation. Our preclinical data of a PDX melanoma model demonstrated that the depletion or inhibition of PPARb delays of blocks tumor formation. Our data suggest that PPARb inhibition can be considered as a therapeutic target for the prevention of UV-induced skin cancers in vulnerable population, by attenuating the DDR and eliminating skin cells with high UV-induced mutational burden.

2024-12-18 | GSE263846 | GEO

Mus musculus

Project description:Comparative expression data between the epidermis and dermis of wild-type (Pparb/d^fl/fl) and fibroblast-selective knockout Pparb/d (FSPCre-Pparb/d^fl/fl) mice

| PRJNA291191 | ENA

Identification of a novel PPARβ/δ / miR-21-3p axis in UV-induced skin inflammation [mouse miRNA]

Project description:Although excessive exposure to UV is widely recognized as a major factor leading to skin perturbations and cancer, the complex mechanisms underlying inflammatory skin disorders resulting from UV exposure remain incompletely characterized. The nuclear hormone receptor PPARβ/δ is known to control cutaneous repair and UV-induced cancer development. Here, we describe a novel PPARβ/δ-dependent molecular cascade involving TGFβ-1 and miR-21-3p, which is activated in the epidermis in response to UV exposure. We establish that the passenger miRNA miR-21-3p, that we identify as a novel UV-induced miRNA in the epidermis, plays a pro-inflammatory function in keratinocytes, and that its high level of expression in human skin is associated with psoriasis and squamous cell carcinomas. Finally, we provide evidence that inhibition of miR-21-3p reduces UV-induced cutaneous inflammation in ex vivo human skin biopsies, thereby underlining the clinical relevance of miRNA-based topical therapies for cutaneous disorders.

2016-06-03 | GSE80428 | GEO

Identification of a novel PPARβ/δ / miR-21-3p axis in UV-induced skin inflammation [human miRNA-seq]

2016-06-03 | GSE80430 | GEO

Identification of a novel PPARβ/δ / miR-21-3p axis in UV-induced skin inflammation [human mRNA]

2016-06-03 | GSE80429 | GEO

Identification of a novel PPARβ/δ / miR-21-3p axis in UV-induced skin inflammation [mouse mRNA]

2016-06-03 | GSE80427 | GEO

Dermal reprogramming through epidermal activation of beta-catenin

Project description:Hair follicle formation depends on reciprocal epidermal-dermal interactions and occurs during skin development, but not in adult life. This suggests that the properties of dermal fibroblasts change during postnatal development. To examine this, we used a PdgfraEGFP mouse line to isolate GFP-positive fibroblasts from neonatal skin, adult telogen and anagen skin and adult skin in which ectopic hair follicles had been induced (EF skin) by transgenic epidermal activation of beta-catenin. We also isolated epidermal cells from each mouse. The gene expression profile of EF epidermis was most similar to that of anagen epidermis, consistent with activation of beta-catenin signalling. In contrast, adult dermis with ectopic hair follicles more closely resembled neonatal dermis than adult telogen or anagen dermis. In particular, genes associated with mitosis were upregulated and extracellular matrix-associated genes were downregulated in neonatal and EF fibroblasts. We confirmed that sustained epidermal beta-catenin activation stimulated fibroblasts to proliferate to reach the high cell density of neonatal skin. In addition, the extracellular matrix was comprehensively remodelled, with mature collagen being replaced by collagen subtypes normally present only in developing skin. The changes in proliferation and extracellular matrix composition originated from a specific subpopulation of fibroblasts located beneath the sebaceous gland. Our results show that adult dermis is an unexpectedly plastic tissue that can be reprogrammed to acquire the molecular, cellular and structural characteristics of neonatal dermis in response to cues from the overlying epidermis.

2011-10-13 | GSE32966 | GEO

Comparative expression data between tumor epithelium of APCmin/+ FSPCre-PPARB -/- and PPARB flox/flox

Project description:Stroma secretes complex regulatory signals, including reactive oxygen species, that are involved in mediating cancer development. Ablation of PPARB expression in fibroblastic cells results in modulation of oxidative stress signals that lead By means of gene expression analysis, we seek to identify key gene expression changes in tumor epithelial cells between FSPCre-PPARB -/- and PPARB flox/flox mice.

2018-08-05 | GSE97339 | GEO

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