Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of high fat diet on mouse prostate development

ABSTRACT: Steroid 5α reductase 2 (SRD5A2) is the predominant enzyme responsible for prostatic development and growth. Despite the introduction of steroid 5α-reductase inhibitors (5ARI) for benign prostatic hyperplasia (BPH), the progression of LUTS is only slowed by 34% with 5ARI-response. Previous literature establishes link between obesity and BPH progression. We hypothesize that high fat diet is associated with prostate development.

ORGANISM(S): Mus musculus

PROVIDER: GSE260450 | GEO | 2024/03/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ESR1+ luminal epithelial cells contribute to androgen-independent prostate survival in the absence of SRD5A2

Project description:Steroid 5α reductase 2 (SRD5A2) is crucial for prostatic development, converting testosterone to dihydrotestosterone (DHT). While 5α reductase inhibitors (5ARI) effectively reduce prostate size in benign prostate hyperplasia (BPH), their limited efficacy against BPH-related lower urinary tract symptoms (LUTS) and mechanisms of 5ARI resistance remain unclear. Here, we developed a Srd5a2-/- mouse model and employed single-cell RNA sequencing (scRNA-seq) to explore the impact of SRD5A2 absence on prostate cellular heterogeneity. Significant alterations in luminal epithelial (LE) populations were observed, alongside increased proportion and proliferative phenotype of estrogen receptor 1 (ESR1)+ Luminal Epithelia 2 (LE2) cells, following an SRD5A2-independent ESR1 differentiation trajectory. LE2 cells exhibited enhanced estrogen response gene signatures, suggesting alternative pathways for prostate growth without SRD5A2. Human prostate biopsy analysis revealed an inverse correlation between SRD5A2 expression and LE2 markers (ESR1 and PKCα). These findings provide insights into prostate biology, 5ARI resistance mechanisms, and potential targeted therapies for BPH-related LUTS.

2023-06-26 | GSE235514 | GEO

Genome-wide analysis of prostatic tissue gene expression from patients with benign prostatic hyperplasia

Project description:Analysis of gene expression in prostatic tissue from BPH patients with and without SRD5A2 gene methylation. The hypothesis is that BPH patients with DNA methylation of the SRD5A2 gene promoter have impaired conversion of testosterone to dihydrotestosterone, and therefore may use an alternative signaling pathway for prostatic tissue growth. Here, we compare gene expression profiles of SRD5A2-methylated vs. unmethylated prostatic tissue to nominate alternative biological pathways relevant in each molecular subtype of BPH.

2017-10-01 | GSE101486 | GEO

Change in prostate tissue gene expression following finasteride or doxazosin administration in the Medical Therapy for Prostatic Symptoms (MTOPS) Study

Project description:Benign prostatic hyperplasia (BPH) may decrease patient quality of life and often leads to acute urinary retention and surgical intervention. While effective treatments are available, many BPH patients do not respond or develop resistance to treatment. To understand molecular determinants of BPH treatment resistance, we investigated gene expression profiles before and after treatments in the prostate transitional zone of 108 participants in the Medical Therapy of Prostatic Symptoms (MTOPS) Trial. Unsupervised clustering revealed molecular subgroups characterized by expression changes in a large set of genes associated with resistance to finasteride, a 5α-reductase inhibitor. Pathway analyses within this gene cluster found finasteride administration induced changes in fatty acid metabolism, amino acid metabolism, immune response, steroid hormone metabolism, and kinase activity within the transitional zone. We found that patients without this transcriptional response were highly likely to develop drug resistance, which is expected in 33% of finasteride-treated patients. Importantly, a patient’s transcriptional response to finasteride was associated with their pre-treatment kinase expression. Further, we identified novel expression signatures of finasteride resistance among the transcriptionally responded patients. These patients showed different gene expression profiles at baseline and increased prostate transitional zone volume compared to the patients who responded to the treatment. Our work suggests molecular mechanisms of resistance to finasteride treatment that could be potentially helpful for personalized BPH treatment as well as new drug development to increase patients drug response.

2024-08-28 | GSE262946 | GEO

Prostates of rats with induced partial bladder outlet obstruction and the effect of Eviprostat on those changes

Project description:Prostatic inflammation plays a role in the progression of benign prostatic hyperplasia (BPH). Eviprostat is an antiinflammatory and antioxidant phytotherapeutic agent widely used to treat lower urinary tract symptoms in BPH. However, because Eviprostat is a mixture of compounds from multiple natural sources, its mechanism of action has been difficult to investigate. In this study, we used oligonucleotide microarrays to identify changes in gene expression that occur in the prostate of rats with surgically induced partial bladder outlet obstruction and the effect of Eviprostat on those changes.

2009-07-21 | GSE16063 | GEO

Opposing Effects of Cyclooxygenase-2 (COX-2) on Estrogen Receptor β (ERβ) Response to 5α-reductase Inhibition in Prostate Epithelial Cells

Project description:Current pharmacotherapies for symptomatic benign prostatic hyperplasia (BPH), an androgen receptor (AR) driven, inflammatory disorder affecting elderly men, include 5α-reductase (5AR) inhibitors (i.e. dutasteride and finasteride) to block the conversion of testosterone to the more potent AR ligand dihydrotestosterone (DHT). Since DHT is the precursor for estrogen receptor β (ERβ) ligands, 5AR inhibitors could potentially limit ERβ activation, which maintains prostate tissue homeostasis. We have uncovered signaling pathways in BPH-derived prostate epithelial cells (BPH-1) that are impacted by 5AR inhibition. The induction of apoptosis and repression of the cell-adhesion protein E-cadherin by the 5AR inhibitor, dutasteride, requires both ERβ and TGFβ. Dutasteride also induces cyclooxygenase type 2 (COX-2), which functions in a negative-feedback loop in TGFβ and ERβ signaling pathways as evidenced by the potentiation of apoptosis induced by dutasteride or finasteride upon pharmacological inhibition or shRNA-mediated ablation of COX-2. Concurrently, COX-2 positively impacts ERβ action through its effect on the expression of a number of steroidogenic enzymes in the ERβ-ligand metabolic pathway. Therefore, effective combination pharmacotherapies, which have included non-steroidal anti-inflammatory drugs, must take into account biochemical pathways affected by 5AR inhibition and opposing effects of COX-2 on the tissue protective action of ERβ.

2016-05-12 | GSE80979 | GEO

Different expressed genes in epithelium and stromal of Benign Prostatic Hyperplasia

Project description:To identify the genes differently expressed in the epithelium and the stromal of Benign Prostatic Hyperplasia (BPH), we collect the epithelium and the stromal from the patients with benign prostatic hyperplasia by laser micro-dissection. And then, Affymetrix HG-U133_Plus_2 gene-chip was used to detect and compare the expression level of genes. To find which genes are most abundantly expressed in epithelium and stromal and what is the role of these genes in the pathogenesis of BPH.

2011-08-10 | GSE31323 | GEO

Gene expression profiling of AR deletion in prostate luminal cells

Project description:Benign prostatic hyperplasia (BPH) is a common urological disease that adversely affects quality of life among elderly males, but its etiology remains poorly understood. We show that the expression of the androgen receptor (AR) is decreased in the luminal epithelial cells of human BPH specimens and is inversely correlated with the degree of regional prostatic inflammation.

2016-09-27 | GSE77646 | GEO

Expression data from benign prostatic hyperplasia samples and normal controls

Project description:To further development of our gene expression signature for benign prostatic hyperplasia, we conducted expression profiles of BPH and normal samples.

2020-05-28 | GSE119195 | GEO

Comparative serum proteome profiling of canine benign prostatic hyperplasia before and after castration

Project description:Benign prostatic hyperplasia (BPH) is the most prevalent prostatic condition in older intact dogs; nonetheless, clinical diagnosis and management remain inconsistent. This study employed in-solution digestion coupled with nano-liquid chromatography-tandem mass spectrometry (nanoLC-MS/MS) to assess serum proteome profiling of dogs with BPH and those dogs after castration.

2024-10-11 | PXD046059 | JPOST Repository

Transcription profiling of human prostatic stromal cells cultured from diseased vs normal tissues

Project description:To obtain a comprehensive view of the transcriptional programs in prostatic stromal cells of different histological/pathological origin, we profiled 18 adult human stromal cell cultures from normal transition zone (TZ), normal peripheral zone (PZ), benign prostatic hyperplasia (BPH), and prostate cancer (CA) using cDNA microarrays.

2006-11-06 | E-SMDB-3867 | 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