Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in vascular smooth muscle cells after 18 weeks of high fat diet

ABSTRACT: Obesity causes diabetes type 2 (DMT2) leading to vascular dysfunction and finally renal end-organ damage. Vascular smooth muscle (VSM) EGF receptor (EGFR) modulates vascular wall homeostasis in part via serum response factor (SRF), a major regulator of VSM differentiation and a sensor for glucose. We investigated the role of VSM-EGFR during obesity-induced renovascular dysfunction and the EGFR-hyperglycemia crosstalk.

ORGANISM(S): Mus musculus

PROVIDER: GSE144838 | GEO | 2020/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in endothelial cells after 18 weeks of high fat diet

Project description:Vascular EGF receptors (EGFR) are supposed to be relevant for function and structure of arterial vessels. Recently, we showed in genetic mouse models that vascular smooth muscle (VSMC) EGFR is required for proper physiological function and structure as well as for pathophysiological alterations induced by angiotensin II or obesity. The importance of endothelial (EC) EGFR in vivo is unknown. Therefore we analyzed the impact of EC-EGFR knockout on vascular and renal function under control condition as well as in obesity in comparison to VSMC-KO.

2021-04-01 | GSE158197 | GEO

Transcriptome analaysis of Bcl11b-deficient aortas

Project description:B-cell leukemia 11b (BCL11B) is a transcription factor known as an essential regulator of T lymphocytes and neuronal development during embryogenesis. A genome-wide association study (GWAS) showed that a gene desert region downstream of BCL11B, known to function as a BCL11B enhancer, harbors single nucleotide polymorphisms (SNPs) associated with increased arterial stiffness. However, a role for BCL11B in the adult cardiovascular system is unknown. Based on these human findings, we sought to examine the relation between BCL11B and arterial function. Here we report that BCL11B is expressed in the vascular smooth muscle (VSM) where it regulates vascular stiffness. RNA sequencing of aortas from WT and Bcl11b null mice (BSMKO) identified the cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) as the most significant differentially regulated signaling pathway in BSMKO compared to WT mice. BSMKO aortas showed decreased levels of PKG1, increased levels of Ca++-calmodulin-dependent serine/threonine phosphatase calcineurin (PP2B) and their common phosphorylation target, vasodilator-stimulated phosphoprotein (pVASPS239), a regulator of cytoskeletal actin rearrangements. Decreased pVASPS239 in BSMKO aortas was associated with increased actin polymerization (F/G actin ratio). Functionally, aortic force, stress, wall tension and stiffness, measured ex vivo in organ baths, were increased in BSMKO aortas, and BSMKO mice had increased pulse wave velocity, the in vivo index of arterial stiffness. Despite having no effect on blood pressure or microalbuminuria, increased arterial stiffness in BSMKO mice was associated with increased incidence of cerebral microbleeds compared to age-matched WT littermates. In conclusion, we have identified VSM BCL11B as a crucial regulator of aortic smooth muscle function and a potential therapeutic target for vascular stiffness.

2021-12-01 | GSE163551 | GEO

Transcriptional impact of EGFR-AT1R-crosstalk (Transient transfection of AT1R in HEK293 cells)

Project description:The impact of AT1R and EGFR on SRF transcriptional activity, signaling pathways and transcriptome regulation were investigated in HEK293, HK-2 and vascular smooth muscle cells, applying reporter gene, protein and mRNA expression techniques as well as RNAseq followed by bioinfor-matic analysis.

2022-01-10 | GSE162769 | GEO

Transcriptional impact of EGFR-AT1R-crosstalk (Stable transfection of AT1R in HEK293 cells)

2022-01-10 | GSE162768 | GEO

Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in vascular smooth muscle cells after 18 weeks of high fat diet

Project description:Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in vascular smooth muscle cells after 18 weeks of high fat diet

| PRJNA605107 | ENA

Obesity drives depot-specific vascular remodeling in white adipose tissue

Project description:Obesity-driven pathological expansion of white adipose tissue (WAT) is a key driver of endothelial dysfunction. Contrary to this paradigm, early vascular alterations associated with over nutrition also exacerbate AT dysfunction. To dissect this complex cause and consequence relationship, here we perform a single-cell transcriptomics screen to generate a detailed landscape of endothelial heterogeneity and vascular alterations in murine model of obesity. Given the differences in ontogeny and function of distinct WAT depots, we demarcate key differences in subcutaneous and visceral WAT vasculature. In addition to descriptive taxonomy, we perform in-depth validation and characterization of our in silico data. We identify a sWAT specific fenestrated endothelial cell subtype, which is drastically reduced in obese conditions. This reduction was associated with a decrease in VEGFA expressing perivascular cells. The novel endothelial subtypes provide a basis for future research and new directions for therapeutic interventions.

2023-05-26 | E-MTAB-12855 | biostudies-arrayexpress

Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in endothelial cells after 18 weeks of high fat diet

Project description:Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in endothelial cells after 18 weeks of high fat diet

| PRJNA664331 | ENA

Vascular smooth muscle-derived TRPV1-expressing progenitors are a new source of cold induced thermogenic adipocytes

Project description:Brown adipose tissue (BAT) functions in energy expenditure in part due its role in thermoregulation. The prominent capacity of BAT to enhance fuel utilization and energy expenditure makes it an attractive target for treating obesity and metabolic disorders. Prolonged cold exposure induces de novo recruitment of brown adipocytes and activates their thermogenic activity. However, the exact source of cold-induced brown adipocytes is not completely understood. In this study, we sought to investigate the cellular origin of cold-induced brown adipocytes using single-cell RNA sequencing. We identified two distinct types of adipocyte progenitors that contribute to de novo recruitment of brown adipocytes in response to cold challenge. One is the previously known Pdgfra-expressing mesenchymal progenitors and the other is a vascular smooth muscle-derived adipocyte progenitor (VSM-APC) population, which expresses the temperature-sensitive ion channel transient receptor potential cation channel subfamily V member 1 (Trpv1). Using flow cytometry and lineage tracing, we demonstrated that the Trpv1pos VSM-APCs were indeed distinct from the Pdgfrapos progenitors and could contribute to brown adipocytes with greater thermogenic potential. Together, these findings illustrate a landscape of thermogenic adipose niche at the single cell resolution and identify a new cellular origin for the development of brown adipocytes.

2021-01-18 | GSE160585 | GEO

Gene expression in brain of interleukin-18 knockout mice at 6 and 12 weeks of age

Project description:Interleukin-18 knockout mice had metabolic syndromes after 24 weeks of age. We examined gene expression profiles in mice brain using genome-wide microarray technology, and compared gene expression profiles between wild-type and interleukin-18 knockout mice. To verify responsible molecules involved in metabolic syndromes such as obesity, we compared the gene expression levels at 6 and 12 weeks of age, and picked up them whose expression was more than 2-fold increase or less than 1/2-fold decrease.

2019-12-20 | GSE64307 | GEO

Gene expression in kidney of interleukin-18 knockout mice at 6 and 12 weeks of age

Project description:Interleukin-18 knockout mice had metabolic syndromes after 24 weeks of age. We examined gene expression profiles in mice kidney using genome-wide microarray technology, and compared gene expression profiles between wild-type and interleukin-18 knockout mice. To verify responsible molecules involved in metabolic syndromes such as obesity, we compared the gene expression levels at 6 and 12 weeks of age, and picked up them whose expression was more than 2-fold increase or less than 1/2-fold decrease.

2018-03-09 | GSE64310 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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