Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Analysis by RNA-seq of the transcriptional profile of left ventricles of WT, CST-KO and CST-KO+CST treated mice

ABSTRACT: Hypertension is a critical risk factor for heart failure (HF), with metabolic inflexibility playing a pivotal role. Chromogranin A (CgA)-derived peptide Catestatin (CST: hCgA352-372) exerts hypotensive and cardioprotective effects, nonetheless CST’s effect on cardiac metabolism remains unexplored. Our transcriptomic approach coupled with filtering through Boolean implication relationships identified a set of gene signatures (fibroblast, cardiomyocyte, and macrophage) that were altered in CST knockout (CST-KO) mice and restored after CST supplementation. These gene signatures obtained from our in vivo experiments corroborated with publicly available HF patient datasets.

ORGANISM(S): Mus musculus

PROVIDER: GSE301063 | GEO | 2026/05/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Catestatin impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways

Project description:Melanoma remains one of the most aggressive and treatment-resistant cancers, emphasizing the need for novel therapeutics. In our current study we report a peptide-based approach as potential therapeutic. The expression and role of Catestatin(CST), a Chromogranin A(CgA)-derived peptide with immunomodulatory and reparative properties in skin injury led us to examine its connection to melanoma. Advancing melanoma stages showed decreased CST expression. CST administration to patient derived cells and melanoma cell lines A375, B16F10, SKMEL28 revealed increased apoptosis, decreased proliferation and metastatic ability of the melanoma cells without affecting cell viability for normal skin fibroblasts. CST reduced growth kinetics and tumor weight in B16F10 derived in vivo melanoma tumors. Transcriptomic analyses of catestatin treated human cell line and mouse tumor revealed downregulation of hypoxia, collagen remodeling, epithelial to mesenchymal transition pathways (EMT), stress adaptive responses that are accountable for melanoma progression. In Vemurafenib-resistant A375 cells, CST increased apoptosis and repressed multiple resistance associated genes. These results highlight CST as a promising therapeutic candidate capable of opposing melanoma progression and overcoming resistance to current targeted treatments.

2026-03-16 | GSE312638 | GEO

Chromogranin A (CgA) Deficiency Attenuates Tauopathy by Altering Epinephrine–Alpha-Adrenergic Receptor Signaling

Project description:Our previous studies have indicated that insulin resistance, hyperglycemia, and hypertension in aged wild-type (WT) mice can be reversed in mice lacking chromogranin-A (CgA-KO mice). These health conditions are associated with a higher risk of Alzheimer’s disease (AD). CgA, a neuroendocrine secretory protein has been detected in protein aggregates in the brains of AD patients. Here, we determined the role of CgA in tauopathies, including AD (secondary tauopathy) and corticobasal degeneration (CBD, primary tauopathy). We found elevated levels of CgA in both AD and CBD brains, which were positively correlated with increased phosphorylated tau in the frontal cortex. Furthermore, CgA ablation in a human P301S tau (hTau) transgenic mice (CgA-KO/hTau) exhibited reduced tau aggregation, resistance to tau spreading, and an extended lifespan, coupled with improved cognitive function. Transcriptomic analysis of mice cortices highlighted altered levels of alpha-adrenergic receptors (Adra) in hTau mice compared to WT mice, akin to AD patients. Since CgA regulates the release of the Adra ligands epinephrine (EPI) and norepinephrine (NE), we determined their levels and found elevated EPI levels in the cortices of hTau mice, AD and CBD patients. CgA-KO/hTau mice exhibited reversal of EPI levels in the cortex and the expression of several affected genes, including Adra1 and 2, nearly returning them to WT levels. Treatment of hippocampal slice cultures with EPI or an Adra1 agonist intensified, while an Adra1 antagonist inhibited, tau hyperphosphorylation and aggregation. These findings reveal a critical role of CgA in regulation of tau pathogenesis via the EPI-Adra signaling axis.

2025-04-07 | GSE274459 | GEO

Chromogranin A (CgA) Deficiency Attenuates Tauopathy by Altering Epinephrine–Alpha-Adrenergic Receptor Signaling

Project description:Chromogranin A (CgA) Deficiency Attenuates Tauopathy by Altering Epinephrine–Alpha-Adrenergic Receptor Signaling

| PRJNA1146456 | ENA

Gut microbial DNA and immune checkpoint gene Vsig4/CRIg are key antagonistic players in healthy aging and age-associated development of hypertension and diabetes

Project description:Aging is associated with the development of insulin resistance and hypertension. Aim of this study was to identify factors regulating these processes. We studied mice with complete knockout (KO) of the neuroendocrine prohormone Chromogranin A (CgA) as a model for healthy aging. These mice display two opposite aging phenotypes: hypertension but heightened insulin sensitivity at young age, whereas the blood pressure normalizes at older age and insulin sensitivity further improves. In comparison, aging WT mice gradually lost glucose tolerance and insulin sensitivity and developed hypertension. Quantitative RT-PCR revealed increased (~35-fold) accumulation of bacterial DNA in the heart of 2-yr-old WT mice compared to only ~2-fold increase in age-matched CgA-KO mice. Similarly, RNA sequencing showed increased expression of the Vsig4 gene (which removes bacterial DNA) in the liver of 2-yr-old CgA-KO mice, which possibly accounts for the very low accumulation of microbial DNA in the heart. The reversal of hypertension in aging CgA-KO mice is possibly due to (i) low accumulation of microbial DNA (i.e., reduced inflammation), and (ii) decreased spillover of norepinephrine (measured by ultra-pressure liquid chromatography) in the heart and kidneys. The reverse is true for aging WT mice. Moreover, while aging WT mice had increased inflammation with higher plasma TNF-⍺, IFN-ɣ, CCL2 and increased mitochondrial fission, these phenotypes were the opposite in aging CgA-KO mice. We conclude that Vsig4 plays a crucial role in “healthy aging” by counteracting age-associated insulin resistance and hypertension.

2022-11-09 | GSE217145 | GEO

Analysis by RNA-seq of the transcriptional profile of left ventricles of WT, CST-KO and CST-KO+CST treated mice

Project description:Analysis by RNA-seq of the transcriptional profile of left ventricles of WT, CST-KO and CST-KO+CST treated mice

| PRJNA1283196 | ENA

SILAC-iPOND analysis of WT vs ATRX KO eHAP cells ± HU

Project description:Mutations in the ATRX chromatin remodeller predispose to a developmental genetic disorder and cancer, but how ATRX safeguards genome and telomere stability remains unresolved. Here, we uncover critical dependencies for the CTC1-STN1-TEN1 (CST) complex and RAD9A-HUS1-RAD1 (9-1-1) clamp in ATRX deficient cells. ATRX:CST synthetic lethality manifests following accumulation of telomeric G-rich ssDNA, which results in telomere loss and cell death. Conversely, we attribute ATRX:9-1-1 synthetic lethality to genome-wide ssDNA lesions, which compromise DNA replication. We further show that ATRX suppresses DNA damage during replication stress by counteracting the activity of the FAM111A protease. We demonstrate that roles of ATRX in telomere maintenance and replication are genetically separable, requiring its ATPase activity and PIP-box, respectively. We also show that such roles protecting genome stability are largely independent of the ATRX-DAXX interaction. Collectively, our data show that functions of ATRX in suppressing toxic ssDNA lesions are context-dependent and are key to global DNA replication and telomere integrity.

2026-05-19 | PXD068487 | Pride

Gene expression in Hypotension

Project description:Rat kidney in normo- and hypotensive animals. Keywords: parallel sample

2005-03-12 | GSE2401 | GEO

miRNA changes after overexpression of uc.372 in HepG2 cells

Project description:To identify putative miRNA targets for uc.372, we overexpressed uc.372 in HepG2 cells and carried out a microarray analysis. A total of 66 miRNAs present in the array demonstrated 1.5-fold upregulation or downregulation of expression upon uc.372 transfection.

2017-11-01 | GSE106366 | GEO

CST interacts with the cohesin complex and promotes chromosome cohesion

Project description:Sister chromatid cohesion (SCC), the pairing of sister chromatids following DNA replication until mitosis, is established by loading of the cohesin complex on newly replicated chromatids. Cohesin must then be maintained until mitosis to prevent segregation defects and aneuploidy. However, how SCC is established and maintained until mitosis remains incompletely understood and emerging evidence suggests that replication stress may lead to premature SCC loss. Here, we report that the single-stranded DNA-binding protein CTC1-STN1-TEN1 (CST) aids in SCC. CST primarily functions in telomere length regulation but also has known roles in replication restart and DNA repair. Following depletion of CST subunits, we observed an increase in the complete loss of SCC. Additionally, we determined that CST associates with the cohesin complex. Unexpectedly, we did not find evidence of altered cohesion or mitotic progression in the absence of CST; however, we did find that treatment with various replication inhibitors increased the association between CST and cohesin. Since replication stress was recently shown to induce SCC loss, we hypothesized that CST may be required to maintain or remodel SCC following DNA replication fork stalling. In agreement with this idea, SCC loss was greatly increased in CST-depleted cells following exogenous replication stress. Based on our findings, we propose that CST aids in the maintenance of SCC at stalled replication forks to prevent premature cohesion loss.

2021-07-28 | PXD026264 | Pride

RNA Sequencing Facilitates Quantitative Analysis of shL3MBTL2 ,CGA-OE and corresponding control Transcriptomes

Project description:L3MBTL2 is a crucial component of ncPRC1.6 and has been implicated in transcriptional repression and chromatin compaction. However, the repression mechanism of L3MBTL2 and its biological functions are largely undefined. CGA encodes the alpha subunit of glycoprotein hormones, however, we showed that CGA plays an individual tumor suppressor role in PDAC. The goals of this part study are to compare transcriptome profiling of PANC-1-shL3MBTL2 cells or PANC-1-CGA-OE cells to their corresponding control cells. By identifying differentially expressed genes (DEGs) and enrichment pathways, the mechanism of L3MBTL2 and CGA in pancreatic cancer can be better studied.

2022-01-01 | GSE184834 | 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