Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema

ABSTRACT: mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema

PROVIDER: PRJNA693620 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13493667_1.fastq.gz	Fastqsanger.gz
	SRR13493667_2.fastq.gz	Fastqsanger.gz
	SRR13493668_1.fastq.gz	Fastqsanger.gz
	SRR13493668_2.fastq.gz	Fastqsanger.gz
	SRR13493669_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema

Project description:Lung diseases develop when telomeres are shortened beyond a critical point. We have constructed a mouse model in which the catalytic subunit of telomerase (mTert), or its catalytically inactive form (mTertCI), is expressed from the p21Cdkn1a promoter. We found that this particular expression of mTert reduces senescence of endothelial cells (EC) in lungs of aged mice, as well as emphysema and pulmonary perivascular fibrosis. We also show that mTert counteracts the decline in capillary density in aged mice and promotes the maintenance of high numbers of Cd34+ cells, identified as a subclass of endothelial cells with proliferative capacity. In line with these results, young p21+/Tert mice treated with a VEGF receptor inhibitor combined with hypoxia are also protected against senescence and emphysema induced by this treatment. The catalytic activity of mTert is required for all the effects observed. However, and unexpectedly, we found that both mTert and mTertCI expression significantly reduced p21 levels in the lungs of aged mice. mTert thus protects against age-related and induced loss of capillary vessels and subsequent lung emphysema.

2023-06-29 | GSE165218 | GEO

mTert induction in p21-positive cells counteracts capillary rarefaction and pulmonary emphysema

Project description:Lung diseases develop when telomeres shorten beyond a critical point. We constructed a mouse model in which the catalytic subunit of telomerase (mTert), or its catalytically inactive form (mTertCI), is expressed from the p21Cdkn1a locus. Expression of either TERT or TERTCI reduces global p21 levels in the lungs of aged mice, highlighting TERT non-canonical function. However, only TERT reduces accumulation of very short telomeres, oxidative damage, endothelial cell (ECs) senescence and senile emphysema in aged mice. Single-cell analysis of the lung reveals that p21 (and hence TERT) is expressed mainly in the capillary ECs. We report that a fraction of capillary ECs marked by CD34 and endowed with proliferative capacity declines drastically with age, and this is counteracted by TERT but not TERTCI. Consistently, only TERT counteracts decline of capillary density. Natural aging effects are confirmed using the experimental model of emphyse-ma induced by VEGFR2 inhibition and chronic hypoxia. We conclude that catalytically active TERT pre-vents exhaustion of the putative CD34+ EC progenitors with age, thus protecting against capillary vessel loss and pulmonary emphysema.

| S-SCDT-10_1038-S44319-023-00041-1 | biostudies-other

Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

Project description:We compared tissue Na+ storage in salt sensitive spontaneously hypertensive rats (SHR) versus salt resistant normotensive Brown Norway (BN) rats after salt loading (10 days drinking 1% NaCl solution), the SHR showed significant parallel increase in osmotically inactive Na+ storage in the skin while no significant changes in skin electrolyte concentrations were observed in BN rats. SHR rats after salt treatment exhibited a nonsignificant decrease in skin blood capillary number (rarefaction) while BN rats showed significantly increased skin blood capillary density. Analysis of dermal gene expression profiles in BN rats after salt treatment showed significant up-regulation of genes involved in angiogenesis and proliferation of endothelial cells contrary to the SHR.

2023-01-01 | E-MTAB-11355 | biostudies-arrayexpress

Identifying novel genes related to the peritubular capillary rarefaction in renal interstitial fibrosis through chip sequencing

Project description:Renal interstitial fibrosis (RIF) is the prominent pathological characteristics of deteriorative chronic kidney disease (CKD), leading to peritubular capillary (PTC) rarefaction accompanied by significant hypoxia. However, the underlying mechanisms remain elusive. To deal with this, we constructed the chip sequencing of HK-2 cells in hypoxia to explore critical genes modulated by HIF-1α through peak annotation. Several biomarkers have been identified on the basis of bioinformatics and deserve further research.

2023-11-15 | GSE234719 | GEO

Vascular rarefaction mediates whitening of brown fat in obesity

Project description:Brown adipose tissue (BAT) is a highly vascularized organ with abundant mitochondria that produce heat through uncoupled respiration. Obesity is associated with a reduction of BAT function; however, it is unknown how obesity promotes dysfunctional BAT. Here, using a murine model of diet-induced obesity, we determined that obesity causes capillary rarefaction and functional hypoxia in BAT, leading to a BAT “whitening” phenotype that is characterized by mitochondrial dysfunction, lipid droplet accumulation, and decreased expression of Vegfa. Targeted deletion of Vegfa in adipose tissue of nonobese mice resulted in BAT whitening, supporting a role for decreased vascularity in obesity-associated BAT. Conversely, introduction of VEGF-A specifically into BAT of obese mice restored vascularity, ameliorated brown adipocyte dysfunction, and improved insulin sensitivity. The capillary rarefaction in BAT that was brought about by obesity or Vegfa ablation diminished β-adrenergic signaling, increased mitochondrial ROS production, and promoted mitophagy. These data indicate that overnutrition leads to the development of a hypoxic state in BAT, causing it to whiten through mitochondrial dysfunction and loss. Furthermore, these results link obesity-associated BAT whitening to impaired systemic glucose metabolism.

2024-12-18 | GSE221854 | GEO

Identifying novel genes related to the peritubular capillary rarefaction in renal interstitial fibrosis through chip sequencing

Project description:Identifying novel genes related to the peritubular capillary rarefaction in renal interstitial fibrosis through chip sequencing

| PRJNA982811 | ENA

Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

Project description:Sodium accumulation and blood capillary rarefaction in the skin predispose spontaneously hypertensive rats to salt sensitive hypertension.

| PRJEB50395 | ENA

The role of NOXO1 in the mouse model of cigarette smoke-induced emphysema and pulmonary hypertension

Project description:NOXO1 KO mice seem to be protected from cigarette smoke-induced emphysema and pulmonary hypertension. Since the molecular mechanisms are not clear yet, this microarray experiment should help to identify the molecular differences in these KO mice compared to the wild-type (WT), figuring out how the protection occurs. Since we believe that vascular altertions could not only be responsible for vascular remodeling but also the trigger for emphysema development, we microdissected pre-capillary vessels from WT and KO mice, both controls and smoke-exposed. In addition, alveolar septa were microdissected to investigate the alveolar changes.

2020-03-01 | GSE112287 | GEO

Gene expression of cardiac tissues in dietary obese mice administered with a dipeptidyl peptidase-4 inhibitor

Project description:Dipeptidyl peptidase-4 (Dpp4) inhibitors are used worldwide to combat diabetes, however, their roles in cardiovascular disorders are yet to be defined. Here we show that a DPP4 inhibitor, linagliptin, contributes for the suppression of capillary rarefaction in cardiac tissues of dietary obese mice model. Imposing a high fat diet into mice induced capillary rarefaction and cardiac dysfunction. These pathologies associated with high DPP4 level in circulation, and the administration of linagliptin into dietary obese mice suppressed the development of capillary rarefaction and ameliorated cardiac dysfunction. Early growth response protein 1 (EGR1), known as an angiogenic transcription factor, is significantly reduced in the cardiac tissue upon metabolic stress, and this suppression was inhibited by the administration of linagliptin.

2017-04-27 | GSE98226 | GEO

Eosinophils promote lung emphysema via CTSL

Project description:Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. Analysis of the accumulated eosinophils revealed differential transcriptomes between the mouse lungs of elastase-induced emphysema and ovalbumin-induced asthma., Eosinophil depletion alleviated elastase-induced emphysema. Notably, eosinophil-derived cathepsin L (CTSL) degraded the extracellular matrix (ECM), causing emphysema in the pulmonary tissue. Eosinophils were positively correlated with serum CTSL levels, which were increased in patients with emphysema than in those without emphysema. Collectively, these results suggest that CTSL expression in eosinophils plays an important role in ECM degradation and remodeling and is related to emphysema in patients with COPD. Therefore, eosinophil-derived CTSL may serve as a potential therapeutic target for patients with emphysema.

2023-10-17 | GSE237749 | 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