Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA897008 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22149482_1.fastq.gz	Fastqsanger.gz
	SRR22149482_2.fastq.gz	Fastqsanger.gz
	SRR22149483_1.fastq.gz	Fastqsanger.gz
	SRR22149483_2.fastq.gz	Fastqsanger.gz
	SRR22149484_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

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

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:AimsAging is associated with the development of insulin resistance and hypertension which may stem from inflammation induced by accumulation of toxic bacterial DNA crossing the gut barrier. The aim of this study was to identify factors counter-regulating these processes. Taking advantage of the Chromogranin A (CgA) knockout (CgA-KO) mouse as a model for healthy aging, we have identified Vsig4 (V-set and immunoglobulin domain containing 4) as the critical checkpoint gene in offsetting age-associated hypertension and diabetes.Methods and resultsThe CgA-KO 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. The gut barrier, compromised in aging WT mice, was preserved in CgA KO mice leading to major 35-fold protection against bacterial DNA-induced inflammation. 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 may account for the very low accumulation of microbial DNA in the heart. The reversal of hypertension in aging CgA-KO mice likely stems from (i) low accumulation of microbial DNA, (ii) decreased spillover of norepinephrine in the heart and kidneys, and (iii) reduced inflammation.ConclusionWe conclude that healthy aging relies on protection from bacterial DNA and the consequent low inflammation afforded by CgA-KO. Vsig4 also plays a crucial role in "healthy aging" by counteracting age-associated insulin resistance and hypertension.

| S-EPMC9691654 | biostudies-literature

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

Project description:Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade

| PRJNA578135 | ENA

Interaction between diabetes and hypertension in a rat model of diabetic nephropathy

Project description:Fisher male Cyp1a1mRen2 rats were allocated into four groups of four biological replicates each: control; streptozotocin-induced diabetes alone; indole-3-carbinol induced hypertension alone; combined induced diabetes and hypertension. <br>Kidneys were harvested for microarray analysis.analysis.

2011-12-31 | E-MEXP-3165 | biostudies-arrayexpress

Antagonistic microorganisms

Project description:Antagonistic microorganisms - Whole Genome Sequencing

| PRJNA1170530 | ENA

Diabetes and hypertension then reversal in a rat model of diabetic nephropathy

Project description:Fisher male Cyp1a1mRen2 rats were allocated into three groups of four or eight biological replicates each: control; combined induced diabetes and hypertension; removal of combined treatments. Kidneys were harvested for gene expression microarray analysis on Affymetrix GeneChip Rat Genome 230 2.0 GeneChips

2013-04-10 | E-MEXP-3739 | biostudies-arrayexpress

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (scRNA-seq dataset: SZ11)

Project description:In this study we searched for primary regulators of cancer-inhibitory inflammation using murine tumors of immune-dependent progressive or regressive fates linked to antagonistic inflammatory tumor microenvironments

2020-11-20 | GSE139046 | GEO

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

2020-11-20 | GSE139045 | GEO

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ3)

2020-11-20 | GSE139044 | GEO

Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

Project description:Antagonistic inflammatory phenotypes dictate tumor fate and response to immune checkpoint blockade (RNA-seq dataset: SZ8)

| PRJNA578140 | ENA