Project description:Contradictorily, both up- and downregulation of miR-25 can reverse heart failure. Importantly, these findings were based on the same animal model of pressure overloaded transverse aortic constriction (TAC) mice. How can we explain and, if possible, reconcile these two conflicting findings? Heart failure is a multi-step process that involves multiple organs, and we hypothesized that determining whether altering miR-25 alone could induce heart failure should provide a mechanistic basis for miR-25âs action in this process. Here, we show that overexpression of miR-25 in normal mice caused cardiomyocyte fibrosis and apoptosis but no obvious kidney impairment. By contrast, inhibition of miR-25 in normal mice led to hypertension, mild heart dilation, and severe kidney dysfunction. With the expectation that restoring miR-25 might ameliorate kidney injury, we demonstrated that increasing miR-25 reversed proteinuria and kidney fibrosis in diabetic nephropathy. MiR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. RNA sequencing of mouse kidneys with elevated and reduced miR-25 identified distinct alterations of a number of putative miR-25 target mRNAs, including those involved in the Ras signaling pathway, oxidant stress. In summary, differences in miR-25 expression during different stages of heart disease and its distinct roles in the heart and kidney, offer a new perspective for the role of miR-25 function in heart failure, which may begin to resolve this catch-22. Detect the mRNA alteration in wildtype and miR-25 agomir or antagomir treated mice

2016-06-10 | E-GEOD-83144 | biostudies-arrayexpress

hereditary spherocytosis

Project description:hereditary spherocytosis

| PRJEB76254 | ENA

cardiorenal failure in rat - Proteomic analysis of the changes in kidney upon chronic heart failure in a rat model. Heart failure develops due to surgically created aorto-venoufistula.

Project description:Proteomic analysis of the changes in kidney upon chronic heart failure in a rat model. Heart failure develops due to surgically created aorto-venoufistula.

2018-09-24 | PXD009296 | Pride

Alteration in microRNA-25 Balance Causes Heart and Kidney Impairment

Project description:Contradictorily, both up- and downregulation of miR-25 can reverse heart failure. Importantly, these findings were based on the same animal model of pressure overloaded transverse aortic constriction (TAC) mice. How can we explain and, if possible, reconcile these two conflicting findings? Heart failure is a multi-step process that involves multiple organs, and we hypothesized that determining whether altering miR-25 alone could induce heart failure should provide a mechanistic basis for miR-25’s action in this process. Here, we show that overexpression of miR-25 in normal mice caused cardiomyocyte fibrosis and apoptosis but no obvious kidney impairment. By contrast, inhibition of miR-25 in normal mice led to hypertension, mild heart dilation, and severe kidney dysfunction. With the expectation that restoring miR-25 might ameliorate kidney injury, we demonstrated that increasing miR-25 reversed proteinuria and kidney fibrosis in diabetic nephropathy. MiR-25 expression in humans is initially decreased at the onset of heart failure but is later increased in end-stage heart failure. RNA sequencing of mouse kidneys with elevated and reduced miR-25 identified distinct alterations of a number of putative miR-25 target mRNAs, including those involved in the Ras signaling pathway, oxidant stress. In summary, differences in miR-25 expression during different stages of heart disease and its distinct roles in the heart and kidney, offer a new perspective for the role of miR-25 function in heart failure, which may begin to resolve this catch-22.

2016-06-10 | GSE83144 | GEO

Excessive O-GlcNAcylation causes heart failure and sudden death

Project description:Excessive O-GlcNAcylation causes heart failure and sudden death

| PRJNA553816 | ENA

DPYS as a potential diagnostic biomarker in hereditary and sporadic PRCC2

Project description:Papillary renal cell carcinoma type 2 (PRCC2) is known to be very aggressive type of tumor without effictive therapy. Hereditary form of PRCC2 is caused by Fumarate Hydratase (FH) gene mutation that accompanied Hereditary Leiomyomatosis and Renal Cell Carcinoma (HLRCC) disorder. In sporadic form of PRCC2 the mutation of FH gene has not been reported. Both forms of tumors have the similar histopathological characteristics with poor survival prognosis. In this study, we profiled the gene expression of renal tumors and normal tissue from PRCC2 (hereditary and sporadic) patients in order to better understand commonalities and differences in the transcriptional landscape of PRCC2. Microarray gene expression profiling was performed on eight normal kidney tissue samples, five hereditary PRCC2 tumor tissue samples and 19 sporadic PRCC2 tumor tissue samples. Hereditary PRCC2 (HPRCC2) patients were confirmed by DNA sequencing of the FH gene.

2016-06-01 | E-GEOD-48352 | 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