Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [Taqman]

ABSTRACT: Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [Taqman]

PROVIDER: PRJNA750866 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [Taqman]

Project description:Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remains limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with non-failing or DCM pediatric patient serum activates the fetal gene program (FGP). Here we show that serum treatment with Proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating microRNAs, promote these pathological changes. Evaluation of the protein secretome showed that midkine (MDK) is up-regulated in DCM serum, and NRVM treatment with MDK activates the FGP. Changes in gene expression in serum-treated NRVMs, evaluated by next-generation RNA sequencing (RNA-Seq), indicates extracellular matrix remodeling and focal adhesion pathways are upregulated in pediatric DCM serum and serum-treated NRVMs, suggesting alterations in cellular stiffness. Cellular stiffness was evaluated by Atomic Force Microscopy, which showed an increase in stiffness in DCM serum-treated NRVMs. Of the proteins increased in DCM sera, secreted frizzled related protein 1 (sFRP1) was a potential candidate for the increase in cellular stiffness, and sFRP1 treatment of NRVMs recapitulated the increase in cellular stiffness observed in response to DCM-serum treatment. Our results show that serum circulating proteins promote pathological changes in gene expression and cellular stiffness, and circulating miRNAs are protective against pathological changes.

2021-07-31 | GSE181048 | GEO

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness

Project description:Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness

| PRJNA750663 | ENA

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [RNA-Seq]

2021-07-31 | GSE181033 | GEO

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [SOMA-proteomics]

2021-07-31 | GSE181091 | GEO

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [RNA-Seq]

Project description:Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [RNA-Seq]

| PRJNA750445 | ENA

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [SOMA-proteomics]

Project description:Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness [SOMA-proteomics]

| PRJNA750667 | ENA

Serum Circulating Proteins from Pediatric Dilated Cardiomyopathy Patients Cause Pathologic Remodeling and Cardiomyocyte Stiffness

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-31 | GSE181051 | GEO

Serum circulating proteins from pediatric patients with dilated cardiomyopathy cause pathologic remodeling and cardiomyocyte stiffness.

Project description:Dilated cardiomyopathy (DCM) is the most common form of cardiomyopathy and main indication for heart transplantation in children. Therapies specific to pediatric DCM remain limited due to lack of a disease model. Our previous study showed that treatment of neonatal rat ventricular myocytes (NRVMs) with serum from nonfailing or DCM pediatric patients activates the fetal gene program (FGP). Here we show that serum treatment with proteinase K prevents activation of the FGP, whereas RNase treatment exacerbates it, suggesting that circulating proteins, but not circulating miRNAs, promote these pathological changes. Evaluation of the protein secretome showed that midkine (MDK) is upregulated in DCM serum, and NRVM treatment with MDK activates the FGP. Changes in gene expression in serum-treated NRVMs, evaluated by next-generation RNA-Seq, indicated extracellular matrix remodeling and focal adhesion pathways were upregulated in pediatric DCM serum and in DCM serum-treated NRVMs, suggesting alterations in cellular stiffness. Cellular stiffness was evaluated by Atomic Force Microscopy, which showed an increase in stiffness in DCM serum-treated NRVMs. Of the proteins increased in DCM sera, secreted frizzled-related protein 1 (sFRP1) was a potential candidate for the increase in cellular stiffness, and sFRP1 treatment of NRVMs recapitulated the increase in cellular stiffness observed in response to DCM serum treatment. Our results show that serum circulating proteins promoted pathological changes in gene expression and cellular stiffness, and circulating miRNAs were protective against pathological changes.

| S-EPMC8525651 | biostudies-literature

Dilated cardiomyopathy vs Myocarditis

Project description:Dilated cardiomyopathy vs Myocarditis

| PRJNA493608 | ENA

Dilated Cardiomyopathy in Dobermans and Boxers

Project description:This study attempts at investigating the changes in cardiac gene expression that occur in Dilated Cardiomyopathy (DCM). DCM in Dobermans and Boxers are the focus of this study. Control heart tissue as well as Pacing tissue used is from mongrel dogs. Keywords: control vs pacing vs disease; strain specific disease 3 Dobermans-DCM, 4 Boxers-DCM, 3 mongrels-control and 3 mongrels-pacing

2008-05-08 | E-GEOD-11015 | 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