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

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

PROVIDER: PRJNA750667 | ENA |

REPOSITORIES: ENA

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

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 | GSE181091 | 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 [Taqman]

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

| PRJNA750866 | ENA

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

2021-07-31 | GSE181048 | GEO

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 [RNA-Seq]

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

| PRJNA750445 | ENA

Mining the stiffness-sensitive transcriptome in human vascular smooth muscle cells identifies long non-coding RNA stiffness regulators

Project description:Vascular extracellular matrix (ECM) stiffening is a risk factor for aortic and coronary artery disease. How matrix stiffening regulates the transcriptome profile of human aortic (Ao) and coronary (Co) vascular smooth muscle cells (VSMCs) is not well understood. Furthermore, the role of long non-coding RNAs (lncRNAs) in the cellular response to stiffening has never been explored. This study characterizes the stiffness-sensitive transcriptome of human Ao and Co VSMCs and identify potentially key lncRNA regulators of stiffness-dependent VSMC functions. Ao and Co VSMCs were cultured on hydrogel substrates mimicking physiologic and pathologic ECM stiffness. Total RNA-seq was performed to compare the stiffness-sensitive transcriptome profiles of Ao and Co VSMCs.

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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