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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.

2017-12-01 | GSE100081 | GEO

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

Key role for Rac in the early transcriptional response to ECM stiffness and the stiffness-dependent repression of ATF3

Project description:The Rho family GTPases, Rac and Rho, play critical roles in transmitting mechanical information contained within the extracellular matrix (ECM) to the cell. Rac and Rho have well described roles in regulating stiffness-dependent actin remodeling, proliferation and motility. However, much less is known about the relative roles of these GTPases in stiffness-dependent transcription, particularly at the genome-wide level. Here, we selectively inhibited Rac and Rho in mouse embryonic fibroblasts cultured on deformable substrata and used RNA sequencing to elucidate and compare the contribution of these GTPases to the early transcriptional response to ECM stiffness. Surprisingly, we found that the stiffness-dependent activation of Rac is dominant over Rho in the initial transcriptional response to ECM stiffness. We also identified Activating Transcription Factor 3 (ATF3) as a major target of stiffness/Rac-mediated signaling and show that ATF3 repression by ECM stiffness helps to explain how the stiffness-dependent activation of Rac results in the induction of cyclin D1.

2023-10-04 | GSE236266 | GEO

Identification of candidate genes affecting juvenile wood stiffness in Pinus radiata

Project description:Wood stiffness is the most important wood quality trait of forest trees for structural timber production. We investigated genes differentially transcribed in radiate pine trees with distinct wood stiffness using bulked segregant analysis (BSA) and cDNA microarrays. Transcript accumulation in earlywood (EW) and latewood (LW) of high (HS) and low stiffness (LS) trees in two progeny trials was compared. Radiata pine trees used for microarray experiment were selected from two progeny trials planted at Flynn and Kromelite, Australia. Based on the IML-based MOE measurement, five families with highest and lowest MOE each were selected from each trial, which represented two segregant populations with contrasting wood stiffness. Two individuals from each selected family were further sampled. Developing xylem tissues of selected trees in Flynn trial were sampled in spring (October) and autumn (April), representing earlywood (EW) and latewood (LW) of juvenile aged trees, respectively. Collection of xylem tissues from Kromelite trial was arranged in summer (late November) when latewood (LW) was formed. The xylem tissues were scraped at breast height with a sharp chisel after the bark was removed. In Flynn trial EW and LW tissues were collected from the same sampled trees on opposite sides of the trunk. Transcript accumulation was compared in trees with highest (HS) and lowest stiffness (LS) using xylem samples from Flynn collected in spring (EW) and autumn (LW), as well as Kromelite in summer (LW), respectively. Bulked segregant analysis (BSA) was used for the experiment design. Total RNA samples extracted from the five trees with HS were pooled at equal amount, and compared to the bulked five individuals with LS. This pooling strategy can partly minimize the genetic variation among different genotypes. Dye swaps were applied in each biological replicate.

2011-06-01 | E-GEOD-23020 | biostudies-arrayexpress

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