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Crosslinked elastin-like polypeptides mediate direct cardiac differentiation of mouse embryonic and induced pluripotent stem cells without use of cardiac differentiation factors

ABSTRACT: Crosslinked elastin-like polypeptides mediate direct cardiac differentiation of mouse embryonic and induced pluripotent stem cells without use of cardiac differentiation factors

PROVIDER: PRJNA607760 | ENA |

REPOSITORIES: ENA

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Crosslinked elastin-like polypeptides mediate direct cardiac differentiation of mouse embryonic and induced pluripotent stem cells without use of cardiac differentiation factors

Project description:Elastin-like polypeptides (ELPs) are promising for biomedical applications due to their unique thermos-responsive and elastic properties. ELP-based biomaterial has been produced through enzymatic crosslinking of modified ELPs. We investigated the role of elastin like polypeptide in cardiomyocyte proliferation and differentiation in mouse ES cells

2024-02-12 | GSE145623 | GEO

Gene expression profiles in Elastin (Eln+/-) mouse aorta and aortic valve tissue

Project description:Elastin wild type Eln+/+ and Eln+/- mouse aorta and aortic valve tissue. In the study, we demonstrated differential gene expression in juvenile elastin deficient mouse valve tissue. In the study, we hybridized RNA from Elastin wild type (Eln+/+) aorta tissue, elastin wild type (Eln+/+) aortic valve tissue, elastin (Eln+/-) aorta tissue and elastin (Eln+/-) aortic valve tissue to Affymetrix GeneChip Mouse Genome 430 2.0 Array

2009-11-30 | E-GEOD-16012 | biostudies-arrayexpress

Effect of elastin insufficiency on gene expression in cultured human aortic smooth muscle cells

Project description:Defective elastin induces aortic smooth muscle cell hyperproliferation. To elucidate gene expression changes with elastin insufficiency, bulk RNA-seq was performed on cultured human aortic smooth muscle cells treated with siRNA targeting elastin.

2025-11-12 | GSE270681 | GEO

Gene expression profiles in Elastin (Eln+/-) mouse aorta and aortic valve tissue

2009-11-30 | GSE16012 | GEO

Effect of elastin-deficiency on gene expression in murine aortic smooth muscle cells at embryonic day 15.5

Project description:Defective elastin induces aortic smooth muscle cell hyperproliferation. As elastin is expressed from embryonic day 14 in the murine aorta, we utilized bulk RNA-seq to reveal molecular differences between Eln(+/+) and Eln(-/-) aortic smooth muscle cells at embryonic day 15.5.

2025-11-12 | GSE270682 | GEO

Brahma safeguards canalization of cardiac mesoderm differentiation

Project description:Brahma safeguards canalization of cardiac mesoderm differentiation

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PDAP1 RIP in UV-crosslinked human T cells

Project description:PDAP1 RIP in UV-crosslinked human T cells

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Analysis of SOX2 overexpression in hESCs undergoing cardiac differentiation.

Project description:SOX2 downregulation is a pre-requisite for proper cardiac differentiation. This study was performed to reveal the neagtive effects of SOX2 on cardiac differentiation.

2015-11-13 | GSE67995 | GEO

Cardiac differentiation of embryonic stem cells recapitulates embryonic cardiac development.

Project description:Mouse embryonic stem cells can differentiate in vitro into spontaneously contracting cardiomyocytes. The main objective of this study was to investigate cardiogenesis in cultures of differentiating embryonic stem cells (ESCs) and to determine how closely it mimics in vivo cardiac development. We identified and isolated a population of cardiac progenitor cells (CPCs) through the use of a reporter DNA construct that allowed the expression of a selectable marker under the control of the Nkx2.5 enhancer. We proceeded to characterize these CPCs by examining their capacity to differentiate into cardiomyocytes and to proliferate. We then performed a large-scale temporal microarray expression analysis in order to identify genes that are uniquely upregulated or downregulated in the CPC population. We determined that the transcriptional profile of the mESC derived CPCs was consistent with pathways known to be active during embryonic cardiac development. We conclude that in vitro differentiation of mESCs recapitulates the early steps of mouse cardiac development. Keywords: embryonic stem cell, differentiation, cardiac progenitor, cardiogenesis

2007-08-30 | GSE5671 | GEO

Dynamic Changes in the Expressions of Elastogenesis- and Elastinolysis-Associated Genes and Remodeling of the Elastin Network in Volume-Overloaded Heart

Project description:Background: In the remodeling process of the volume-overloaded heart, the extracellular matrix (ECM) may be dynamically modified to adapt to hemodynamic stress. We investigated the expression of ECM-related genes and modification of the elastin network in the remodeling process of the left ventricles (LVs) of rats with aortocaval fistulae. Methods and Findings: Gene array analysis identified 36 upregulated and 11 downregulated ECM-related genes during evolution from the compensated to the late decompensated phase. Ingenuity Pathway Analysis identified the formation of elastic fibers as an important biological function. Real-time PCR confirmed persistent upregulation of elastogenesis-associated genes, including elastin, lysyl oxidase, lysyl oxidase like-1, fibrillin 1, fibulin 2, versican and latent transforming growth factor beta binding protein 2 at various intervals. The expression levels and enzymatic activities of potent elastases, cathepsin S and cathepsin K increased during the early phase. Immunofluorescence confocal microscopy showed that the microstructure of the elastin network was preserved during the early phase, degraded during the compensated phase, partially repaired during the early decompensated phase, and reinforced during the late decompensated phase. Assessment of elastin concentrations in the LVs showed a consistent temporal pattern throughout the course. Conclusions: In the volume-overloaded heart, upregulation of potent elastases during the early phase and persistent upregulation of elastogenesis-related genes result in early degradation followed by repair and reinforcement of the elastin network of the LV. Remodeling of the elastin network may contribute to changes in the mechanical property of the volume-overloaded heart.

2018-03-31 | GSE97044 | GEO

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