Single cell transcriptional profiles of endothelial cells sorted from the hearts with ablation of Wnt/beta-catenin signaling activating cardiomyocytes and without ablation [scRNA-seq]
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ABSTRACT:
PROVIDER: PRJNA926357 | ENA |
REPOSITORIES: ENA
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Project description:To understand how Wnt/β-catenin signaling-activated cardiomyocytes (β-cat ON CMs) promote coronary vessel development, we performed single-cell RNA sequencing of endothelial cells (ECs) sorted from the hearts ablated β-cat ON CMs and those from control hearts, respectively. Our analyses indicated that β-cat ON CMs regulates coronary vessel development by promoting arterialization, a step in the transition of endocardial ECs to coronary ECs.
2024-08-23 | GSE223461 | GEO
Project description:β-Catenin signaling pathway regulates cardiomyocytes proliferation and differentiation, though its involvement in metabolic regulation of cardiomyocytes remains unknown. We used one-day-old mice with cardiac-specific knockout of β-catenin and neonatal rat ventricular myocytes treated with β-catenin inhibitor to investigate the role of β-catenin metabolism regulation in perinatal cardiomyocytes. Transcriptomics of perinatal β-catenin-ablated hearts revealed a dramatic shift in the expression of genes involved in metabolic processes. Further analysis indicated an inhibition of lipolysis and glycolysis in both in vitro and in vivo models. Finally, we showed that β-catenin deficiency leads to mitochondria dysfunction via the downregulation of Sirt1/PGC-1α pathway. We conclude that cardiac-specific β-catenin ablation disrupts the energy substrate shift that is essential for postnatal heart maturation, leading to perinatal lethality of homozygous β-catenin knockout mice.
2021-08-31 | GSE153995 | GEO
Project description:single cell transcriptomic analysis of embyronic hearts with fibroblast ablation
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Project description:BRAFV600E mutation frequently occurs in papillary thyroid cancer (PTC). β-catenin, encoded by CTNNB1, is a key downstream component of canonical Wnt signaling pathway and is often overexpressed in PTC. BRAFV600E-driven PTC tumors rely on Wnt/β-catenin signaling to sustain their growth and progression. In the present study, we investigated the tumorigenicity of thyroid cancer cells derived from BrafV600E PTC mice after Ctnnb1 ablation (BVE-Ctnnb1null). Remarkably, the tumorigenic potential of BVE-Ctnnb1null tumor cells was lost in nude mice. RNA-Seq analysis of the BVE-Ctnnb1null tumor cells showed up-regulation of NKG2D receptor activating ligands (H60a, H60b, H60c, Raet1a, Raet1b, Raet1c, Raet1d, Raet1e and Ulbp1) and down-regulation of inhibitory MHC class I molecules H-2L and H-2K2 in the BVE-Ctnnb1null tumor cells. In vitro cytotoxicity assay demonstrated that BVE-Ctnnb1wt tumor cells were resistant to NK cell-mediated cytotoxicity whereas BVE-Ctnnb1null tumor cells were sensitive to NK cell-mediated killing. Furthermore, overexpression of any one of these NKG2D ligands in the BVE-Ctnnb1wt cell line resulted in significant reduction of tumor growth in nude mice. Our results indicate that active β-catenin signaling inhibits NK cell-mediated immune response against thyroid cancer cells. Targeting β-catenin signaling pathway may have significant therapeutic benefit for thyroid cancer by not only inhibiting tumor growth but also enhancing host immune surveillance.
2023-02-09 | GSE207695 | GEO
Project description:Combinatorial ablation of the major cardiac-expressed novel protein kinase C isoforms, PKCdelta and PKCepsilon, in murine cadiac myocytes unmasked functionally redundant growth-limiting effects of these kinases in hemodynamically stressed adult hearts and during normal embryonic cardiac development, mediated in part by shared transcriptional de-repression of ERK and periostin signaling. 14 cardiac polyA+-RNA profiles from unstressed, 12 week-old C57BL/6J-background mice (4 wild-type, 3 postnatal cardiac PKCdelta ablation, 3 germline PKCepsilon knockout, 4 combined knockouts) and 15 profiles generated 4 weeks after TAC induction (4 wild-type, 3 PKCdelta, 4 PKCepsilon, 4 combined knockout) were generated on Illumina HiSeq 2000 instruments.
2015-04-21 | E-GEOD-62689 | biostudies-arrayexpress
Project description:Combinatorial ablation of the major cardiac-expressed novel protein kinase C isoforms, PKCdelta and PKCepsilon, in murine cadiac myocytes unmasked functionally redundant growth-limiting effects of these kinases in hemodynamically stressed adult hearts and during normal embryonic cardiac development, mediated in part by shared transcriptional de-repression of ERK and periostin signaling.
2015-04-21 | GSE62689 | GEO
Project description:Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. However, the in vivo role of fibroblasts in structuring the basal ECM network is poorly understood. To examine the effects of fibroblast loss on the microenvironment in the adult murine heart, we generated mice with reduced fibroblast numbers and evaluated the tissue microenvironment during homeostasis and after injury. We determined that a 60-80% reduction in fibroblasts numbers did not overtly change the fibrillar collagen network but did alter the distribution and abundance of type VI collagen, a microfibrillar collagen that forms an open network with the basement membrane. In fibroblast ablated mice, myocardial infarction did not result in ventricular wall rupture, and heart function was more effectively preserved during angiotensin II/phenylephrine (AngII/PE) induced fibrosis. Analysis of cardiomyocyte contractility demonstrated weaker contractions and slower calcium release and reuptake in uninjured and AngII/PE infused fibroblast ablated animals. Moreover, fibroblast ablated hearts have a similar gene expression prolife to hearts with exercise-induced and physiological hypertrophy after AngII/PE infusion. These results suggest that hearts are resilient to a significant degree of fibroblast loss and that fibroblasts can directly impact cardiomyocyte function. Furthermore, a reduction in fibroblasts may have cardioprotective effects heart after injury suggesting that manipulation of the number of fibroblasts may have therapeutic value.
2023-03-10 | PXD021741 | Pride
Project description:Fibroblasts produce the majority of collagen in the heart and are thought to regulate extracellular matrix (ECM) turnover. However, the in vivo role of fibroblasts in structuring the basal ECM network is poorly understood. To examine the effects of fibroblast loss on the microenvironment in the adult murine heart, we generated mice with reduced fibroblast numbers and evaluated the tissue microenvironment during homeostasis and after injury. We determined that a 60-80% reduction in fibroblasts numbers did not overtly change the fibrillar collagen network but did alter the distribution and abundance of type VI collagen, a microfibrillar collagen that forms an open network with the basement membrane. In fibroblast ablated mice, myocardial infarction did not result in ventricular wall rupture, and heart function was more effectively preserved during angiotensin II/phenylephrine (AngII/PE) induced fibrosis. Analysis of cardiomyocyte contractility demonstrated weaker contractions and slower calcium release and reuptake in uninjured and AngII/PE infused fibroblast ablated animals. Moreover, fibroblast ablated hearts have a similar gene expression prolife to hearts with exercise-induced and physiological hypertrophy after AngII/PE infusion. These results suggest that hearts are resilient to a significant degree of fibroblast loss and that fibroblasts can directly impact cardiomyocyte function. Furthermore, a reduction in fibroblasts may have cardioprotective effects heart after injury suggesting that manipulation of the number of fibroblasts may have therapeutic value.
2023-03-10 | PXD021739 | Pride
Project description:Human colon carcinoma cells SKCO1 were deprived of either beta-catenin alone or beta-catenin together with TNFR1 and changes in mRNA levels were examined before and after TNFR1 ablation SKCO1 cells were transfected with either beta-catenin-specific siRNA alone or beta-catenin-specific siRNA together with a TNFR1-specific siRNA and changes in mRNA levels were examined before and after TNFR1 ablation
2014-10-02 | E-GEOD-61961 | biostudies-arrayexpress
Project description:The Wnt pathway is a key regulator of embryonic development, cell growth, differentiation, polarity formation, neural development, carcinogenesis, and stem cell self-renewal, and deregulation of the Wnt signalling is associated with many human disease. The central player in the Wnt pathway is β-catenin, A recent study has shown that β-catenin/Tcf/Lef signaling pathway is an essential growth-regulatory pathway in cardiomyocytes. We used DNA microarrays to detail the global trends in gene expression underlying β-catenin-overexpressed cardiomyocytes and identified distinct classes of up- or down-regulated genes during this process. Our findings suggest that β-catenin plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how β-catenin modulates heart diseases. Cardiomyocytes were infected with GFP control or β-catenin adenoviruses for RNA extraction and hybridization on Affymetrix microarrays. We sought to define the effects of β-catenin on the global programme of gene expression in primary cardiomyocytes. To that end, neonatal rat cardiomyocytes were infected with GFP control (G) or β-catenin adenovirus (B) for 24 hours.
2011-12-30 | E-GEOD-34772 | biostudies-arrayexpress