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Single cell transcriptomic analysis of embyronic hearts with fibroblast ablation

ABSTRACT: single cell transcriptomic analysis of embyronic hearts with fibroblast ablation

PROVIDER: PRJNA1134740 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29791535_1.fastq.gz	Fastqsanger.gz
	SRR29791535_2.fastq.gz	Fastqsanger.gz
	SRR29791536_1.fastq.gz	Fastqsanger.gz
	SRR29791536_2.fastq.gz	Fastqsanger.gz
	SRR29791537_1.fastq.gz	Fastqsanger.gz

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Consequences of fibroblast ablation in adult murine hearts

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

Consequences of fibroblast ablation in adult murine hearts

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single cell transcriptomic analysis of embyronic hearts with fibroblast ablation

Project description:Control and ablated embryonic hearts from the Pdgfra-CreER; Rosa-DTA mice were isolated, dissociated, and multiplexed using the MULTI-seq approach, profiled with the 10X scRNA-seq platform and sequenced with Illumina NovaSeq X.

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RNA-sequencing of unstressed and pressure-overloaded C57 mouse hearts with single or combined ablation of PKCdelta and PKCepsilon

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.

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RNA-sequencing of unstressed and pressure-overloaded C57 mouse hearts with single or combined ablation of PKCdelta and PKCepsilon

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Fibroblast-specific Proteo-transcriptomes of Human Sinoatrial Node in Non-failing and Failing Hearts

Project description:Sinoatrial node (SAN), and right atrial (RA) fibroblasts were isolated from explanted non-failing (nHF) and HF human hearts, cultured, passaged once, and treated +/- transforming growth factor beta 1(TGF beta-1). Fibroblast pellets were subjected to comprehensive high-throughput proteomic analyses.

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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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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]

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.

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Project description:Post-injury remodeling is a complex process involving temporal specific cellular interactions in the injured tissue where the resident fibroblasts play multiple roles, including inflammation induction and tissue remodeling. To dissect the molecular basis of these interactions, we performed single-cell and spatial transcriptome analysis in human and mouse hearts after myocardial infarction. A subset of fibroblasts identified by unique high expression of CD248 was strongly correlated with collagen synthesis and remodeling, and genetic deletion of CD248 in fibroblast ameliorated cardiac fibrosis and dysfunction following ischemia/reperfusion, highlighting the functional importance of CD248 positive fibroblasts in post-injury pathological remodeling. CD248 stabilizes TGF-βR Ⅰ protein and activates ACKR3 expression in fibroblast, leading to enhanced T cell adhesion and retention. This CD248 mediated fibroblast-T cell interaction is required to sustain fibroblast activation and scar expansion in injured heart. Disruption of this interaction using monoclonal antibody or Chimeric antigen receptor T cell reduces T cell infiltration, ameliorates ischemia/reperfusion-induced cardiac fibrosis and improves heart function. Therefore, single cell molecular profiling in post-injury heart has uncovered a CD248 specific subclass of fibroblast with a critical role in fibroblast-T cell interaction and a new potential therapy to treat tissue fibrosis.

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