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Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [CUT&Tag]

ABSTRACT: Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [CUT&Tag]

PROVIDER: PRJNA1152975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30420771_1.fastq.gz	Fastqsanger.gz
	SRR30420771_2.fastq.gz	Fastqsanger.gz
	SRR30420772_1.fastq.gz	Fastqsanger.gz
	SRR30420772_2.fastq.gz	Fastqsanger.gz

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Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [CUT&Tag]

Project description:Zebrafish heart regeneration is a complex process consisting of tempo-spatial coordination of cardiomyocyte (CM) and endothelial cell (EC) regeneration, fibrosis and inflammation. While myocardial, endocardial, and epicardial signaling have been reported to modulate this process, little is known about how leukocyte especially platelet signaling is involved in this regenerative process. Here we report that cloche/npas4l (neuronal PAS domain protein 4 like) is a pro-regenerative platelet factor for adult zebrafish heart regeneration. We found that injury triggered npas4l expression as early as 1 h post ventricular amputation, and haploinsufficiency of npas4l disrupted CM and EC proliferation and heart regeneration in clofv087b/+ and clom39/+ mutants after ventricular resection or nitroreductase (NTR)-mediated CM ablation. By constructing a single-cell transcriptomic atlas, we discovered that npas4l was dynamically expressed in platelets in response to heart injury with robust platelet-CM or -EC interactions via ligand-receptor activity analysis. Decreasing platelets in NTR-mediated depletion or mpl mutants impaired CM and EC proliferation, and over-expression of npas4l in platelets sufficiently made uninjured and injured CM reentry into the cell-cycle and rescued CM and EC proliferation in clofv087b/+ mutants. Furthermore, Npas4l positively regulated Bmp6 expression in platelets and either BMP6 inhibitors or siRNAs decreased CM proliferation and heart regeneration. This work demonstrates, for the first time, that injury-induced platelets are essential for zebrafish heart regeneration and Npas4l is a core platelet transcription factor for fine-tuning heart regeneration partially via Bmp6 signaling.

2025-04-22 | GSE275789 | GEO

Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration

Project description:Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration

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Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [bulk RNA-seq]

2025-04-22 | GSE223226 | GEO

Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [10x scRNA-seq]

2025-04-22 | GSE224111 | GEO

Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [10x scRNA-seq]

Project description:Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [10x scRNA-seq]

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Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [bulk RNA-seq]

Project description:Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration [bulk RNA-seq]

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Cloche is a pro-regenerative platelet factor during zebrafish heart regeneration

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-04-22 | GSE224125 | GEO

Osr1 controls the pro-regenerative response of Fibro-Adipogenic Progenitors

Project description:Purpose: To study the requirement of Osr1 expression for FAP function during skeletal muscle regeneration. Methods: We sequenced total mRNAs isolated from adult FAPs FACS sorted from 3 and 7 day post injured hindlimb skeletal muscle of Ctrl (Osr1flox/+ CAGG Cre+) and Osr1 cKO (Osr1flox/flox CAGG Cre+) mice. Results: Loss of Osr1 leads to pro-fibrotic orientation of FAPs and impairs both FAP-macrophage and FAP-MuSCs communication network resulting in impaired regenerative myogenesis and persistent fibrosis. Conclusions: Osr1 is a key transcriptional regulator of FAP regenerative function protecting FAPs from assuming a detrimental pro-fibrotic and anti-myogenic state.

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GSDMD-mediated metabolic crosstalk licenses a pro-regenerative niche for tissue repair

Project description:GSDMD-mediated metabolic crosstalk licenses a pro-regenerative niche for tissue repair

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