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Activation of Nkx2.5 Transcriptional Program is Required for Adult Myocardial Repair

ABSTRACT: Activation of Nkx2.5 Transcriptional Program is Required for Adult Myocardial Repair

PROVIDER: PRJNA692707 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13450052.fastq.gz	Fastqsanger.gz
	SRR13450053.fastq.gz	Fastqsanger.gz
	SRR13450054.fastq.gz	Fastqsanger.gz
	SRR13450055.fastq.gz	Fastqsanger.gz
	SRR13450056.fastq.gz	Fastqsanger.gz

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Activation of Nkx2.5 Transcriptional Program is Required for Adult Myocardial Repair

Project description:We show that cardiac-specific RNA-sequencing studies reveal a disrupted embryonic Nkx2.5 transcriptional profile despite histologically normal, Nkx2.5 loss-of-function adult myocardium. Yet, adult nkx2.5-/- fish exhibit an impaired ability to recover following ventricular apex amputation as illustrated by retention of fibrin and collagen in the injured area. Complex network analyses illuminate that Nkx2.5 is required to mount a proliferative response for cardiomyocyte renewal and to provoke proteolytic pathways necessary for sarcomere disassembly. Moreover, direct Nkx2.5 targets embedded in these distinct gene regulatory modules coordinate appropriate, multi-faceted injury responses. Altogether, our findings support a previously unrecognized, Nkx2.5-dependent regenerative circuit that invokes myocardial proliferation and dedifferentiation to ensure effective regeneration in the teleost heart.

2022-04-05 | GSE164966 | GEO

Activation of Nkx2.5 transcriptional program is required for adult myocardial repair.

Project description:The cardiac developmental network has been associated with myocardial regenerative potential. However, the embryonic signals triggered following injury have yet to be fully elucidated. Nkx2.5 is a key causative transcription factor associated with human congenital heart disease and one of the earliest markers of cardiac progenitors, thus it serves as a promising candidate. Here, we show that cardiac-specific RNA-sequencing studies reveal a disrupted embryonic transcriptional profile in the adult Nkx2.5 loss-of-function myocardium. nkx2.5-/- fish exhibit an impaired ability to recover following ventricular apex amputation with diminished dedifferentiation and proliferation. Complex network analyses illuminate that Nkx2.5 is required to provoke proteolytic pathways necessary for sarcomere disassembly and to mount a proliferative response for cardiomyocyte renewal. Moreover, Nkx2.5 targets embedded in these distinct gene regulatory modules coordinate appropriate, multi-faceted injury responses. Altogether, our findings support a previously unrecognized, Nkx2.5-dependent regenerative circuit that invokes myocardial cell cycle re-entry, proteolysis, and mitochondrial metabolism to ensure effective regeneration in the teleost heart.

| S-EPMC9142600 | biostudies-literature

Enhanced Myocardial Repair with CardioClusters

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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. This SuperSeries is composed of the SubSeries listed below.

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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

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Endocardial HDAC3 is required for myocardial trabeculation

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The DiGeorge Syndrome gene TBX1 is required to specify the nkx2.5+ cardiopharyngeal lineage

Project description:Hemizygous microdeletions on chromosome 22q11.2 cause a broad spectrum of congenital cardiovascular and craniofacial anomalies known collectively as DiGeorge Syndrome (DGS) that appear to arise from reduced expression of TBX1, a gene in the typically deleted region. Although mice lacking tbx1 display similar, yet more severe, cardiovascular and craniofacial defects, the mechanisms underlying these devastating phenotypes remain incompletely understood. Here, we report that Tbx1 is required prior to pharyngeal arch development to specify the nkx2.5+ cardiopharyngeal cell lineage that gives rise to the cardiovascular and crainiofacial structures absent in tbx1 null zebrafish. Importantly, the role of Tbx1 during cardiopharyngeal lineage specification is conserved in mammals. Further, we learned that DVR1, the zebrafish homolog of mammalian GDF1/3, functions downstream of Tbx1 for pharyngeal progenitor specification. Together, these studies unveil a new paradigm potentially underlying the cardiovascular and craniofacial defects observed in the DGS population.

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Project description:The neonatal mammalian heart retains transient regenerative capacity that diminishes shortly after birth. Reactivation of cardiomyocyte proliferation represents a promising strategy for cardiac repair. This study identifies the nuclear-enriched long non-coding RNA FIRRE (Firre) as a critical regulator of cardiac development and regeneration. In vitro overexpression of Firre significantly enhanced cardiomyocyte proliferation, evidenced by increased S-phase entry. In vivo, AAV9-mediated cardiac-specific delivery of Firre extended the regenerative window in neonatal mice by promoting cardiomyocyte proliferation and reducing fibrotic scar area following myocardial injury. Remarkably, Firre administration improved cardiac function, attenuated infarct size, and stimulated cardiomyocyte proliferation in adult mice post-myocardial infarction. Mechanistically, RNA immunoprecipitation revealed direct interaction between Firre and Polypyrimidine Tract Binding Protein 1 (PTBP1). Transcriptome profiling demonstrated Firre-mediated activation of the PI3K/AKT signaling pathway. Furthermore, we identified Phlda3 (Pleckstrin Homology-like Domain Family A Member 3) as a downstream effector, through which Firre facilitates cardiac regeneration by modulating SFPQ-NONO heteromer stability and enhancing DNA repair capacity. These findings establish Firre as a potential therapeutic target for augmenting myocardial repair and regeneration.

2025-04-07 | GSE293638 | GEO

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