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Egr1 is a master regulator of regenerative senescence and cardiac repair

ABSTRACT: Egr1 is a master regulator of regenerative senescence and cardiac repair

PROVIDER: PRJNA1073899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27890429_1.fastq.gz	Fastqsanger.gz
	SRR27890429_2.fastq.gz	Fastqsanger.gz
	SRR27890430_1.fastq.gz	Fastqsanger.gz
	SRR27890430_2.fastq.gz	Fastqsanger.gz
	SRR27890431_1.fastq.gz	Fastqsanger.gz

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Egr1 is a master regulator of regenerative senescence and cardiac repair

Project description:The protein signatures in two mouse models of cardiac regeneration reveal enriched senescence gene sets, and Egr1 is the key regulator for regenerative senescence.Cathepsin S, a regenerative senescence-secreted component, promotes the degradation of the extracellular matrix, contributing to cardiac repair.

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Egr1 is a master regulator of regenerative senescence and cardiac repair

Project description:Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA-sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and Agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, Agrin-induced senescence and repair require Egr1, activated by the integrin/FAK-ERK/Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype (SASP) components that promote ECM degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process.

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Project description:Therapy-related myeloid neoplasms (t-MN) share many similarities with AML de novo in the elderly. One common factor is that they arise in the setting of chronic inflammation, likely due to advanced age or chemotherapy-induced senescence. Here, we examined the impact of haploinsufficient loss of the del(5q) tumor suppressor gene, EGR1, commonly deleted in high-risk MNs. In mice, under the exogenous inflammatory stress of either serial transplant or successive doses of the alkylating agent ENU, Egr1-haploinsufficient hematopoietic stem cells (HSCs) exhibit a clonal advantage. Complete loss of EGR1 function is incompatible with transformation; mutations of EGR1 are rare and are not observed in the remaining allele in del(5q) patients and complete knockout of Egr1 in mice leads to HSC exhaustion. Using chromatin immunoprecipitation sequencing (ChIP-seq), we identify EGR1 binding sites in human CD34+ cord blood-derived stem and progenitor cells (HSPCs) and show that EGR1 binds genes critical for stem cell differentiation, inflammatory signaling, and the DNA damage response. Notably, in the chromosome 5 sequences frequently deleted in patients, there is a significant enrichment of innate and inflammatory genes, which may confer a fitness advantage in an inflammatory environment. Short hairpin RNA (shRNA) mediated silencing of EGR1 biases HSPCs towards a self-renewal transcriptional signature. In the absence of EGR1, cells upregulate MYC-driven proliferative signals, downregulate CDKN1A (p21), disrupt the DNA damage response, and downregulate inflammation - adaptations anticipated to confer a relative fitness advantage for stem cells especially in an environment of chronic inflammation.

2022-09-01 | GSE184931 | GEO

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