The role of Egr1 and FosB in the 6 hour injury response
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA851397 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19764212_1.fastq.gz | Fastqsanger.gz | |||
| SRR19764212_2.fastq.gz | Fastqsanger.gz | |||
| SRR19764213_1.fastq.gz | Fastqsanger.gz | |||
| SRR19764213_2.fastq.gz | Fastqsanger.gz | |||
| SRR19764214_1.fastq.gz | Fastqsanger.gz |
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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:EGR1 is an early growth response zinc finger transcription factor with broad actions, including in differentiation, mitogenesis, tumor suppression, and neuronal plasticity. Here we demonstrate that Egr1-/- C57BL/6-background mice have normal eyelid development, but back-crossing to BALB/c background for 4-5 generations resulted in defective eyelid development by embryonic day E15.5, at which time EGR1 was expressed in eyelids of WT mice. Defective eyelid formation correlated with profound ocular anomalies evident by post-natal days 1-4, including severe cryptophthalmos, microphthalmia or anophthalmia, retinal dysplasia, keratitis, corneal neovascularization, cataracts, and calcification. The BALB/c albino phenotype-associated Tyrc tyrosinase mutation appeared to contribute to the phenotype, as crossing the independent Tyrc-2J allele to Egr1-/- C57BL/6 mice also produced ocular abnormalities, albeit less severe than those in Egr1-/- BALB/c mice. Thus, EGR1 in a genetic background-dependent manner plays a critical role in mammalian eyelid development and closure, with subsequent impact on ocular integrity.
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Project description:Egr1 regulates genes involved in cholesterol biosynthesis in liver. ChIP-chip assays were performed on H4IIE liver cells that were either treated or untreated with insulin for one hour. This experiment includes a custom ChIP-chip design incorporating many genes that are dynamically regulated by insulin signaling. The Egr1 antibody used was from Santa Cruz sc-189. Egr1 ChIP samples from untreated and 1h insulin treated cells were hybridized.
2011-07-22 | E-GEOD-30823 | biostudies-arrayexpress
Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.
2019-06-27 | PXD011767 | Pride
Project description:Egr1 regulates genes involved in cholesterol biosynthesis in liver. ChIP-chip assays were performed on H4IIE liver cells that were either treated or untreated with insulin for one hour. This experiment includes a custom ChIP-chip design incorporating many genes that are dynamically regulated by insulin signaling. The Egr1 antibody used was from Santa Cruz sc-189.
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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:The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Egr1 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China). H/R was used to mimic IRI in vitro. Briefly, cells were incubated in glucose-free medium in a tri-gas incubator (94% N2, 5% CO2 and 1.0% O2) at 37 °C for 6 hours. Subsequently, cells were incubated in complete medium under normal conditions for 18 hours for reoxygenation. Cells were then collected by 1ml TRIzol (Invitrogen, Carlsbad), and sent to Annoroad Corporation (Beijing, China) for high throughout Illumina NovaSeq 6000 sequencing (GPL24247) (Illumina, San Diego, CA, USA). Results: To determine the possible pathways and downregulated genes of Egr1 in protecting mice primary renal tubular epithelial cells from injury, we conduct the transcriptomotic sequencing. After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) on isolated mouse renal tubular epithelial cells of 3 groups, negtive control(Sham group) treated with H/R (H/R group) or Egr1 overexpression plasmid (Egr1OV group). Egr1-responsive genes showed significant enrichment in proliferation pathway.
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Project description:Role of EGR1 in vasculogenic mimicry of MDA-MB-231 cells
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