ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Early growth response (EGR)-1 is required for timely cell-cycle entry and progression in hepatocytes after acute carbon tetrachloride exposure in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- A Shared EGR1-IL-32-Macrophage Polarisation Signature in Rheumatoid Arthritis and Metabolic Dysfunction-Associated Steatotic Liver Disease.Journal of inflammation research · 2026Article
- Atlas of expression of acyl CoA binding protein/diazepam binding inhibitor (ACBP/DBI) in human and mouse.Cell death & disease · 2025Article
- EGR1 is crucial for the chlorogenic acid-provided promotion on liver regeneration and repair after APAP-induced liver injury.Cell biology and toxicology · 2023Article
- Lentinan induces apoptosis of mouse hepatocellular carcinoma cells through the EGR1/PTEN/AKT signaling axis.Oncology reports · 2023Article
- Adefovir Dipivoxil as a Therapeutic Candidate for Medullary Thyroid Carcinoma: Targeting RET and STAT3 Proto-Oncogenes.Cancers · 2023Article
- Egr1 confers protection against acetaminophen‑induced hepatotoxicity via transcriptional upregulating of Acaa2.International journal of biological sciences · 2022Article
- Participation of 5-lipoxygenase and LTB4 in liver regeneration after partial hepatectomy.Scientific reports · 2019Article
- HCMV miR-US22 down-regulation of EGR-1 regulates CD34+ hematopoietic progenitor cell proliferation and viral reactivation.PLoS pathogens · 2019Article
- Attenuation of liver cancer development by oral glycerol supplementation in the rat.European journal of nutrition · 2018Article
- Role of early growth response 1 in liver metabolism and liver cancer.Hepatoma research · 2017Article
- Pesticide toxicogenomics across scales: in vitro transcriptome predicts mechanisms and outcomes of exposure in vivo.Scientific reports · 2016Article
- Inhibition of miR-21 rescues liver regeneration after partial hepatectomy in ethanol-fed rats.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Moderate (2%, v/v) Ethanol Feeding Alters Hepatic Wound Healing after Acute Carbon Tetrachloride Exposure in Mice.Biomolecules · 2016Article
- Differential effects of hyaluronan synthase 3 deficiency after acute vs chronic liver injury in mice.Fibrogenesis & tissue repair · 2016Article
- Dysregulated serum response factor triggers formation of hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2015Article
- Constitutive Activation of the Nlrc4 Inflammasome Prevents Hepatic Fibrosis and Promotes Hepatic Regeneration after Partial Hepatectomy.Mediators of inflammation · 2015Article
- P2Y2 purinergic receptor activation is essential for efficient hepatocyte proliferation in response to partial hepatectomy.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Toxicogenomic analysis reveals profibrogenic effects of trichloroethylene in autoimmune-mediated cholangitis in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Modeling toxicodynamic effects of trichloroethylene on liver in mouse model of autoimmune hepatitis.Toxicology and applied pharmacology · 2014Article
- AAV-mediated liver-specific MPV17 expression restores mtDNA levels and prevents diet-induced liver failure.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cell-cycle induction in hepatocytes protects from prolonged tissue damage after toxic liver injury. Early growth response (Egr)-1(-/-) mice exhibit increased liver injury after carbon tetrachloride (CCl(4)) exposure and reduced TNF-α production. Because TNF-α is required for prompt cell-cycle induction after liver injury, here, we tested the hypothesis that Egr-1 is required for timely hepatocyte entry into the cell cycle after CCl(4)-induced liver injury. Acute liver injury was induced by a single injection of CCl(4). Assays were employed to assess indices of the cell cycle in liver after CCl(4) exposure. Bromodeoxyuridine incorporation peaked in wild-type mice at 48 h after CCl(4) but was reduced by 80% in Egr-1(-/-) mice. Proliferating-cell nuclear-antigen immunohistochemistry revealed blocks in cell-cycle entry and progression to DNA synthesis in Egr-1-deficient mice 48 h after CCl(4). Cyclin D, important for G0/G1 progression, was reduced at baseline and 36 h after CCl(4). Cyclin E1, required for G1/S-phase transition, was reduced in Egr-1(-/-) mice 24 and 48 h after CCl(4) exposure and was associated with reduced phosphorylation of the retinoblastoma protein. Proliferation in Egr-1(-/-) mice was delayed, rather than blocked, because indices of cell-cycle progression were restored 72 h after CCl(4) exposure. We concluded that Egr-1 was required for prompt cell-cycle entry (G0- to G1-phase) and G1/S-phase transition after toxic liver injury. These data support the hypothesis that Egr-1 provides hepatoprotection in the CCl(4)-injured liver, attributable, in part, to timely cell-cycle induction and progression.
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