ArticleCellular and molecular gastroenterology and hepatology2019
Myeloid Cell-Derived HB-EGF Drives Tissue Recovery After Pancreatitis.
Article in Cellular and molecular gastroenterology and hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting CCR1 Remodels the Tumor Microenvironment and Relieves Immunosuppression in Pancreatic Cancer.Cancer immunology research · 2026Article
- Longitudinal single-cell multiomic atlas of high-risk neuroblastoma reveals chemotherapy-induced tumor microenvironment rewiring.Nature genetics · 2025Article
- Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.Developmental cell · 2025Article
- FRA1 controls acinar cell plasticity during murine KrasDevelopmental cell · 2024Article
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- Acinar to β-like cell conversion through inhibition of focal adhesion kinase.Nature communications · 2024Article
- Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.bioRxiv : the preprint server for biology · 2024Article
- Neutrophils facilitate the epicardial regenerative response after zebrafish heart injury.Developmental biology · 2024Article
- The CA125 level postoperative change rule and its prognostic significance in patients with resectable pancreatic cancer.BMC cancer · 2023Article
- Article
- Myeloid- and Epithelial-derived Heparin-Binding Epidermal Growth Factor-like Growth Factor Promotes Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- ADAM17-mediated EGFR ligand shedding directs macrophage-promoted cancer cell invasion.JCI insight · 2022Article
- Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer.PLoS genetics · 2022Article
- Mitochondrial bioenergetics boost macrophage activation, promoting liver regeneration in metabolically compromised animals.Hepatology (Baltimore, Md.) · 2022Article
- Progranulin mediates immune evasion of pancreatic ductal adenocarcinoma through regulation of MHCI expression.Nature communications · 2022Article
- Extrinsic KRAS Signaling Shapes the Pancreatic Microenvironment Through Fibroblast Reprogramming.Cellular and molecular gastroenterology and hepatology · 2022Article
- M2 macrophages have unique transcriptomes but conditioned media does not promote profibrotic responses in lung fibroblasts or alveolar epithelial cells in vitro.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Serum Amphiregulin and Heparin-Binding Epidermal Growth Factor as Biomarkers in Patients with Idiopathic Inflammatory Myopathy.Journal of clinical medicine · 2021Article
- The Gustatory Sensory G-Protein GNAT3 Suppresses Pancreatic Cancer Progression in Mice.Cellular and molecular gastroenterology and hepatology · 2021Article
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Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsPancreatitis is a major cause of morbidity and mortality and is a risk factor for pancreatic tumorigenesis. Upon tissue damage, an inflammatory response, made up largely of macrophages, provides multiple growth factors that promote repair. Here, we examine the molecular pathways initiated by macrophages to promote pancreas recovery from pancreatitis.
methodsTo induce organ damage, mice were subjected to cerulein-induced experimental pancreatitis and analyzed at various times of recovery. CD11b-DTR mice were used to deplete myeloid cells. Hbegf
resultsMacrophages infiltrating the pancreas in experimental pancreatitis make high levels of HB-EGF. Both depletion of myeloid cells and ablation of myeloid cell HB-EGF delayed recovery from experimental pancreatitis, resulting from a decrease in cell proliferation and an increase in apoptosis. Mechanistically, ablation of myeloid cell HB-EGF impaired epithelial cell DNA repair, ultimately leading to cell death. Soluble HB-EGF induced EGFR nuclear translocation and methylation of histone H4, facilitating resolution of DNA damage in pancreatic acinar cells in vitro. Consistent with its role as the primary receptor of HB-EGF, in vivo ablation of EGFR from pancreatic epithelium during recovery from pancreatitis resulted in accumulation of DNA damage.
conclusionsBy using novel conditional knockout mouse models, we determined that HB-EGF derived exclusively from myeloid cells induces epithelial cell proliferation and EGFR-dependent DNA repair, facilitating pancreas healing after injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.