ArticleJournal of cellular and molecular medicine2018
Lipopolysaccharide enhances TGF-β1 signalling pathway and rat pancreatic fibrosis.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 61 citations in OpenAlex.
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- Mechanistic insights into pancreatic cancer progression from circadian rhythm disruption and gut microbiota dysbiosis (Review).International journal of molecular medicine · 2026Review
- Proof-of-concept study: APOE4 brain endothelial cells as a phenotypic compound screen.Alzheimer's research & therapy · 2026Article
- The Novel Soluble Guanylate Cyclase Stimulator Attenuates Acute Lung Injury via Inhibiting Pericyte Phenotypic Transition.International journal of molecular sciences · 2026Article
- Prenatal exposure to polystyrene nanoparticles induces neuroimmune dysregulation in the adult mouse brain.Zoological research · 2025Article
- Review
- Intelligent berberine-loaded erythrocytes attenuated inflammatory cytokine productions in macrophages.Scientific reports · 2024Article
- Pancreatitis affects gut microbiota via metabolites and inflammatory cytokines: an exploratory two-step Mendelian randomisation study.Molecular genetics and genomics : MGG · 2024Article
- Zinc-nanoparticles alleviate the ovarian damage induced by bacterial lipopolysaccharide (LPS) in pregnant rats and their fetuses.Histochemistry and cell biology · 2023Article
- Pancreatic Stellate Cells and the Targeted Therapeutic Strategies in Chronic Pancreatitis.Molecules (Basel, Switzerland) · 2023Review
- Lobeglitazone inhibits LPS-induced NLRP3 inflammasome activation and inflammation in the liver.PloS one · 2023Article
- Evogliptin Directly Inhibits Inflammatory and Fibrotic Signaling in Isolated Liver Cells.International journal of molecular sciences · 2022Article
- Overexpressing HPGDS in adipose-derived mesenchymal stem cells reduces inflammatory state and improves wound healing in type 2 diabetic mice.Stem cell research & therapy · 2022Article
- Article
- Vitamin D: A Potential Star for Treating Chronic Pancreatitis.Frontiers in pharmacology · 2022Review
- Pancreatic stellate cells - rising stars in pancreatic pathologies.Physiological research · 2021Review
- Microbiota in Pancreatic Diseases: A Review of the Literature.Journal of clinical medicine · 2021Review
- High Mobility Group Box 1 (HMGB1) Induces Toll-Like Receptor 4-Mediated Production of the Immunosuppressive Protein Galectin-9 in Human Cancer Cells.Frontiers in immunology · 2021Article
- Update on Pharmacological Activities, Security, and Pharmacokinetics of Rhein.Evidence-based complementary and alternative medicine : eCAM · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic stellate cells (PSCs) play a critical role in fibrogenesis during alcoholic chronic pancreatitis (ACP). Transforming growth factor-beta1 (TGF-β1) is a key regulator of extracellular matrix production and PSC activation. Endotoxin lipopolysaccharide (LPS) has been recognized as a trigger factor in the pathogenesis of ACP. This study aimed to investigate the mechanisms by which LPS modulates TGF-β1 signalling and pancreatic fibrosis. Sprague-Dawley rats fed with a Lieber-DeCarli alcohol (ALC) liquid diet for 10 weeks with or without LPS challenge during the last 3 weeks. In vitro studies were performed using rat macrophages (Mφs) and PSCs (RP-2 cell line). The results showed that repeated LPS challenge resulted in significantly more collagen production and PSC activation compared to rats fed with ALC alone. LPS administration caused overexpression of pancreatic TLR4 or TGF-β1 which was paralleled by an increased number of TLR4-positive or TGF-β1-positive Mφs or PSCs in ALC-fed rats. In vitro, TLR4 or TGF-β1 production in Mφs or RP-2 cells was up-regulated by LPS. LPS alone or in combination with TGF-β1 significantly increased type I collagen and α-SMA production and Smad2 and 3 phosphorylation in serum-starved RP-2 cells. TGF-β pseudoreceptor BAMBI production was repressed by LPS, which was antagonized by Si-TLR4 RNA or by inhibitors of MyD88/NF-kB. Additionally, knockdown of Bambi with Si-Bambi RNA significantly increased TGF-β1 signalling in RP-2 cells. These findings indicate that LPS increases TGF-β1 production through paracrine and autocrine mechanisms and that LPS enhances TGF-β1 signalling in PSCs by repressing BAMBI via TLR4/MyD88/NF-kB activation.
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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.