ArticleJournal of gastroenterology2017
Bone morphogenetic protein-binding endothelial regulator of liver sinusoidal endothelial cells induces iron overload in a fatty liver mouse model.
Article in Journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Restoration of oxidative stress by HNF4α deletion in VWA8-null hepatocytes.Biochemistry and biophysics reports · 2026Article
- Ferroptosis and gut microbiota: A new horizon in alcohol-associated liver disease management.Cellular and molecular life sciences : CMLS · 2025Review
- Differences in DNA methylation of HAMP in blood cells predicts the development of type 2 diabetes.Molecular metabolism · 2023Article
- Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023Review
- The Association between Excess Body Mass and Disturbances in Somatic Mineral Levels.International journal of molecular sciences · 2020Review
- Deletion of the Mitochondrial Protein VWA8 Induces Oxidative Stress and an HNF4α Compensatory Response in Hepatocytes.Biochemistry · 2019Article
- Hepcidin levels correlate to liver iron content, but not steatohepatitis, in non-alcoholic fatty liver disease.BMC gastroenterology · 2018Article
- GFRAL is the receptor for GDF15 and the ligand promotes weight loss in mice and nonhuman primates.Nature medicine · 2017Article
- Vascular Endothelial Regulation of Obesity-Associated Insulin Resistance.Frontiers in cardiovascular medicine · 2017Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is frequently accompanied by iron overload. However, because of the complex hepcidin-regulating molecules, the molecular mechanism underlying iron overload remains unknown. To identify the key molecule involved in NAFLD-associated iron dysregulation, we performed whole-RNA sequencing on the livers of obese mice.
methodsMale C57BL/6 mice were fed a regular or high-fat diet for 16 or 48 weeks. Internal iron was evaluated by plasma iron, ferritin or hepatic iron content. Whole-RNA sequencing was performed by transcriptome analysis using semiconductor high-throughput sequencer. Mouse liver tissues or isolated hepatocytes and sinusoidal endothelial cells were used to assess the expression of iron-regulating molecules.
resultsMice fed a high-fat diet for 16 weeks showed excess iron accumulation. Longer exposure to a high-fat diet increased hepatic fibrosis and intrahepatic iron accumulation. A pathway analysis of the sequencing data showed that several inflammatory pathways, including bone morphogenetic protein (BMP)-SMAD signaling, were significantly affected. Sequencing analysis showed 2314 altered genes, including decreased mRNA expression of the hepcidin-coding gene Hamp. Hepcidin protein expression and SMAD phosphorylation, which induces Hamp, were found to be reduced. The expression of BMP-binding endothelial regulator (BMPER), which inhibits BMP-SMAD signaling by binding BMP extracellularly, was up-regulated in fatty livers. In addition, immunohistochemical and cell isolation analyses showed that BMPER was primarily expressed in the liver sinusoidal endothelial cells (LSECs) rather than hepatocytes.
conclusionsBMPER secretion by LSECs inhibits BMP-SMAD signaling in hepatocytes and further reduces hepcidin protein expression. These intrahepatic molecular interactions suggest a novel molecular basis of iron overload in NAFLD.
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