ArticleInflammation2012
Downregulation of ferroportin 1 expression in hFOB1.19 osteoblasts by hepcidin.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Reducing iron accumulation: A potential approach for the prevention and treatment of postmenopausal osteoporosis.Experimental and therapeutic medicine · 2015Article
- Effects of mouse hepcidin 1 treatment on osteoclast differentiation and intracellular iron concentration.Inflammation · 2015Article
- Iron regulates the expression of ferroportin 1 in the cultured hFOB 1.19 osteoblast cell line.Experimental and therapeutic medicine · 2014Article
- Iron homeostasis in osteoporosis and its clinical implications.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to address the relationship between iron homeostasis and bone metabolism. Cultured hFOB 1.19 osteoblasts were incubated with selected concentrations of hepcidin (50, 100, and 200 nmol/L) for 20 h, harvested for extraction of total RNA and proteins, and the expression of ferroportin 1 was analyzed by RT-PCR and western blotting. The results showed the presence of ferroportin 1 expression in cultured hFOB 1.19 cells. Furthermore, the ferroportin 1 had a similar expression pattern in hFOB cells as in hepatocytes and enterocytes and was downregulated by hepcidin. Our data indicate that osteoblasts are target cells for hepcidin, suggest that hepcidin may have many more targets than previously recognized, and support the role of hepcidin in the development of osteoporosis.
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Registered trials
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