The Hepcidin/Ferroportin axis modulates proliferation of pulmonary artery smooth muscle cells.

Scientific Reports
Latha RamakrishnanGregory J Quinlan

Abstract

Studies were undertaken to examine any role for the hepcidin/ferroportin axis in proliferative responses of human pulmonary artery smooth muscle cells (hPASMCs). Entirely novel findings have demonstrated the presence of ferroportin in hPASMCs. Hepcidin treatment caused increased proliferation of these cells most likely by binding ferroportin resulting in internalisation and cellular iron retention. Cellular iron content increased with hepcidin treatment. Stabilisation of ferroportin expression and activity via intervention with the therapeutic monoclonal antibody LY2928057 reversed proliferation and cellular iron accumulation. Additionally, IL-6 treatment was found to enhance proliferation and iron accumulation in hPASMCs; intervention with LY2928057 prevented this response. IL-6 was also found to increase hepcidin transcription and release from hPASMCs suggesting a potential autocrine response. Hepcidin or IL-6 mediated iron accumulation contributes to proliferation in hPASMCs; ferroportin mediated cellular iron excretion limits proliferation. Haemoglobin also caused proliferation of hPASMCs; in other novel findings, CD163, the haemoglobin/haptoglobin receptor, was found on these cells and offers a means for cellular uptake of...Continue Reading

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Citations

Jun 4, 2019·Proceedings of the National Academy of Sciences of the United States of America·Samira Lakhal-LittletonPeter A Robbins
Feb 11, 2020·Internal and Emergency Medicine·Thomas SonnweberGünter Weiss
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Jul 1, 2021·Clinical Kidney Journal·Lucia Del VecchioUNKNOWN ERA-EDTA European Renal and Cardiovascular Medicine Working (EURECA-m) Group

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Methods Mentioned

BETA
ELISA
confocal microscopy
Assay
FCS
PCR
protein assay

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