The iron regulatory hormone hepcidin reduces ferroportin 1 contentand iron release in H9C2 cardiomyo.pdf
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The iron regulatory hormone hepcidin reduces ferroportin 1 contentand iron release in H9C2 cardiomyo
Available online at
istry 20 (2009) 860–865Journal of Nutritional BiochemThe iron regulatory hormone hepcidin reduces ferroportin 1 content
and iron release in H9C2 cardiomyocytes
Xiao Hu Gea, Qin Wanga, Zhong Ming Qiana,c,?, Li Zhua,c, Fang Dub, Wing Ho Yungb,
Lei Yangb, Ya Keb,?
aNational Key Laboratory of Chinese Medicine and Molecular Pharmacology (Shenzhen) and Laboratory of Brain Iron Metabolism,
Department of Applied Biology and Chemical Technology, Hong Kong Polytechnic University, Hong Kong
bDepartment of Physiology, The Chinese University of Hong Kong, Faculty of Medicine, NT, Shatin, Hong Kong
cDepartment of Neurobiology and Neurobiochemistry and Jiangsu Key Laboratory of Neuroregeneration, Nantong University,
Nantong 226001, Peoples Republic of China
Received 19 March 2008; received in revised form 23 June 2008; accepted 31 July 2008Abstract
Iron plays a key pathophysiological role in a number of cardiac diseases. Studies on the mechanisms of heart iron homeostasis are
therefore crucial for understanding the causes of excessive heart iron. In addition to iron uptake, cellular iron balance in the heart also
depends on iron export. We provided evidence for the existence of iron exporter ferroportin 1 (Fpn1) in the heart in a recent study. The
presence of hepcidin, a recently discovered iron regulatory hormone, was also confirmed in the heart recently. Based on these findings and
the inhibiting role of hepcidin on Fpn1 in other tissues, we speculated that hepcidin might be able to bind with, internalize and degrade Fpn1
and then decrease iron export in heart cells, leading to an abnormal increase in heart iron and iron mediated cell injury. We therefore
investigated the effects of hepcidin on the contents of Fpn1 and iron release in H9C2 cardiomyocyte cell line. We demonstrated that hepcidin
has the ability to reduce Fpn1 content as well as iron release in this cell. The similar regulation patterns of hepcidin on the Fpn1 and iron
release suggested that th
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