title: Serum hepcidin-20 is elevated during the acute phase of myocardial infarction.
abstract: Hepcidin, a key iron-regulator secreted from the liver, consists of 25 amino acids (hepcidin-25), blocks iron release from macrophages via internalization and degradation of cellular iron exporter ferroportin, and restrains the use of iron in organs. Hepcidin mRNA and protein are also expressed in the human heart. A short form of hepcidin that lacks 5 amino-acid residues in the N-terminus (hepcidin-20) has been found in human serum, although its physiological role is unknown. Here, we successfully measured the serum levels of hepcidin-25 and hepcidin-20 in 12 patients with acute myocardial infarction (AMI) using surface-enhanced laser desorption ionization time of flight mass spectrometry. Among the selected 10 patients, whose blood samples were taken within 4 hours after a heart attack, all the patients showed elevated serum levels of hepcidin-20 [between 31.7 and 285.1 arbitrary unit (AU); normal level < 9.3 AU], while 8 patients showed high levels of hepcidin-25 (9.3-271.4; normal < 25.5 AU). The hepcidin-20 level was decreased to nearly the normal level on day 7 (range of 2.9 to 12.5 AU) in the 12 patients, whereas the hepcidin-25 level remained high on day 7 in 8 patients. Furthermore, the elevated levels of hepcidin-25 and hepcidin-20 were not correlated with the serum levels of markers for inflammation, interleukin-6 and C-reactive protein, in the patients with AMI. In conclusion, the serum hepcidin-20 is transiently elevated in response to acute cardiac ischemia. Measurement of serum hepcidin-20, rather than hepcidin-25, is helpful for diagnosis of acute myocardial infarction.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Suzuki
authors.forename: Ken
authors.initials: K
authors.lastname: Toba
authors.forename: Kiminori
authors.initials: K
authors.lastname: Kato
authors.forename: Takuya
authors.initials: T
authors.lastname: Ozawa
authors.forename: Naohisa
authors.initials: N
authors.lastname: Tomosugi
authors.forename: Masato
authors.initials: M
authors.lastname: Higuchi
authors.forename: Taro
authors.initials: T
authors.lastname: Kusuyama
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Iso
authors.forename: Naohiko
authors.initials: N
authors.lastname: Kobayashi
authors.forename: Sin-ichiro
authors.initials: S
authors.lastname: Yokoyama
authors.forename: Noboru
authors.initials: N
authors.lastname: Fukuda
authors.forename: Hideki
authors.initials: H
authors.lastname: Saitoh
authors.forename: Kohei
authors.initials: K
authors.lastname: Akazawa
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000595:Amino Acid Sequence; D023181:Antimicrobial Cationic Peptides / Q000097:blood* / Q000737:chemistry; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D004921:Erythropoietin / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D064451:Hepcidins; D006801:Humans; D007249:Inflammation / Q000097:blood; D007328:Insulin / Q000737:chemistry; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D009203:Myocardial Infarction / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood* / Q000737:chemistry; D017386:Sequence Homology, Amino Acid; D013997:Time Factors
chemical_list: D023181:Antimicrobial Cationic Peptides; D015415:Biomarkers; C578702:HAMP protein, human; D064451:Hepcidins; D007328:Insulin; D015850:Interleukin-6; D010446:Peptide Fragments; C542573:hepcidin (6-25), human; D004921:Erythropoietin; D002097:C-Reactive Protein; D003402:Creatine Kinase