Investigation for iron sensing mechanism via the direct regulation of hepcidin expression by serum ferritin protein

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09446
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Hematology
• Research Institution: Asahikawa Medical College
• Principal Investigator: IKUTA KATSUYA 旭川医科大学, 医学部, 講師 (00396376)
• Co-Investigator(Kenkyū-buntansha): 進藤 基博 旭川医科大学, 医学部, 講師 (10396377) ; 伊藤 巧 旭川医科大学, 大学病院, 特任助教 (80548686) ; 土岐 康通 旭川医科大学, 大学病院, 医員 (90596280)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 鉄代謝 / フェリチン / ヘプシジン / 鉄感知機構

Outline of Final Research Achievements

The present study was performed to determine the possibility that serum ferritin protein which increases in iron overload directly regulate iron regulatory peptide hepcidin produced from hepatocytes. Upregulation of HAMP (hepcidin) gene in human hepatoma-derived HepG2 cells was observed when cells were incubated with human spleen-derived ferritin protein. Because ferritin protein is present as heteropolymer of L- (FTL) and H- (FTH) subunit of ferritin, the influences of each subunit were then determined. The medium incubated with FTL- or FTH-overexpressed HEK293 cells, and FTL or FTH protein purified from transformed E. Coli were used; however, HAMP expression was decreased contrary. The results obtained from this study seemed to be discrepant, but there is a possibility that ferritin might manipulate HAMP expression quite finely utilizing bidirectional effect. This study will be further continued considering iron contents in ferritin, and the ratio of each subunit in heteropolymer.

Free Research Field

鉄代謝