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Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus

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Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus. / Li, Lin; Hölscher, Christian; Chen, Bing-Bing et al.

In: Biological Trace Element Research, Vol. 143, No. 3, 12.2011, p. 1581-1593.

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Li L, Hölscher C, Chen B-B, Zhang Z-F, Liu Y-Z. Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus. Biological Trace Element Research. 2011 Dec;143(3):1581-1593. doi: 10.1007/s12011-011-8967-3

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@article{1af4dd571e9f4fa8ae69f128d3a4cd8d,
title = "Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus",
abstract = "Elevated iron levels are considered to play a role in the neurodegenerative mechanisms that underlie Alzheimer's and Parkinson's disease. The linkage between hepcidin (Hepc) and ferroportin-1 (FPN1), the divalent metal transporter 1 (DMT1), and ceruloplasmin (CP) in the brain is unknown. To discern the role of Hepc in regulating the expression of these proteins, we investigated FPN1, DMT1, and CP protein and mRNA expression in the brain after the intracerebroventricular injection of Hepc. Our results show that after Hepc injection, expression of FPN1 mRNA and FPN1 protein was inhibited in the cerebral cortex and hippocampus. Furthermore, we showed a clear change of DMT1 and CP protein and mRNA levels in the brain. The immunohistochemical analysis revealed an increase of DMT1 and a decrease of CP levels. Semi-quantitative analysis using PCR methods showed an increase of DMT1(+IRE) mRNA, and a decrease of DMT1(-IRE) mRNA and CP mRNA levels. Since alterations in iron levels in the brain are causally linked to degenerative conditions such as Alzheimer's disease, an improved understanding of the regulation of iron transport protein expression such as FPN1, DMT1, and CP could lead to novel strategies for treatments.",
keywords = "Animals, Antimicrobial Cationic Peptides, Base Sequence, Cation Transport Proteins, Cerebral Cortex, Ceruloplasmin, DNA Primers, Hepcidins, Hippocampus, Immunohistochemistry, Male, Polymerase Chain Reaction, RNA, Messenger, Rats, Rats, Wistar",
author = "Lin Li and Christian H{\"o}lscher and Bing-Bing Chen and Zhi-Feng Zhang and Yue-Ze Liu",
year = "2011",
month = dec,
doi = "10.1007/s12011-011-8967-3",
language = "English",
volume = "143",
pages = "1581--1593",
journal = "Biological Trace Element Research",
issn = "0163-4984",
publisher = "Humana Press",
number = "3",

}

RIS

TY - JOUR

T1 - Hepcidin treatment modulates the expression of divalent metal transporter-1, ceruloplasmin, and ferroportin-1 in the rat cerebral cortex and hippocampus

AU - Li, Lin

AU - Hölscher, Christian

AU - Chen, Bing-Bing

AU - Zhang, Zhi-Feng

AU - Liu, Yue-Ze

PY - 2011/12

Y1 - 2011/12

N2 - Elevated iron levels are considered to play a role in the neurodegenerative mechanisms that underlie Alzheimer's and Parkinson's disease. The linkage between hepcidin (Hepc) and ferroportin-1 (FPN1), the divalent metal transporter 1 (DMT1), and ceruloplasmin (CP) in the brain is unknown. To discern the role of Hepc in regulating the expression of these proteins, we investigated FPN1, DMT1, and CP protein and mRNA expression in the brain after the intracerebroventricular injection of Hepc. Our results show that after Hepc injection, expression of FPN1 mRNA and FPN1 protein was inhibited in the cerebral cortex and hippocampus. Furthermore, we showed a clear change of DMT1 and CP protein and mRNA levels in the brain. The immunohistochemical analysis revealed an increase of DMT1 and a decrease of CP levels. Semi-quantitative analysis using PCR methods showed an increase of DMT1(+IRE) mRNA, and a decrease of DMT1(-IRE) mRNA and CP mRNA levels. Since alterations in iron levels in the brain are causally linked to degenerative conditions such as Alzheimer's disease, an improved understanding of the regulation of iron transport protein expression such as FPN1, DMT1, and CP could lead to novel strategies for treatments.

AB - Elevated iron levels are considered to play a role in the neurodegenerative mechanisms that underlie Alzheimer's and Parkinson's disease. The linkage between hepcidin (Hepc) and ferroportin-1 (FPN1), the divalent metal transporter 1 (DMT1), and ceruloplasmin (CP) in the brain is unknown. To discern the role of Hepc in regulating the expression of these proteins, we investigated FPN1, DMT1, and CP protein and mRNA expression in the brain after the intracerebroventricular injection of Hepc. Our results show that after Hepc injection, expression of FPN1 mRNA and FPN1 protein was inhibited in the cerebral cortex and hippocampus. Furthermore, we showed a clear change of DMT1 and CP protein and mRNA levels in the brain. The immunohistochemical analysis revealed an increase of DMT1 and a decrease of CP levels. Semi-quantitative analysis using PCR methods showed an increase of DMT1(+IRE) mRNA, and a decrease of DMT1(-IRE) mRNA and CP mRNA levels. Since alterations in iron levels in the brain are causally linked to degenerative conditions such as Alzheimer's disease, an improved understanding of the regulation of iron transport protein expression such as FPN1, DMT1, and CP could lead to novel strategies for treatments.

KW - Animals

KW - Antimicrobial Cationic Peptides

KW - Base Sequence

KW - Cation Transport Proteins

KW - Cerebral Cortex

KW - Ceruloplasmin

KW - DNA Primers

KW - Hepcidins

KW - Hippocampus

KW - Immunohistochemistry

KW - Male

KW - Polymerase Chain Reaction

KW - RNA, Messenger

KW - Rats

KW - Rats, Wistar

U2 - 10.1007/s12011-011-8967-3

DO - 10.1007/s12011-011-8967-3

M3 - Journal article

C2 - 21274654

VL - 143

SP - 1581

EP - 1593

JO - Biological Trace Element Research

JF - Biological Trace Element Research

SN - 0163-4984

IS - 3

ER -