Erythrocytic ferroportin reduces intracellular iron accumulation, hemolysis, and malaria risk-Reference-Cited by-同舟云学术

Erythrocytic ferroportin reduces intracellular iron accumulation, hemolysis, and malaria risk

Published:2018-03-30 Issue:6383 Volume:359 Page:1520-1523
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Zhang De-Liang¹^ORCID,Wu Jian²^ORCID,Shah Binal N.³,Greutélaers Katja C.⁴,Ghosh Manik C.¹,Ollivierre Hayden¹,Su Xin-zhuan²^ORCID,Thuma Philip E.⁵^ORCID,Bedu-Addo George⁶,Mockenhaupt Frank P.⁴^ORCID,Gordeuk Victor R.³^ORCID,Rouault Tracey A.¹^ORCID

Affiliation:

1. Section on Human Iron Metabolism, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.

2. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

3. Sickle Cell Center, University of Illinois at Chicago, Chicago, IL 60612, USA.

4. Charité–Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Tropical Medicine and International Health, Berlin 13353, Germany.

5. Malaria Research Trust, Choma 630166, Zambia.

6. Komfo Anokye Teaching Hospital, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana.

Abstract

Iron's grip on malaria Malaria parasites have coevolved with their human and mammalian hosts. These Plasmodium species invade the iron-rich environment of red blood cells. Zhang et al. found that the iron transporter ferroportin persists on the surface of mature mammalian red blood cells. Red blood cells are at risk of oxidative damage if their hemoglobin releases its iron; ferroportin is thus important to expel this iron. The authors also found that the transporter can deprive malaria parasites of the iron they need for proliferation. The Q248H mutation in the human ferroportin gene enhances ferroportin expression during development and seems to provide protection against malaria. This effect may explain the enrichment of the Q248H mutation among African populations. Science , this issue p. 1520

Funder

National Institute of Allergy and Infectious Diseases

The intramural program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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