期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 101, 期 9, 页码 2700-2705出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0306622101
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资金
- NIDDK NIH HHS [R01 DK059429, DK59429, R01 DK056160, DK56160] Funding Source: Medline
Copper is known to play a role in iron recycling from macrophages. To examine whether cellular copper status affects expression of the iron exporter ferroportin-1 (FPN1), J774 macrophage cells were exposed to 10-100 muM CuSO4 for up to 20 h. Copper treatment significantly increased FPN1 mRNA in a close- and time-dependent manner. After 20 h, 100 muM CuSO4 up-regulated FPN1 transcript levels approximate to13-fold compared to untreated controls. Induction was detected 8 h after copper treatment was initiated and markedly increased thereafter. A corresponding increase in FPN1 protein levels was observed upon copper treatment. Induction of J774 cell FPN1 expression by copper was also associated with a dose-dependent increase in Fe-59 release after erythrophagocytosis of labeled red blood cells. Thus, a previously uncharacterized role for copper in the regulation of macrophage iron recycling is suggested by the induction of FPN1 gene expression and iron efflux by this metal.
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