期刊
PEDIATRIC HEMATOLOGY AND ONCOLOGY
卷 24, 期 4, 页码 237-243出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/08880010701360700
关键词
ferritin; hepcidin; hypertransfusion iron overload; iron regulatory proteins; sickle cell disease; beta-thalassemia
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR001271] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL056169, P60HL020985] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R37DK020251, R01DK020251, N01DK092310, R56DK020251, R01DK057778] Funding Source: NIH RePORTER
- NCRR NIH HHS [M01RR01271] Funding Source: Medline
- NHLBI NIH HHS [HL-56169, HL-20985, HL-07951] Funding Source: Medline
- NIDDK NIH HHS [DK-057778, N01-DK-92310, DK-20251] Funding Source: Medline
Hypertransfusional (> 8 transfusions/year) iron in liver biopsies collected immediately after transfusions in beta- thalassemia and sickle cell disease correlated with increased expression ( RNA) for iron regulatory proteins 1 and 2 (3-, 9- to 11-fold) and hepcidin RNA: (5- to 8-fold) ( each p <. 01), while ferritin H and L RNA remained constant. A different H: L ferritin ratio in RNA ( 0.03) and protein ( 0.2-0.6) indicated disease-specific trends and suggests novel post-transcriptional effects. Increased iron regulatory proteins could stabilize the transferrin receptor mRNA and, thereby, iron uptake. Increased hepcidin, after correction of anemia by transfusion, likely reflects excess liver iron. Finally, the absence of a detectable change in ferritin mRNA indicates insufficient oxidative stress to significantly activate MARE/ARE promoters.
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