Abstract
Haem is a structural component of numerous cellular proteins which contributes significantly to iron metabolic processes in mammals but its toxicity demands that cellular levels must be tightly regulated. Breast Cancer Resistance Protein (BCRP/ABCG2), an ATP Binding Cassette G-member protein has been shown to possess porphyrin/haem efflux function. The current study evaluated the expression and regulation of Abcg2 mRNA and protein levels in mouse tissues involved in erythropoiesis. Abcg2 mRNA expression was enhanced in bone marrow hemopoietic progenitor cells from mice that were treated with phenylhydrazine (PHZ). Abcg2 mRNA expression was increased particularly in the extramedullary haematopoietic tissues from all the mice models with enhanced erythropoiesis. Haem oxygenase (ho1) levels tended to increase in the liver of mice with enhanced erythropoiesis and gene expression patterns differed from those observed in the spleen. Efflux of haem biosynthetic metabolites might be dependent on the relative abundance of Abcg2 or ho1 during erythropoiesis. Abcg2 appears to act principally as a safety valve regulating porphyrin levels during the early stages of erythropoiesis and its role in systemic haem metabolism and erythrophagocytosis, in particular, awaits further clarification.
Highlights
Iron turnover in mammals is largely explained by the production and breakdown of erythrocytes
This study investigates the expression and regulation of abcg2 and ho1 in tissues of mice with enhanced erythropoiesis
Abcg2 and tfr1 mRNA expression were enhanced in bone marrow cells from mice treated with PHZ (Figure 1)
Summary
Iron turnover in mammals is largely explained by the production (biosynthesis) and breakdown (biodegradation) of erythrocytes. Abcg is a half ATPBinding Cassette (ABC) G-member transporter with a nucleotide binding domain (NBD) at its amino terminus and a transmembrane domain at its carboxyl end (Krishnamurthy and Schuetz, 2006). It functions conventionally as a plasma membrane protein extruding endogenous and exogenous toxic xenobiotics from the intestine, liver, placenta, and the blood/brain barrier. This transporter, in some instances, confers resistance to anticancer drugs
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