Levels of EPOR Protein and Gene Expression of SLC11A2, SLC40A1 in Children with Iron Deficiency Anemia

Abstract

Iron has many different roles in the body. About 65 to 80 percent of the body’s iron is in the blood in the form of hemoglobin. Hemoglobin is a protein in red blood cells that transports oxygen to tissues in the body. If iron is lacking in the diet, iron reserves in the body are used. Once this supply is depleted the formation of hemoglobin is affected. This means the red blood cells cannot carry oxygen needed by the cells. When this happens, iron deficiency occurs and anemia results. The Solute Carrier Family 11 Member 2 (SLC11A2) and Solute Carrier Family 40Member 1 (SLC40A1)gene plays a crucial role in iron metabolism and homeostasis in the body, The erythropoietin receptor (EPOR) gene plays a crucial role in erythropoiesis and iron metabolism, with its protein product playing a central role in erythroid cell survival and proliferation.

The study included 50 children with iron deficiency anemia and healthy control group of 30 children for comparison analysis and measuring the expression levels of certain genes. The methods included collecting of blood samples from male and female children aged (eleven months to nine years), all diagnosed with iron deficiency anemia and free from chronic conditions. The diagnosis of iron deficiency anemia was verified with a complete blood count (CBC) and an iron assay for each sample.

The studies of gene expression of SLC11A2 and SLC40A1 in IDA children and healthy children observed significant increase of gene (SLC11A2) expression and non-significant decrease of gene (SLC40A1). Study showed significant negative correlation between SLC11A2 and SLC40A1gene expression. Observed increase in EPOR level in IDA children when compared with healthy children but this increasing was non-significant. The concluding SLC11A2 gene expression elevates in iron deficiency anemia to increase intestinal iron absorption, while SLC40A1 gene expression diminishes in correlation with the severity of iron deficiency to keep cellular iron levels. Also we conclude that the EPOR level rises in response to iron insufficiency, with the increase being proportionate to the extent of iron reduction to prevent the formation of deformed red blood cells.