
Transferrin Receptor Expression in Normal, Iron‐deficient and Iron‐overloaded Rats
Author(s) -
Lu Jianping,
Hayashi Keiki,
Awai Michiyasu
Publication year - 1989
Publication title -
acta patholigica japonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
ISSN - 0001-6632
DOI - 10.1111/j.1440-1827.1989.tb02427.x
Subject(s) - red pulp , spleen , endocrinology , transferrin receptor , medicine , duodenum , chemistry , transferrin , kidney , iron deficiency , hemoglobin , total iron binding capacity , serum iron , biology , anemia
The distribution of transferrin receptor (TfR) positive cells and their staining intensity were examined in the liver, duodenum, pancreas, spleen, kidney and brain of iron deficient, iron‐overloaded and normal Wistar rats to elucidate the regulatory effects of iron on TfR expression in vivo. Iron deficiency was produced by an iron deficient food and water regimen, and iron overload by repeated intraperitoneal injections of ferric nitrilotriacetate (Fe 3 ‐NTA) for 12 weeks. In iron deficient rats, levels of hemoglobin (Hb= 5.9 ± 0.7) and serum iron (Sl = 29.9 ± 4.4) were lower, and total iron binding capacity (TIBC = 624.4 ± 72.7) was higher than in normal rats (Hb = 15.6 ± 0.9, Sl = 206.5 # 20.5, TIBC = 416.0 ± 56.0), and Wee versa for SI (217.7 ± 15.5) and TIBC (307.1 ± M45.4) in iron‐overloaded rats. In normal rats, TfR positive granules were observed in hepatocytes and Kupffer cells of the liver, absorptive epithelium of the duodenum, acinar and Langerhans islet cells of the pancreas, macrophages and red pulp erythro‐blasts of the spleen, and distal convoluted tubular epithelium of the kidney. Although the tissue distribution pattern of TfR positive cells was similar in normal, iron deficient and iron overloaded rats, the staining intensity and number of TfR positive cells were obviously higher in iron deficient, and lower in iron overloaded rats. We conclude that TfR expression is negatively regulated by the tissue concentration of iron. Acta Pathol Jpn 39: 759‐764, 1989.