Abe Y, Muta K, Nishimura J, Nawata H
Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Am J Hematol. 1992 Aug;40(4):270-5. doi: 10.1002/ajh.2830400406.
We investigated the regulatory mechanism of human erythroblast transferrin receptors (Tf.R) under conditions of iron deprivation and iron loading. Treatment of erythroblasts with an iron chelator, desferrioxamine, induced an increase in surface Tf.R number associated with an elevation of biosynthetic rate and the mRNA level of Tf.R. Reduced cellular iron pool increased the Tf.R number by altering the level of mRNA, as in nonhemoglobin-producing cells. Although treatment of erythroblasts with hemin induced a decrease in the biosynthetic rate and in the level of mRNA, the number of surface Tf.R did not decrease. This phenomenon may explain the fact that a high level of serum iron has no influence on the surface Tf.R number in vivo, as we reported previously. We suggest the existence of a regulatory mechanism specific for hemoglobin-producing cells that keeps surface Tf.R expression constant despite iron loading.
我们研究了人成红细胞转铁蛋白受体（Tf.R）在缺铁和铁负荷条件下的调节机制。用铁螯合剂去铁胺处理成红细胞，可诱导表面Tf.R数量增加，这与Tf.R生物合成速率和mRNA水平的升高有关。细胞内铁池减少通过改变mRNA水平增加了Tf.R数量，这与不产生血红蛋白的细胞情况相同。尽管用血红素处理成红细胞会导致生物合成速率和mRNA水平下降，但表面Tf.R的数量并未减少。这一现象可能解释了我们之前报道的高血清铁水平在体内对表面Tf.R数量没有影响这一事实。我们认为存在一种对产生血红蛋白的细胞特异的调节机制，尽管有铁负荷，该机制仍能使表面Tf.R表达保持恒定。
