Erythropoietin production by macrophages from preterm infants: implications regarding the cause of the anemia of prematurity

Pediatr Res. 1994 Feb;35(2):169-70. doi: 10.1203/00006450-199402000-00008.

Abstract

In the human fetus, liver macrophages appear to be the primary source of erythropoietin (Epo). Epo production shifts from the liver to peritubular cells in the kidney sometime during the 3rd trimester. Some preterm infants experience a hyporegenerative anemia that appears to be caused by inadequate Epo production. It is not clear whether this anemia is due to deficient Epo production by liver macrophages or renal peritubular cells. To assess this situation, we measured Epo mRNA and protein in macrophages obtained from cord blood of preterm and term infants and from peripheral blood of adults. Macrophages from preterm infants generated Epo mRNA and protein as effectively as those from term infants and adults. It appears that the anemia of prematurity is not due to defective Epo production by macrophages.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Anemia, Neonatal / blood
  • Anemia, Neonatal / etiology*
  • Anemia, Neonatal / genetics
  • Erythropoietin / biosynthesis*
  • Erythropoietin / blood
  • Erythropoietin / genetics
  • Fetal Blood / cytology
  • Fetal Blood / metabolism
  • Humans
  • In Vitro Techniques
  • Infant, Newborn
  • Infant, Premature
  • Macrophages / metabolism*
  • RNA, Messenger / blood
  • RNA, Messenger / genetics

Substances

  • RNA, Messenger
  • Erythropoietin