Hemin-induced erythroid differentiation changes the sensitivity of K562 cells to tumor necrosis factor-α

X. F. Li, J. Anderson, D. Hutzler, G. David Roodman

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Tumor necrosis factor-α (TNF) can inhibit the growth of erythroid progenitors (erythroid colony-forming units [CFU-E] and erythroid burst-forming units [BFU-E]) at picomolar concentrations, but only if added within the first 48 h of culture. These data suggested that cells undergoing erythroid differentiation become resistant to TNF. To test this hypothesis, K562 cells were treated with hemin to induce erythroid differentiation and then tested for their sensitivity to TNF in terms of growth and TNF receptor expression. TNF inhibited the growth of untreated K562 cells, but not hemin-treated K562 cells. Untreated K562 cells expressed TNF receptors, whereas few hemin-treated K562 cells expressed TNF receptors within 23 h of exposure to hemin. These data show that K562 cells induced to differentiate along the erythroid pathway are resistant to TNF because they lack TNF receptors and suggest that the resistance of erythropoietin-treated human bone marrow cells to TNF added after 48 h of culture may also reflect loss of TNF receptors associated with erythroid differentiation.

Original languageEnglish (US)
Pages (from-to)1059-1062
Number of pages4
JournalExperimental Hematology
Volume17
Issue number11
StatePublished - 1989
Externally publishedYes

Fingerprint

Hemin
K562 Cells
Tumor Necrosis Factor Receptors
Erythroid Precursor Cells
Tumor Necrosis Factor-alpha
Growth
Erythroid Cells
Erythropoietin
Bone Marrow Cells

Keywords

  • erythroid differentiation
  • K562
  • receptors
  • TNF

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Genetics
  • Hematology
  • Oncology
  • Transplantation

Cite this

Hemin-induced erythroid differentiation changes the sensitivity of K562 cells to tumor necrosis factor-α. / Li, X. F.; Anderson, J.; Hutzler, D.; Roodman, G. David.

In: Experimental Hematology, Vol. 17, No. 11, 1989, p. 1059-1062.

Research output: Contribution to journalArticle

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