Open AccessFLT3/FLK‐2 (STK‐1) Ligand Does Not Stimulate Human Megakaryopoiesis In Vitro
Author(s) -
Ratajczak Mariusz Z.,
Ratajczak Janina,
Ford John,
Kregenow Robert,
Marlicz Wojtek,
Gewirtz Alan M.
Publication year - 1996
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.140146
Subject(s) - biology , megakaryocyte , in vitro , microbiology and biotechnology , receptor , growth factor , recombinant dna , haematopoiesis , immunology , stem cell , genetics , gene
It has not yet been determined if the FLT3/FLK‐2 or STK‐1 Ligand (STK‐1 L)/FLT3/FLK‐2 or STK‐1 receptor (STK‐1R) axis has the ability to regulate human megakaryopoiesis in vitro. To address this question, we exposed normal human CD34 + marrow mononuclear cells to recombinant human STK‐1L alone, or in combination with other growth factors. Colony‐forming unit‐megakaryocytic/thrombocytes (CFU‐Meg) and BFU‐E‐derived colonies were then enumerated, and effects on colony size and maturation noted. As assessed by these parameters, STK‐1L had no demonstrable effect on megakaryocyte colony formation. Similarly, suppressing STK‐1R expression with oligodeoxynucleotides also had no influence on CFU‐Meg‐derived colony formation. To begin to derive a physiologic explanation for these findings, we examined freshly isolated normal human megakaryocytes for the presence of STK‐1L and STK‐1R mRNA. In contrast to a growing number of growth factors and growth factor receptors which appear to be expressed by megakaryocytes, normal mature human megakaryocytes express neither STK‐1R or STK‐1L mRNA. Accordingly, our results led us to hypothesize that if STK‐1/ STK‐1L have any effects on megakaryocyte development in vitro, they are likely subtle and of uncertain physiologic significance.