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Carboxy‐terminal peptides (C1–24 and C13–24 but not C1–13) of platelet factor 4 inhibit murine megakaryocytopoiesis, an activity which is neutralized by heparin
Author(s) -
Lebeurier Isabelle,
Basara Nada,
Aïdoudi Sallouha,
Amiral Jean,
Caen Jacques,
Chao Han Zhong
Publication year - 1996
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1996.296828.x
Subject(s) - megakaryocytopoiesis , platelet factor 4 , megakaryocyte , platelet , in vivo , heparin , in vitro , chemistry , microbiology and biotechnology , biology , haematopoiesis , biochemistry , immunology , stem cell
Negative regulation of megakaryocytopoiesis is a complex process involving various cytokines. One of these cytokines is platelet factor 4 (PF4), a megakaryocyte/platelet specific protein. PF4 and a carboxy‐terminal peptide related to PF4 have been reported to inhibit human and murine megakaryocytopoiesis. The growth of several megakaryoblastic cell lines: human erythroleukaemia cell line (HEL), Meg‐01 and Dami, was also inhibited by PF4 and a 13–24 carboxy‐terminal peptide related to PF4. We report that peptides corresponding to the 1–24 and 13–24 but not 1–13 carboxy‐terminal region of PF4 inhibit murine megakaryocytopoiesis both in vivo (5 μg/inj) and in vitro (2.5 and 5 μg/ml). Moreover, such an inhibitory activity of PF4‐related peptides is abrogated by heparin (5 IU/dish). These overall data indicate that carboxy‐terminal PF4‐related peptides retain the inhibitory effect of PF4 on both murine single MK and CFU‐MK in vivo and in vitro by acting on an early stage of megakaryocytopoiesis and strongly suggest that the inhibitory activity of the multi‐functional PF4 might be localized in a short carboxy‐terminal region which might include, in part, the PF4 heparin binding domain.