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Blood, Vol. 94 No. 6 (September 15), 1999:
pp. 1961-1970
Transforming Growth Factor- 1 (TGF-1) Induces Thrombopoietin From
Bone Marrow Stromal Cells, Which Stimulates the Expression of TGF-
Receptor on Megakaryocytes and, in Turn, Renders Them Susceptible to
Suppression by TGF- Itself With High Specificity
Sumio Sakamaki,
Yasuo Hirayama,
Takuya Matsunaga,
Hiroyuki Kuroda,
Toshiro Kusakabe,
Takehide Akiyama,
Yuichi Konuma,
Katsunori Sasaki,
Naoki Tsuji,
Tetsuro Okamoto,
Masayoshi Kobune,
Katsuhisa Kogawa,
Junji Kato,
Rishu Takimoto,
Ryuzo Koyama, and
Yoshiro Niitsu
From the 4th Department of Internal Medicine, Sapporo Medical
University School of Medicine, Sapporo, Japan; and the Hokkaido
Prefectural Sapporo Kitano Hospital, Sapporo, Japan.
The present study was designed to test the concept that platelets
release a humoral factor that plays a regulatory role in megakaryopoiesis. The results showed that, among various
hematoregulatory cytokines examined, transforming growth factor- 1
(TGF-1) was by far the most potent enhancer of mRNA expression of
bone marrow stromal thrombopoietin (TPO), a commitment of lineage
specificity. The TPO, in turn, induced TGF- receptors I and II on
megakaryoblasts at the midmegakaryopoietic stage; at this stage,
TGF-1 was able to arrest the maturation of megakaryocyte
colony-forming units (CFU-Meg). This effect was relatively specific
when compared with its effect on burst-forming unit-erythroid
(BFU-E) or colony-forming unit-granulocyte-macrophage
(CFU-GM). In patients with idiopathic thrombocytopenic
purpura (ITP), the levels of both TGF-1 and stromal TPO mRNA were
correlatively increased and an arrest of megakaryocyte maturation was
observed. These in vivo findings are in accord with the aforementioned
in vitro results. Thus, the results of the present investigation
suggest that TGF-1 is one of the pathophysiological feedback
regulators of megakaryopoiesis.
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