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TGF-beta1 drives and accelerates erythroid differentiation in the epo-dependent UT-7 cell line even in the absence of erythropoietin.

Abstract：

OBJECTIVE:TGF-beta1 is a powerful inhibitor of erythropoiesis. However, its mechanisms of action are not fully elucidated yet at the cellular level. In this work we have studied the effects of TGF-beta on UT-7 cell survival, proliferation and differentiation. MATERIALS AND METHODS:UT-7 cell line is strictly dependent on growth factors for cell survival, growth, and differentiation. Epo (2 U/mL) induces erythroid differentiation as assessed by up regulation of glycophorin A and the presence of 5%-10% benzidine positive cells (BPC). In contrast, even in the presence of Epo (2 U/mL), GM-CSF (1 ng/mL) inhibits erythroid differentiation. RESULTS:When UT-7 cells were switched from GM-CSF to Epo, TGF-beta1 (2 ng/mL) induced a rapid (3 days [Epo+TGF-beta1] vs 8 days [Epo]) and marked erythroid differentiation (80% [Epo+TGF-beta1] vs 10% [Epo] BPC) including Hemoglobin A synthesis (HbA/HbF ratio of 1 [Epo] vs 4 [Epo+TGF-beta1]). In the presence of GM-CSF, although to a lesser extent, TGF-beta1 induced erythroid differentiation (40% BPC). This effect was not a consequence of TGF-beta1-induced apoptosis because, in the presence of Epo or GM-CSF, apoptosis occurred only at day 8 or 10, respectively. Moreover, although SCF inhibited apoptotic effect of TGF-beta1, SCF+TGF-beta1+Epo was the best combination to give rise to the highest number of hemoglobinized cells. We further demonstrated that induction of erythroid differentiation by TGF-beta1 was not due to an autocrine loop involving Epo/Epo-R or to a prolongation of the G1 phase of the cell cycle. CONCLUSION:Taken together, these data suggest that TGF-beta1 is an inducer of erythroid differentiation, even stronger than Epo at the cellular level.

journal_name

Exp Hematol

journal_title

Experimental hematology

authors

Zermati Y,Varet B,Hermine O

doi

10.1016/s0301-472x(99)00155-1

keywords:

subject

Has Abstract

pub_date

2000-03-01 00:00:00

pages

256-66

issue

3

eissn

0301-472X

issn

1873-2399

pii

S0301-472X(99)00155-1

journal_volume

28

pub_type

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