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Follistatin-like 1 attenuates differentiation and survival of erythroid cells through Smad2/3 signaling.

Abstract：

:Hematopoiesis is a complex process tightly controlled by sets of transcription factors in a context-dependent and stage-specific manner. Smad2/3 transcription factor plays a central role in differentiation and survival of erythroid cells. Here we report that follistatin-like 1 (FSTL1) treatment impairs hemin-induced erythroid differentiation and cell survival. FSTL1 differentially regulates transforming growth factor beta (TGF-β) and bone morphogenetic protein (BMP) signaling. Blockade of Smad2/3 signaling with the ALK5/type I TGF-βR kinase inhibitor, SB-525334, was efficacious for rescue of erythroid differentiation blockage and apoptosis. Reversely, activation of Smad1/5/8 signaling with BMP4 cannot rescue FSTL1-mediated erythroid differentiation blockage and apoptosis. Collectively, these data provide mechanistic insight into the regulation of erythropoiesis by FSTL1 signaling and lay a foundation for exploring FSTL1 signaling as a therapeutic target for anemia.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wu J,Dong Y,Teng X,Cheng M,Shen Z,Chen W

doi

10.1016/j.bbrc.2015.09.044

subject

Has Abstract

pub_date

2015-10-30 00:00:00

pages

711-6

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(15)30561-1

journal_volume

466

pub_type

杂志文章

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