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Anticancer Res ; 39(8): 4495-4502, 2019 Aug.
Article in English | MEDLINE | ID: mdl-31366551

ABSTRACT

BACKGROUND/AIM: In mice, fetal liver is the first tissue of definitive erythropoiesis for definitive erythroid expansion and maturation. ZFAT, originally identified as a candidate susceptibility gene for autoimmune thyroid disease, has been reported to be involved in primitive hematopoiesis and T cell development. The aim of this study was to examine whether or not Zfat is involved in definitive erythropoiesis in the fetal liver during mammalian development. MATERIALS AND METHODS: The role of Zfat during mouse fetal erythropoiesis in the fetal liver was examined using tamoxifen-inducible CreERT2 Zfat-deficient mice. RESULTS: Zfat-deficient mice exhibit moderate anemia with small and pale fetal liver through a decreased number of erythroblasts by E12.5. Apoptosis sensitivity in fetal liver erythroid progenitors was enhanced by Zfat-deficiency ex vivo. Moreover, Zfat knockdown partially inhibited CD71-/lowTer119- to CD71highTer119- transition of fetal liver erythroid progenitors with impairment in the elevation of CD71 expression. CONCLUSION: Zfat plays a critical role for erythropoiesis in the fetal liver.


Subject(s)
Antigens, CD/genetics , Erythropoiesis/genetics , Liver/growth & development , Receptors, Transferrin/genetics , Transcription Factors/genetics , Animals , Apoptosis/genetics , Cell Differentiation/genetics , Erythroid Cells/metabolism , Erythroid Cells/pathology , Fetal Development/genetics , Fetus , Gene Expression Regulation, Developmental , Gene Knockdown Techniques , Humans , Liver/metabolism , Mice , T-Lymphocytes/cytology , T-Lymphocytes/metabolism , Thyroiditis, Autoimmune/genetics , Thyroiditis, Autoimmune/pathology
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