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A link between the interleukin‐6/Stat3 anti‐apoptotic pathway and microRNA‐21 in preimplantation mouse embryos
Author(s) -
Shen XingHui,
Han YoungJoon,
Zhang DingXiao,
Cui XiangShun,
Kim NamHyung
Publication year - 2009
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.21048
Subject(s) - biology , blastocyst , apoptosis , stat3 , microrna , embryo , microbiology and biotechnology , signal transduction , embryogenesis , gene , genetics
Signal transducers and activators of transcription‐3 (Stat3) plays a central role in interleukin‐6 (IL‐6)‐mediated cell proliferation by inhibiting apoptosis in a variety of cell types. MicroRNA‐21 (miRNA‐21), a ubiquitous miRNA, acts as an anti‐apoptotic factor that seems to be indirectly but strictly linked to Stat3. In order to determine whether the IL‐6 induced Stat3 anti‐apoptosis pathway is linked with miRNA‐21, we first determined the effects of recombinant mouse IL‐6 on Stat3 expression, mouse embryo viability, and the mRNA levels of apoptosis related genes and miRNA‐21 during mouse embryo development in vitro. Addition of 10 or 100 ng/ml of recombinant IL‐6 to the culture medium did not affect the developmental ability of 2‐cell stage embryos into blastocysts. However, total cell number was significantly increased and apoptosis was reduced in blastocyst stage embryos cultured in the presence of 100 ng/ml of recombinant IL‐6. Furthermore, addition of recombinant IL‐6 to the culture medium significantly increased the copy numbers of anti‐apoptotic miRNA‐21, up‐regulated Bcl2l1, and down‐regulated casp3. Similarly, the injection of mature miRNA‐21 into cells up‐regulated Bcl2l1 and down‐regulated casp3. These results suggest that the induction of the Stat3 anti‐apoptotic pathway by IL‐6 is linked to miRNA‐21 expression, which possibly results in the regulation of cell apoptosis in early mouse embryo development. Mol. Reprod. Dev. 76: 854–862, 2009. © 2009 Wiley‐Liss, Inc.