Cofilin translocation to the nucleus is a key feature of decidualization

Decidualization (D), the differentiation of stromal fibroblasts (SF) into decidual cells, is critical for pregnancy establishment. D requires the reorganization of the actin cytoskeleton that is governed by phosphorylation (P) of myosin light chain and actin dynamics. Manipulation of actin dynamics by jasplakinolide prevents D of human SF. Actin dynamics are regulated by actin‐binding proteins, one of which is cofilin. The activity of cofilin depends on its P, which is regulated by LIMK1 and LIMK2. D of human SF is associated with changes in the distribution and activity of the proteins of the LIMK‐cofilin pathway. D induced by a stimulus of embryonic origin, interleukin‐1β (IL‐1β) and steroid hormones (H), is accompanied by an upregulation of LIMK1, a downregulation of LIMK2 and the translocation of inactivated (phosphorylated) cofilin from the nucleus into the cytosol. On the other hand, D induced by an artificial stimulus cAMP (with H) is characterized by a significant decrease in phosphorylated cofilin and unchanged amounts of LIMK1 and LIMK2. Despite the differences in molecular mechanisms underlying the D induced by H alone, IL‐1β+H or cAMP+H, the most striking observation during D is the translocation of cofilin from the cytosol to the nucleus. Taken together, the stabilization of F‐actin significantly inhibits D; and the translocation of cofilin to the nucleus is a key feature of D. Supported by HD044713