Activin A regulates trophoblast cell adhesive properties: implications for implantation failure in women with endometriosis-associated infertility.

Background: During implantation, the embryo adheres to the endometrium via cell adhesion molecules (CAMs) present on blastocyst trophectoderm and endometrial epithelial cells. CAMs, including integrins and extracellular matrix (ECM) ligands, are most likely regulated by hormones, cytokines and growth factors. We hypothesized first that activin A affects the adhesive properties of trophoblast cells and second that alterations in dimeric activin A levels in the uterine cavity could disrupt adhesion, thereby causing implantation failure.

Depletion of high-abundance serum proteins from human uterine lavages enhances detection of lower-abundance proteins.

Two-dimentional electrophoresis, 2-DE, of human uterine lavages demonstrated the abundance of serum proteins. Two methods of serum protein removal were assessed. Multiple affinity removal system was most effective in depleting abundant serum proteins.

A distinct cohort of the TGFbeta superfamily members expressed in human endometrium regulate decidualization.

Background: Successful blastocyst implantation requires the differentiation of human endometrial stromal cells (HESC), a process known as decidualization. Activin A, a transforming growth factor beta (TGFbeta) superfamily member, enhances HESC decidualization and localizes to decidual cells in human endometrium. Other TGFbeta superfamily members, including BMP2, BMP4, BMP7, GDF5, GDF8, GDF11, TGFbetas and Nodal, may also play a role during decidualization.

Interleukin 1 beta is induced by interleukin 11 during decidualization of human endometrial stromal cells, but is not released in a bioactive form.

Blastocyst implantation is dependent on the differentiation of endometrial stromal cells (ESC) into decidual cells. Decidualization of human ESC in vitro is enhanced by interleukin 11 (IL11), with associated changes in gene expression. Genes downstream of IL11 may provide targets for the treatment of implantation failure or the development of non-hormonal contraceptives.