Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
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BIOLOGY OF REPRODUCTION 78, 1–1 (2008)
DOI: 10.1095/biolreprod.107.066837
© 2008 by the Society for the Study of Reproduction, Inc.

Highlights

Mutant mice provide keys to decidualization and maintenance of pregnancy. Mice lacking interleukin 11 receptor alpha (IL11RA) because of a null mutation are infertile due to defective decidualization and uncontrolled trophoblast invasion and the absence of decidual proteinase inhibitors. Furthermore, decidua are smaller in uteri of pseudopregnant Il11ra-null mice in the absence of trophoblast cells. On p. 127, Li and co-workers report that defective decidualization in the mutant mice is due to dysregulation of key molecules involved in decidual cell growth and differentiation. Specifically, they found down-regulation of expression of cyclin D3 and BIRC5 (formerly known as survivin) in Il11ra-null mice while, on the other hand, IL11 increased expression of cyclin D3 and the cell differentiation factor CDKN1A (p21). Thus, the mutant mice have revealed that targets of IL11 include cyclin D3, CDKN1A, and BIRC5, and that these regulatory factors are essential for growth and differentiation of decidual cells and maintenance of normal pregnancy.

Feixue Li, Y. Sangeeta Devi, Lei Bao, Jifang Mao, and Geula Gibori. Involvement of Cyclin D3, CDKN1A (p21), and BIRC5 (Survivin) in Interleukin 11 Stimulation of Decidualization in Mice. Biol Reprod 2008; 78: 127–133. Published online in BOR-Papers In Press 19 September 2007; 10.1095/biolreprod.107.063313





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