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BOR - Papers in Press, published online ahead of print May 30, 2007.
Biol Reprod 2007, 10.1095/biolreprod.107.062414
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BIOLOGY OF REPRODUCTION 77, 425–432 (2007)
DOI: 10.1095/biolreprod.107.062414
© 2007 by the Society for the Study of Reproduction, Inc.

Maternal Pentraxin 3 Deficiency Compromises Implantation in Mice1

Susanne Tranguch 4, Anindita Chakrabarty 5, Yong Guo 3 5, Haibin Wang 5, and Sudhansu K Dey 2 4 5 6

Departments of Cell & Developmental Biology,4 Pediatrics,5 and Pharmacology,6 Vanderbilt University Medical Center, Nashville, Tennessee 37232

ABSTRACT

Reduced litter sizes in mice missing pentraxin 3 (Ptx3) have been attributed to fertilization failure. However, our global gene expression studies showed high uterine Ptx3 expression at the implantation site in mice, suggesting its role in blastocyst implantation. We initiated molecular and genetic studies in mice to explore the importance of uterine Ptx3 in this process. We found that Ptx3 is expressed in a unique and transient fashion at implantation sites. With the initiation of implantation on midnight of Day 4 of pregnancy, Ptx3 is expressed exclusively in stromal cells at the site of blastocysts. On Day 5, its expression is more intense in decidualizing stromal cells, but it disappears on Day 6. The expression again becomes evident in the deciduum on Day 7, followed by a more robust expression on Day 8, particularly at the antimesometrial pole. From Day 9, with the initiation of placentation, Ptx3 expression becomes undetectable. These results suggest a role for PTX3 in implantation and decidualization. Indeed, deletion of Ptx3 results in both compromised implantation and decidualization. Interleukin 1B (IL1B), a known inducer of Ptx3, is also transiently expressed in stromal cells at the implantation site, suggesting that IL1B is an inducer of uterine Ptx3 expression. In fact, uterine Ptx3 expression follows that of Il1b induced by lipopolysaccharide treatment on Day 7 of pregnancy. Collectively, these findings provide evidence for an important role for PTX3 in implantation and decidualization. This study has clinical implications, since PTX3 is expressed in the receptive endometrium, and trophoblast cells influence decidual Ptx3 expression in humans.

embryo, implantation, pregnancy, uterus


FOOTNOTES

3Current address: Department of Animal Science and Technology, Beijing University of Agriculture, Beijing, China.

1Supported in part by National Institute of Child Health & Human Development grants HD 12304 (to S.K.D.) and HD050315 (to H.W.). S.T. is supported by a National Institutes of Health National Research Service Award individual pre-doctoral fellowship from the National Institute of Drug Abuse (F31 DA021062).

Correspondence: 2Sudhansu K. Dey, Department of Pediatrics, Division of Reproductive and Developmental Biology, Vanderbilt University Medical Center, MCN-D4100, Nashville, TN 37232-2678. FAX: 615 322 4704; e-mail: sk.dey{at}vanderbilt.edu




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R. M. Popovici, M. S. Krause, J. Jauckus, A. Germeyer, I. S. Brum, C. Garlanda, T. Strowitzki, and M. von Wolff
The Long Pentraxin PTX3 in Human Endometrium: Regulation by Steroids and Trophoblast Products
Endocrinology, March 1, 2008; 149(3): 1136 - 1143.
[Abstract] [Full Text] [PDF]




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Copyright © 2007 by the Society for the Study of Reproduction.