Ubp43 gene expression is required for normal Isg15 expression and fetal development
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BioMed Central
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Ubp43 gene expression is required for normal Isg15 expression and fetal development Lea A Rempel1,2, Kathleen J Austin1, Kenneth J Ritchie3, Ming Yan3, Meifeng Shen3, Dong-Er Zhang3, Luiz E Henkes4 and Thomas R Hansen*1,4 Address: 1Department of Animal Science, University of Wyoming, Laramie, Wyoming, 82071, USA, 2Currently Institute of Maternal-Fetal Biology and the Division of Cancer & Developmental Biology, Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, USA, 3Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA and 4Department of Biomedical Sciences, Animal Reproduction and Biotechnology Laboratory, Colorado State University, Fort Collins, Colorado 80523, USA Email: Lea A Rempel - [email protected]; Kathleen J Austin - [email protected]; Kenneth J Ritchie - [email protected]; Ming Yan - [email protected]; Meifeng Shen - [email protected]; Dong-Er Zhang - [email protected]; Luiz E Henkes - [email protected]; Thomas R Hansen* - [email protected] * Corresponding author
Published: 26 March 2007 Reproductive Biology and Endocrinology 2007, 5:13
doi:10.1186/1477-7827-5-13
Received: 19 January 2007 Accepted: 26 March 2007
This article is available from: http://www.rbej.com/content/5/1/13 © 2007 Rempel et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Isg15 covalently modifies murine endometrial proteins in response to early pregnancy. Isg15 can also be severed from targeted proteins by a specific protease called Ubp43 (Usp18). Mice lacking Ubp43 (null) form increased conjugated Isg15 in response to interferon. The Isg15 system has not been examined in chorioallantoic placenta (CP) or mesometrial (MM) components of implantation sites beyond 9.5 days post coitum (dpc). It was hypothesized that deletion of Ubp43 would cause disregulation of Isg15 in implantation sites, and that this would affect pregnancy rates. Methods: Heterozygous (het) Ubp43 mice were mated and MM and CP implantation sites were collected on 12.5 and 17.5 days post-coitum (dpc). Results: Free and conjugated Isg15 were greater on 12.5 versus 17.5 dpc in MM. Free and conjugated Isg15 were also present in CP, but did not differ due to genotype on 12.5 dpc. However, null CP had greater free and conjugated Isg15 when compared to het/wt on 17.5 dpc. Null progeny died in utero with fetal genotype ratios (wt:het:null) of 2:5:1 on 12.5 and 2:2:1 on 17.5 dpc. Implantation sites were disrupted within the junctional zone and spongiotrophoblast, contained less vasculature based on lectin B4 staining and contained greater Isg15 mRNA and VEGF protein in Ubp43 null when compared to wt placent
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