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Prepublished online as a Blood First Edition Paper on August 21, 2003; DOI 10.1182/blood-2003-05-1467. This Article Full Text (PDF) All Versions of this Article: 2003-05-1467v1 102/13/4410    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Koseki-Kuno, S. Articles by Ichinose, A. Search for Related Content PubMed PubMed Citation Articles by Koseki-Kuno, S. Articles by Ichinose, A. Social Bookmarking                   What's this? Submitted May 9, 2003 Accepted July 24, 2003 Factor XIII A subunit-deficient mice developed severe uterine bleeding events and subsequent spontaneous miscarriages Shiori Koseki-Kuno, Mitsunori Yamakawa, Gerhard Dickneite, and Akitada Ichinose* Department of Molecular Patho-Biochemistry and Patho-Biology, Yamagata University School of Medicine, Yamagata, Japan Second Department of Pathology, Yamagata University School of Medicine, Yamagata, Japan Department of Preclinical Pharmacology and Toxicology, Aventis Behring, Marburg, Germany * Corresponding author; email: aichinos{at}med.id.yamagata-u.ac.jp. In order to understand the molecular pathology of factor XIII (XIII) deficiency in vivo, its A subunit (XIIIA)-knockout (KO) mice were functionally analyzed. Although homozygous XIIIA female KO mice were capable of becoming pregnant, most of them died due to excessive vaginal bleeding during gestation. Abdominal incisions revealed that the uteri of the dead mice were filled with blood and that some embryos were much smaller than others within a single uterus. A series of histological examinations of the pregnant animals suggested that massive placental hemorrhage and subsequent necrosis developed in the uteri of the XIIIA KO mice on day 10 of gestation. This was true regardless of the genotypes of fetuses. These results are reminiscent of spontaneous miscarriage in human female patients with factor XIII deficiency, and indicate that maternal XIII plays a critical role in uterine hemostasis and maintaining the placenta during gestation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. E. Iismaa, B. M. Mearns, L. Lorand, and R. M. Graham Transglutaminases and Disease: Lessons From Genetically Engineered Mouse Models and Inherited Disorders Physiol Rev, July 1, 2009; 89(3): 991 - 1023. [Abstract] [Full Text] [PDF] J. Cho and D. F. Mosher Enhancement of thrombogenesis by plasma fibronectin cross-linked to fibrin and assembled in platelet thrombi Blood, May 1, 2006; 107(9): 3555 - 3563. [Abstract] [Full Text] [PDF] M. Nahrendorf, K. Hu, S. Frantz, F. A. Jaffer, C.-H. Tung, K.-H. Hiller, S. Voll, P. Nordbeck, D. Sosnovik, S. Gattenlohner, et al. Factor XIII Deficiency Causes Cardiac Rupture, Impairs Wound Healing, and Aggravates Cardiac Remodeling in Mice With Myocardial Infarction Circulation, March 7, 2006; 113(9): 1196 - 1202. [Abstract] [Full Text] [PDF] S. M. Jobe, L. Leo, J. S. Eastvold, G. Dickneite, T. L. Ratliff, S. R. Lentz, and J. Di Paola Role of FcR{gamma} and factor XIIIA in coated platelet formation Blood, December 15, 2005; 106(13): 4146 - 4151. [Abstract] [Full Text] [PDF]

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