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Blood, 1 November 2005, Vol. 106, No. 9, pp. 3055-3057. Prepublished online as a Blood First Edition Paper on June 28, 2005; DOI 10.1182/blood-2005-02-0577. This Article Full Text (PDF) All Versions of this Article: 2005-02-0577v1 106/9/3055    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 Cheng, Q. Articles by Gailani, D. Search for Related Content PubMed PubMed Citation Articles by Cheng, Q. Articles by Gailani, D. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 10, 2005 Accepted June 17, 2005 The effects of intrinsic pathway protease deficiencies on plasminogen deficient mice Qiufang Cheng, Yong Zhao, William E Lawson, Vasiliy V Polosukhin, Joyce E Johnson, Timothy S Blackwell, and David Gailani* Department of Pathology, Vanderbilt University, Nashville, TN, USA Department of Medicine, Vanderbilt University, Nashville, TN, USA Department of Medicine, Vanderbilt University, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA Department of Pathology, Vanderbilt University, Nashville, TN, USA; Department of Medicine, Vanderbilt University, Nashville, TN, USA * Corresponding author; email: dave.gailani{at}vanderbilt.edu. Plasminogen (Plg) deficient mice experience wasting and have decreased longevity due to disseminated fibrin deposition. We generated mice with combined deficiencies of Plg and coagulation factor IX (fIX) or XI (fXI), to determine the effects on the Plg null phenotype. Mice lacking Plg and fIX (Plg-/-/fIX-/-) have lower mortality at age six months than Plg-/-/fIX+/+ mice (15% and 67%, respectively), and less severe wasting, consistent with the importance of fIX in fibrin formation. In contrast, combined Plg and fXI deficiency (Plg-/-/fXI-/-) reduces life span ( > 90% mortality at 6 months), and is associated with leukocyte infiltration of the lungs and pulmonary fibrosis. These abnormalities are not seen in Plg-/- or Plg-/-/fIX-/- animals. Activated fXI is thought to function primarily as a factor IX activator; however, our observation suggests that fXI may have functions in regulation of inflammation or tissue repair distinct from its role in coagulation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Gailani and T. Renne Intrinsic Pathway of Coagulation and Arterial Thrombosis Arterioscler Thromb Vasc Biol, December 1, 2007; 27(12): 2507 - 2513. [Abstract] [Full Text] [PDF]

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