Zobrazeno 1 - 10
of 55
pro vyhledávání: '"Thomas J, Podor"'
Autor:
Xiaozhen Wang, Joanna Leung, Theresa A. Deisher, Thomas J. Podor, Alexandra Kerjner, Heather L. Heine, Stéphane Y. Corbel, Nana Rezai, Fabio M.V. Rossi, Bruce M. McManus
Publikováno v:
Cardiovascular Pathology. 19:36-47
Granulocyte-colony stimulating factor (G-CSF) mobilizes progenitors from the bone marrow (BM) and into the circulation. In cardiac transplantation, G-CSF pretreatment of both donors and recipients has been found to improve cardiac function. The aim o
Autor:
J. R. Day, Marlene L. Rose, Gopal Ghimire, A. D. McCormack, John D. Smith, Hon S. Leong, Thomas J. Podor, Balakrishnan Mahesh
Publikováno v:
Journal of Leukocyte Biology. 83:263-271
Anti-vimentin antibodies (AVA) are asso- ciated with autoimmunity and solid organ transplan- tation, conditions associated with vascular disease, but their contribution to disease pathogenesis is un- known. Here, we have examined interactions be- twe
Autor:
Darya Dabiri, Alexandra Kerjner, Bruce M. McManus, Thomas J. Podor, Fabio M.V. Rossi, Nana Rezai, Stéphane Y. Corbel
Publikováno v:
Laboratory Investigation. 85:982-991
Currently, there is intense debate regarding the origin of reparative cells in injured hearts and vasculature. To determine the contribution of recipient bone marrow (BM)-derived cells to the regeneration of cells in the vasculature of transplanted h
Publikováno v:
Artificial Organs. 28:142-151
Adult bone marrow-derived stem/progenitor cells have traditionally been considered to be tissue-specific cells with limited capacity for differentiation. However, recent discoveries have generated tremendous excitement regarding possible applications
Autor:
Jonathan C. Choy, Bobby Yanagawa, Bruce M. McManus, John C.K. Lai, Thomas J. Podor, David J. Granville, David C. Walker
Publikováno v:
Cardiovascular Toxicology. 3:269-282
Atheromatous diseases are lipid and cell-rich vascular disorders that include coronary artery disease (CAD), transplant vascular disease (TVD), and restenosis. Considering the inflammatory nature of these diseases, cytotoxic immune mechanisms such as
Autor:
Philip D. Walton, Cynthia B. Peterson, David H. Farrell, Stephanie Campbell, Thomas J. Podor, Jeffrey I. Weitz, Paul A. Chindemi, Denise M. Foulon
Publikováno v:
Journal of Biological Chemistry. 277:7520-7528
Vitronectin is an abundant plasma protein that regulates coagulation, fibrinolysis, complement activation, and cell adhesion. Recently, we demonstrated that plasma vitronectin inhibits fibrinolysis by mediating the interaction of type 1 plasminogen a
Autor:
Richard C. Austin, Davindra Singh, Ghislain Boudreau, Richard F. Davies, Robert S. McKelvie, Thomas J. Podor, Jeffrey I. Weitz, Paul A. Chindemi, Denise M. Foulon
Publikováno v:
Journal of Biological Chemistry. 277:7529-7539
Type 1 plasminogen activator inhibitor (PAI-1), the primary inhibitor of tissue-type plasminogen activator (t-PA), is found in plasma and platelets. PAI-1 circulates in complex with vitronectin (Vn), an interaction that stabilizes PAI-1 in its active
Publikováno v:
Journal of Biological Chemistry. 275:25402-25410
Plasminogen activator inhibitor-type 1 (PAI-1) is the primary inhibitor of endogenous plasminogen activators that generate plasmin in the vicinity of a thrombus to initiate thrombolysis, or in the pericellular region of cells to facilitate migration
Autor:
Stephen G. Shaughnessy, Thomas J. Podor, Jack Hirsh, José C.O Ribau, Thomas J. Venner, Edward Young
Publikováno v:
Thrombosis Research. 96:373-381
The binding of unfractionated heparin to endothelium is thought to be responsible for the rapid and saturable phase of unfractionated heparin clearance. Thrombin can induce endothelial cells to express and/or secrete a number of heparin binding prote
Autor:
J. I. Weitz, Jun Li, Sudesh K. Sood, S. I. Pfeifer, Thomas J. Podor, P. A. Outinen, Sushmita Pamidi, Richard C. Austin
Publikováno v:
Blood. 94:959-967
Alterations in the cellular redox potential by homocysteine promote endothelial cell (EC) dysfunction, an early event in the progression of atherothrombotic disease. In this study, we demonstrate that homocysteine causes endoplasmic reticulum (ER) st