Nature Medicine
7, 324 - 330 (2001)
doi:10.1038/85471
Plasma fibronectin supports neuronal survival and reduces brain injury following transient focal cerebral ischemia but is not essential for skin-wound healing and hemostasis.Takao Sakai1, Kamin J. Johnson1, 3, 4, Michihiro Murozono2, 5, Keiko Sakai1, Marc A. Magnuson6, Tadeuz Wieloch2, Tobias Cronberg2, Atsushi Isshiki5, Harold P. Erickson4
& Reinhard Fässler11
Department of Experimental Pathology, Lund University, Lund, Sweden
2
Wallenberg Neuroscience Center, Lund University, Lund, Sweden
3
Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island, USA
4
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA
5
Department of Anesthesiology, Tokyo Medical University, Tokyo, Japan
6
Departments of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Tennesee, USA
Correspondence should be addressed to Reinhard Fässler reinhard.fassler@pat.lu.seFibronectin performs essential roles in embryonic development and is prominently expressed during tissue repair. Two forms of fibronectin have been identified: plasma fibronectin (pFn), which is expressed by hepatocytes and secreted in soluble form into plasma; and cellular fibronectin (cFn), an insoluble form expressed locally by fibroblasts and other cell types and deposited and assembled into the extracellular matrix. To investigate the role of pFn in vivo, we generated pFn-deficient adult mice using Cre-loxP conditional gene-knockout technology. Here we show that pFn-deficient mice show increased neuronal apoptosis and larger infarction areas following transient focal cerebral ischemia. However, pFn is dispensable for skin-wound healing and hemostasis.
|
