Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published online as doi:10.1189/jlb.1106687 on March 29, 2007

Published online before print March 29, 2007
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.1106687v1
81/6/1496    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bezuidenhout, L.
Right arrow Articles by Davies, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bezuidenhout, L.
Right arrow Articles by Davies, N.
(Journal of Leukocyte Biology. 2007;81:1496-1503.)
© 2007 by Society for Leukocyte Biology

Ang-2 and PDGF-BB cooperatively stimulate human peripheral blood monocyte fibrinolysis

Louise Bezuidenhout*, Mona Bracher*, Glenda Davison{dagger}, Peter Zilla* and Neil Davies*,1

* Cardiovascular Research Unit and
{dagger} Department of Hematology, University of Cape Town, Cape Town, South Africa

1 Correspondence: Cardiovascular Research Unit, Chris Barnard Building, University of Cape Town Medical School, Anzio Road, Observatory, 7925, Cape Town, South Africa. E-mail: neil.davies{at}uct.ac.za

Angiopoietin-2 (Ang-2) is a growth factor, which was identified originally as playing a critical role in vessel remodeling during angiogenesis. More recent evidence has indicated additional involvement in vascular homeostatic responses such as coagulation and inflammation, which are central to wound healing. We therefore determined whether a relationship existed between Ang-2 and monocytes, one of the initial cell types to be recruited to a wound, in the context of fibrin clot invasion. Ang-2 significantly increased monocyte invasion of fibrin in the presence of serum. In the absence of serum, it required a combination of Ang-2 and platelet-derived growth factor BB (PDGF-BB) to increase invasion by threefold. Furthermore, it was shown that the heightened invasion was dependent on serine proteases and matrix metalloproteinases (MMPs) and that the combination of Ang-2 and PDGF-BB increased urokinase plasminogen-activator receptor expression, as well as MMP-9 and membrane type 1 MMP expression. These data give further credence to the concept of Ang-2 as a key regulator of several essential phases of wound healing.

Key Words: wound healing • proteases • matrix metalloproteinases • invasion






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the Society for Leukocyte Biology.