Premium
Ang‐2 and PDGF‐BB cooperatively stimulate human peripheral blood monocyte fibrinolysis
Author(s) -
Bezuidenhout Louise,
Bracher Mona,
Davison Glenda,
Zilla Peter,
Davies Neil
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1106687
Subject(s) - biology , matrix metalloproteinase , angiogenesis , wound healing , platelet derived growth factor receptor , angiopoietin , fibrinolysis , monocyte , platelet derived growth factor , microbiology and biotechnology , inflammation , growth factor , immunology , endocrinology , medicine , cancer research , receptor , vascular endothelial growth factor , biochemistry , vegf receptors
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.