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Angiogenic Role of MMP‐2/9 Expressed on the Cell Surface of Early Endothelial Progenitor Cells/Myeloid Angiogenic Cells
Author(s) -
KanayasuToyoda Toshie,
Tanaka Takeshi,
IshiiWatabe Akiko,
Kitagawa Hiroko,
Matsuyama Akifumi,
Uchida Eriko,
Yamaguchi Teruhide
Publication year - 2015
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25002
Subject(s) - progenitor cell , angiogenesis , cell , matrix metalloproteinase , microbiology and biotechnology , in vivo , myeloid , biology , in vitro , endothelial stem cell , chemistry , cancer research , stem cell , biochemistry , genetics
Since the introduction of angiogenic cell therapy using early endothelial progenitor cells (EPCs), myeloid angiogenic cells (MACs) have been expected to be useful in treating ischemic diseases. In order to elucidate the angiogenic properties of MACs/EPCs, we clarified the characteristics of MACs as compared to M2 macrophages (Mϕs). Comparison of the gene expression profiles of MACs and late EPCs revealed that MACs expressed greater amounts of metalloproteinase (MMP)‐9. It should be noted that the profile of MMP‐2/9 expression on the cell surface of MACs was similar to that of M2 Mϕs, and that cell surface MMP‐2/9 might be an active form based on molecular size. In addition, the invasion of MACs was prohibited not only by MMP‐2/9 inhibitor, but also by the hyaluronidase treatment that caused the down‐regulation of MMP‐9 on the cell surface of MACs and inhibited their invasion activity. These results indicate that cell surface MMP‐2/9 plays an important role in the high invasion ability of MACs. The conditioned medium of both MACs and M2 Mϕs stimulated tube formation of endothelial cells in vitro. MACs caused an increase in vessel formation in in vivo models through the production of IL‐8. We propose that the role of MACs with cell surfaces expressing MMP‐2/9 is rapidly invading ischemic tissue. J. Cell. Physiol. 9999: 2763–2775, 2015. © 2015 Wiley Periodicals, Inc.