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Stromelysin-1 (MMP-3)-Independent Gelatinase Expression and
Activation in Mice
H.R. Lijnen,
J. Silence,
B. Van Hoef, and
D. Collen
From the Center for Molecular and Vascular Biology, University of
Leuven, Leuven, Belgium.
A potential physiological role of stromelysin-1 (MMP-3) in the
expression or activation of gelatinase A (MMP-2) or gelatinase B
(MMP-9) in the wall of injured arteries was studied with the use of
homozygous MMP-3-deficient (MMP-3 /) mice. One week
after perivascular electric injury of the carotid or femoral artery in
wild-type (MMP-3+/+) or MMP-3/ mice,
70 kD and 65 kD proMMP-2 levels were enhanced by twofold to fourfold,
with corresponding increases of 20- to 40-fold for active 61 kD and 58 kD MMP-2, and of 10- to 80-fold for 94 kD proMMP-9. Active MMP-2
species represented approximately one third of the total MMP-2
concentration for both MMP-3+/+ and
MMP-3/ mice. Active 83 kD MMP-9 was not detected in
noninjured carotid or femoral arteries, whereas one week after injury
its contribution to the total MMP-9 level was 11% to 18% for
MMP-3+/+ and MMP-3/ mice.
Immunostaining of arterial sections confirmed enhanced expression of
both MMP-2 and MMP-9 after vascular injury. Double immunostaining
showed colocalization of MMP-9 with macrophages in the adventitia,
whereas MMP-2 was also detected mainly in the adventitia but failed to
colocalize with smooth muscle cells. Cell culture experiments confirmed
comparable ratios of active versus latent MMP-2 in skin fibroblasts and
smooth muscle cells derived from MMP-3+/+ and
MMP-3/ mice. Addition of plasmin(ogen) did not
significantly affect activation of proMMP-2. In
MMP-3+/+ and MMP-3/ macrophages,
comparable levels of 94 kD proMMP-9 were detected, and
plasmin(ogen)-mediated conversion to 83 kD MMP-9 was obtained in both
genotypes. These data thus indicate that proMMP-2 activation may occur
via a plasmin- and MMP-3-independent mechanism, whereas plasmin can
directly activate proMMP-9 via a MMP-3-independent mechanism.
Blood, Vol. 91 No. 6 (March 15), 1998:
pp. 2045-2053
© 1998 by The American Society of Hematology.
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