CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 6, November/December 2011
318
AFRICA
artery after injury, followed by a gradual increase in staining
intensity. After the administration of AMD3100, an antagonist
against the interaction between CXCR4 and SDF-1
a
, the expres-
sion of CXCR4 mRNA and protein was significantly decreased.
The intensity of CXCR4-positive staining was also less and the
time to when CXCR4-positive staining occurred was delayed.
After three months, the two groups were no longer showing
CXCR4-positive staining, which may have been because the
interaction between SDF-1
a
and CXCR4 occurred only in the
early injury period.
Carotid artery hyperplasia was observed with H&E staining
after balloon injury. We found that compared with the control
group after one and three months, hyperplasia of the neo-intima
had occurred in groups S and A (
p
<
0.05 and 0.01). The degree
of intimal hyperplasia in group A was lower than in group S after
one month (
p
<
0.05), and the difference between the two groups
remained after three months (
p
<
0.05).
We therefore postulated that the expression of SDF-1
a
mRNA in the left common carotid artery was increased after
injury, leading to an elevated plasma level of SDF-1
a
, which
exerted chemotactic effects on the migration of CD34
+
CXCR4
+
cells into the injured tissues as a result of the concentration
gradient of SDF-1
a
. The deposited cells then took part in the
neo-intimal repair or even caused restenosis.
The results demonstrated that intimal repair was closely
associated with the interaction between SDF-1
a
and its recep-
tor CXCR4. The elevated plasma levels of SDF-1
a
after injury
recruited peripheral CD34
+
CXCR4
+
cells into the damaged
endothelium, thus leading to formation of the neo-intima. In the
injured artery, the expression of CXCR4 mRNA and protein,
as well as the CXCR4-positive staining in the neo-intima was
observed to be increased.
With an antagonist (AMD3100) against the interaction
between SDF-1
a
and CXCR4, the expression of CXCR4
mRNA and protein, as well as the CXCR4-positive staining was
decreased. H&E staining also showed that after the intervention
of AMD3100, the rat carotid artery neo-intimal thickness was
still more than the normal control group, but thinner than in
the non-intervention group. Therefore, we speculated that the
SDF-1
a
/CXCR4 axis played an important role in neo-intimal
proliferation.
Conclusion
In this study, we investigated short- and long-term changes in
the SDF-1
a
/CXCR4 axis in the rat common carotid artery neo-
intima after injury. More studies are required to explore the long-
term changes in neo-intimal proliferation after administration of
AMD3100, and the specific signalling pathway involved in the
SDF-1
a
/CXCR4 axis. This may provide useful information for
prevention of restenosis after PTCA or PCI.
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