CARDIOVASCULAR JOURNAL OF AFRICA • Vol 22, No 6, November/December 2011
316
AFRICA
tion models.
9
We speculated that, besides stem/progenitor cells
being involved in intimal repair, their abnormal implantation in
the neo-intima may be the main cause of vascular restenosis, in
which SDF-1, an important chemokine, plays a crucial role.
SDF-1, a small (~ 8–14 kDa) pro-inflammatory chemokine,
10
is the main regulator of cell trafficking and adhesion.
11
It binds
and activates a subset of G protein-coupled receptors with seven
transmembrane domains called CXCR4, which are expressed on
the surface of target cells.
12
Although CXCR7 is also the receptor
of SDF-1, CXCR4 is the only receptor known to have a definite
physical role in cell trafficking, and SDF-1 is the only physical
ligand for CXCR4.
The rat SDF-1 gene encodes three splice variants:
α
,
β
and
γ
. SDF-1
α
is mainly observed in the liver, spleen, kidney, heart,
brain and lung and SDF-1
β
in the liver, kidney, spleen and
thymus. SDF-1
γ
is predominately noted in the heart, lung, brain
and peripheral nerve system.
13
Although the levels of SDF-1
γ
in the heart are high, significant changes in the expression of
Fig. 4. A: In group S, the positive staining for CXCR4 was detectable one day after injury and lasted for at least one
month. Discontinuous brown spots were shown at the injured area. With time, the spots gradually fused to form a
brown line with a slowly enhancing intensity. B: In group A, the positive staining was observed four days after injury
and was sustained for one month, with a weak intensity when compared with that in group S.
A
S
0
(40 ×)
S
1d
(40 ×)
S
4d
(40 ×)
S
7d
(40 ×)
S
1m
(40 ×)
S
3m
(40 ×)
B
A
0
(40 ×)
A
1d
(40 ×)
A
4d
(40 ×)
A
7d
(40 ×)
A
1m
(40 ×)
A
3m
(40 ×)
