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tissue (Fig. 6.5) [37]. Similarly to A
2A
deficient mice, mice lacking the adapter
protein in the pathway of Toll-like receptors MyD88 heal at a markedly slower
rate than wounds in wild-type mice, showing delayed contraction, decreased and
delayed granulation tissue formation, and reduced new blood vessel density. The
A
2A
receptor agonist CGS21680 promoted wound closure and angiogenesis in wild
Fig. 6.5
Histological examination of representative sections of untreated and CGS-21680-treated
excisional wounds in wild-type mice and air pouch wall in wild-type and A
2A
receptor deficient
mice. (
a
) On day 3 after wounding, mice were killed and the wounds dissected out, embedded
in paraffin, and stained with H&E using standard techniques. Original magnifications
400 1:
Wild-type mouse treated with vehicle 2: Wild-type mouse treated with CGS-21680, arrows indi-
cate blood vessels containing erythrocytes. (
b
) Subcutaneous vesicles were formed on the backs
of wild-type and knockout mice by injecting 3 ml of steril air and were reinflated later with
1.5 ml of steril air two days. After 6 days, the mice were killed and the pouches dissected out.
The dissected pouches were fixed, embedded in paraffin, and stained with H&E using standard
techniques (
1
and
2
) or stained immunohistologically with a goat anti-Factor VIII antibody, visu-
alized by immunoperoxidase-mediated conversion of diaminobenzidine, and counterstained with
hematoxylin (
3
and
4
).
1:
Shown is a representative section from a pouch wall from a female wild-
type mouse (original magnification,
×
100).
2:
Shown is a representative section from a pouch wall
from a female A
2A
receptor knockout mouse (original magnification,
×
×
100).
3:
Shown is a repre-
sentative section from a pouch wall from a female wild-type mouse (same block as in
1
; original
magnification,
400).
4:
Shown is a representative section from a pouch wall from a female knock-
out mouse (same block as in
2
; original magnification
×
×
400). Reprinted from [37] with permission
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