Expression of angiopoietin-2 and vascular endothelial growth factor in mice cerebral cortex after permanent focal cerebral ischemia.
Abstract
AIM: To study the expressions of vascular endothelial growth factor (VEG F),
angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), Tie-1, and Tie-2 in C57BL/6 mouse
brain after permanent focal cerebral ischemia.
METHODS: The mRNA levels of VEGF, Ang-1, Ang-2, Tie-1, and Tie-2 were measured by
semiquantitative reverse transcription polymerase chain reaction (RT-PCR). The
protein express ions of VEGF and Ang-2 were determined by immunohistochemistry.
RESULTS: Low mRNA levels of VEGF, Ang-1, Ang-2, Tie-1, and Tie-2 were
constitutively expressed in the normal cortex of mouse. After middle cerebral
artery occlusion (MCAO), the expressions of VEGF, Ang-2, and Tie-2 mRNA were
dramatically increased in the infarcted cortex and the elevation was remained
through 7 d of ischemia. However, the levels of Ang-1 and Tie-1 mRNA were
unchanged in the infarcted cortex. Immunoreactivities of Ang-2 or VEGF were
hardly observed in the normal cortex. Ang-2 protein was evidently detected in the
infarct core 8 h after MCAO and in t he perifocal area 1 d after MCAO. Expression
of VEGF protein was elevated in the infarct core 2 h after MCAO and in the
perifocal area 1 d after MCAO. Immunoreaction was restricted to endothelial cells
and glial-like cells within the infarct core and perifocal area.
CONCLUSION: The expressions of An g-2 and VEGF are induced after focal cerebral
ischemia, which may contribute to the angiogenic response in the cortex of
ischemic brain.
Keywords:
angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), Tie-1, and Tie-2 in C57BL/6 mouse
brain after permanent focal cerebral ischemia.
METHODS: The mRNA levels of VEGF, Ang-1, Ang-2, Tie-1, and Tie-2 were measured by
semiquantitative reverse transcription polymerase chain reaction (RT-PCR). The
protein express ions of VEGF and Ang-2 were determined by immunohistochemistry.
RESULTS: Low mRNA levels of VEGF, Ang-1, Ang-2, Tie-1, and Tie-2 were
constitutively expressed in the normal cortex of mouse. After middle cerebral
artery occlusion (MCAO), the expressions of VEGF, Ang-2, and Tie-2 mRNA were
dramatically increased in the infarcted cortex and the elevation was remained
through 7 d of ischemia. However, the levels of Ang-1 and Tie-1 mRNA were
unchanged in the infarcted cortex. Immunoreactivities of Ang-2 or VEGF were
hardly observed in the normal cortex. Ang-2 protein was evidently detected in the
infarct core 8 h after MCAO and in t he perifocal area 1 d after MCAO. Expression
of VEGF protein was elevated in the infarct core 2 h after MCAO and in the
perifocal area 1 d after MCAO. Immunoreaction was restricted to endothelial cells
and glial-like cells within the infarct core and perifocal area.
CONCLUSION: The expressions of An g-2 and VEGF are induced after focal cerebral
ischemia, which may contribute to the angiogenic response in the cortex of
ischemic brain.