Expression of angiopoietin-2 and vascular endothelial growth factor in mice cerebral cortex after permanent focal cerebral ischemia.
OBJECTIVE
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.


CONCLUSIONS
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.
Wang
Ren-Gang
RG
Department of Pharmacology, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Zhu
Xing-Zu
XZ
D043925:Angiogenesis Inducing Agents / Q000096:biosynthesis* / Q000235:genetics; D042683:Angiopoietin-1; D042702:Angiopoietin-2; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D016228:Endothelial Growth Factors / Q000096:biosynthesis* / Q000235:genetics; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis* / Q000235:genetics; D008222:Lymphokines / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020794:Receptor Protein-Tyrosine Kinases / Q000096:biosynthesis / Q000235:genetics; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D011956:Receptors, Cell Surface / Q000096:biosynthesis / Q000235:genetics; D042764:Receptors, TIE; D020133:Reverse Transcriptase Polymerase Chain Reaction; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
D043925:Angiogenesis Inducing Agents; D042683:Angiopoietin-1; D042702:Angiopoietin-2; C467628:Angpt1 protein, mouse; D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; C105373:MEN1 protein, human; D008562:Membrane Glycoproteins; D009363:Neoplasm Proteins; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D020794:Receptor Protein-Tyrosine Kinases; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D042764:Receptors, TIE