EGFL7 expression in various CNS pathologies. (A) Representative pictures of different human pathology specimens include (a) angioma, a vascular malformation without neoplastic potential associated with no or low levels of EGFL7 expression; (b) hemangioblastoma (World Health Organization grade I), a slowly growing neoplasm characterized by moderate EGFL7 levels; (c) necrotic meningioma exhibiting tissue remodeling and high levels of EGFL7; (d) angiosarcoma, a fast-growing neoplasm associated with strong EGFL7 expression and nonneoplastic lesions; (e) granulation tissue; and (f) infarct resorption characterized by very strong EGFL7 protein levels. Bar represents 50 µm. (B) Costaining of a human hemangiosarcoma with anti-EGFL7 and anti-PECAM (a blood vessel marker) antibodies revealed that most EGFL7 is detected in blood vessels. Bar represents 10 µm. (C) For statistical analysis, the endothelial MIB-1 score was used as ordinal scaled response variable and analyzed together with the ordinal explanatory variable (EGFL7 expression: low expression, n = 10; moderate expression, n = 3; strong expression, n = 4) using a contingency table followed by likelihood-ratio test (low vs moderate EGFL7 expression, *P = .002; moderate vs strong EGFL7 expression, **P = .0084; low vs strong EGFL7 expression, ***P = .0008). Statistical analysis was performed using JMP 8.0 software (SAS, Cary, NC). (D) qRT-PCR revealed a significant upregulation of EGFL7 in the penumbra of stroke 24 and 72 hours after cerebral ischemia induction using a reversible MCAO mouse model (mean ± SEM, n = 6, *P < .01, **P < .005). (E) Likewise, VEGF levels were maximally elevated 3 hours postinduction (mean ± SEM, n = 6, *P < .01). (F) Twenty-four hours postinduction of cerebral ischemia, EGFL7 expression was restricted to blood vessels in the stroke penumbra (G) but was not spotted in blood vessels of the contralateral hemisphere as detected by immunohistochemical staining using EGFL7- and PECAM-specific antibodies. Bar represents 50 µm.