Increase in circulating endothelial cells correlates with vascular dysfunction caused by epileptic seizures

• Published in: The FASEB journal Vol. 20; no. 4; pp. A732 - A733
• Main Authors: Zimmermann, Aliz, Leffler, Charles W., Parfenova, Helena
• Format: Journal Article
• Language: English
• Published: Federation of American Societies for Experimental Biology 01-03-2006
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.20.4.A732-b

Circulating endothelial cells (CEC) are non‐hematopoetic mononuclear cells in the peripheral blood that are dislodged from vessel walls. The number of CEC has been shown to increase during pathological conditions accompanied by endothelial damage, such as cardiovascular diseases and inflammation. However, correlation between CEC and cerebrovascular insults has not been established. Epileptic seizures cause sustained vascular dysfunction as indicated by reduced reactivity of cerebral arterioles. We investigated if seizures cause endothelial sloughing from cerebral vessels and increase the number of CEC. Seizures were induced by iv. bicuculline administration in anesthetized and paralyzed newborn pigs. Venous blood samples were collected before, 1h, 2 h and 4 h after seizure induction. The mononuclear cell fraction was isolated from the whole blood by density centrifugation. CEC were identified by immunostaining for CD146, an endothelial cell‐specific membrane glycoprotein. Brain‐derived CEC (BCEC) were identified by double immunostaining for CD146 and GLUT‐1, the brain‐specific glucose transporter. In control blood, only a few CEC were detected. Seizures induced time‐dependent elevation in CEC, with the most notable increase in BCEC number occurring 4h after the seizure onset. These data indicate that epileptic seizures cause endothelial cells to dislodge from cerebral vessels and appear in circulating blood. The BCEC increase correlates with sustained postictal cerebral vascular damage. Therefore, detection of BCEC may be of clinical importance as a non‐invasive marker of cerebrovascular injury.