Different expressions of AQP1, AQP4, eNOS, and VEGF proteins in ischemic versus non-ischemic cerebropathy in rats: potential roles of AQP1 and eNOS in hydrocephalic and vasogenic edema formation.
10.5115/acb.2011.44.4.295
- Author:
Jaehyun KIM
1
;
Yongwook JUNG
Author Information
1. Department of Anatomy, Dongguk University College of Medicine, Gyeongju, Korea. jungyw@dongguk.ac.kr
- Publication Type:Original Article
- Keywords:
Aquaporin 1;
Blood-CSF barrier;
eNOS;
Blood-brain barrier;
Brain edema
- MeSH:
Animals;
Aquaporin 1;
Blood-Brain Barrier;
Brain Edema;
Brain Injuries;
Capillary Permeability;
Choroid Plexus;
Edema;
Epithelium;
Hippocampus;
Hyponatremia;
Immunoglobulin G;
Infarction, Middle Cerebral Artery;
Neurons;
Nitric Oxide;
Nitric Oxide Synthase Type III;
Plasma;
Proteins;
Rats;
Vascular Endothelial Growth Factor A
- From:Anatomy & Cell Biology
2011;44(4):295-303
- CountryRepublic of Korea
- Language:English
-
Abstract:
In this study, expressions of aquaporin (AQP) 1, AQP4, endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor in blood-cerebrospinal fluid (CSF) barrier and blood-brain barrier (BBB) are examined in rat choroid plexus and peri-infarcted hippocampal formation (HF) following systemic hyponatremia (SH) and permanent middle cerebral artery occlusion (pMCAO). These events are thought to cause the development of hydrocephalic and vasogenic edemas. The importance of CSF overproduction and intact blood-CSF barrier during hydrocephalic edema formation is demonstrated by the high expression of AQP1 (329.86+/-10.2%, n=4 , P<0.01) and trapped plasma immunoglobulin G (IgG) in choroid plexus epithelium after 24 hours of SH. However, the increased eNOS expression in peri-infarcted HF (130+/-3%, n=4, P<0.01) and extravasation of plasma IgG into the extravascular compartment after 24 hours of pMCAO suggest that increased microvascular permeability, probably due to elevated levels of nitric oxide, leads to development of vasogenic brain edema via BBB breakdown. Based on these findings, the authors suggest that modulation of different protein expression, dependent on the type of brain edema, is required for primary (pMCAO) and secondary (SH) brain injuries to attenuate brain edema and neuronal degeneration.
