Small GTPase RhoA and Its Effector Rho Kinase Mediate Oxygen Glucose Deprivation-Evoked In Vitro Cerebral Barrier Dysfunction | Zendy

Claire Allen | Zendy; Kirtiman Srivastava | Zendy; Ulvi Bayraktutan | Zendy

Open Access

Small GTPase RhoA and Its Effector Rho Kinase Mediate Oxygen Glucose Deprivation-Evoked In Vitro Cerebral Barrier Dysfunction

Author(s) -

Claire Allen,

Kirtiman Srivastava,

Ulvi Bayraktutan

Publication year - 2010

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.109.574939

Subject(s) - rhoa , microbiology and biotechnology , rho associated protein kinase , myosin light chain kinase , stress fiber , actin cytoskeleton , protein kinase c , blood–brain barrier , biology , medicine , focal adhesion , signal transduction , myosin , cytoskeleton , biochemistry , endocrinology , cell , central nervous system

Enhanced vascular permeability attributable to disruption of blood-brain barrier results in the development of cerebral edema after stroke. Using an in vitro model of the brain barrier composed of human brain microvascular endothelial cells and human astrocytes, this study explored whether small GTPase RhoA and its effector protein Rho kinase were involved in permeability changes mediated by oxygen-glucose deprivation (OGD), key pathological phenomena during ischemic stroke.

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