S
Svetlana M. Stamatovic
Researcher at University of Michigan
Publications - 38
Citations - 3673
Svetlana M. Stamatovic is an academic researcher from University of Michigan. The author has contributed to research in topics: Blood–brain barrier & Tight junction. The author has an hindex of 24, co-authored 31 publications receiving 3023 citations.
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Journal ArticleDOI
Brain endothelial cell-cell junctions: how to "open" the blood brain barrier.
TL;DR: The route and possible factors involved in BBB disruption in a variety of neuropathological disorders (e.g. CNS inflammation, Alzheimer’s disease, Parkinson's disease, epilepsy) are highlighted and proposed signal transduction pathways that may be involved inBBB “opening” are summarized.
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Potential role of MCP-1 in endothelial cell tight junction `opening': signaling via Rho and Rho kinase
TL;DR: It is suggested that a small GTPase Rho and Rho kinase have a pivotal role in MCP-1-induced junction disarrangement and contributes to increased brain endothelial permeability.
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Monocyte Chemoattractant Protein-1 Regulation of Blood–Brain Barrier Permeability:
Svetlana M. Stamatovic,Parvin Shakui,Richard F. Keep,Bethany B. Moore,Steven L. Kunkel,Nico van Rooijen,Anuska V. Andjelkovic +6 more
TL;DR: The results showed that MCP-1 induces a significant increase in the BBB permeability surface area product for fluorescein isothiocyanate (FITC)-albumin under in vivo conditions, particularly during prolonged exposure.
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Absence of the Chemokine Receptor CCR2 Protects Against Cerebral Ischemia/Reperfusion Injury in Mice
TL;DR: It is suggested that inhibiting the CCL2/CCR2 axis affects brain reperfusion outcome by reducing brain edema, leukocyte infiltration, and inflammatory mediator expression.
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Junctional proteins of the blood-brain barrier: New insights into function and dysfunction
TL;DR: This review summarizes the characteristics of brain endothelial tight, adherens and gap junctions and highlights structural and functional alterations in junctional proteins that may contribute to BBB dysfunction.