期刊
NEURON
卷 82, 期 3, 页码 603-617出版社
CELL PRESS
DOI: 10.1016/j.neuron.2014.03.003
关键词
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资金
- AHA [12BGIA11560014]
- NMSS [RG4673A1/1, RG3936A7/1, RG3936BG/1]
- NIH [1R01 HL116995-01, 1P01NS37520-08]
- Rita Allen Foundation
- Whitehall Foundation
- NIH (New Innovator Award) [1DP2NS083038]
- NIH (Cancer Center Core Grant) [2P30CA014195]
- Nakajima Foundation
- Mary K. Chapman Foundation
- Jesse and Caryl Philips Foundation
- Stanford University School of Medicine Dean's Fellowship
- Russell and Elisabeth Siegelman Foundation
- Bernard and Ronni Lacroute Foundation
- William Randolph Hearst Foundation
- Myelin Repair Foundation
Brain endothelial cells form a paracellular and transcellular barrier to many blood-borne solutes via tight junctions (TJs) and scarce endocytotic vesicles. The blood-brain barrier (BBB) plays a pivotal role in the healthy and diseased CNS. BBB damage after ischemic stroke contributes to increased mortality, yet the contributions of paracellular and transcellular mechanisms to this process in vivo are unknown. We have created a transgenic mouse strain whose endothelial TJs are labeled with eGFP and have imaged dynamic TJ changes and fluorescent tracer leakage across the BBB in vivo, using two-photon microscopy in the t-MCAO stroke model. Although barrier function is impaired as early as 6 hr after stroke, TJs display profound structural defects only after 2 days. Conversely, the number of endothelial caveolae and transcytosis rate increase as early as 6 hr after stroke. Therefore, stepwise impairment of transcellular followed by paracellular barrier mechanisms accounts for the BBB deficits in stroke.
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