A novel role of Semaphorin3A on the increase of vascular permeability

 

High vascular permeability is closely related to the increase of neuronal damage and the loss of brain functions in stroke brain. To find out the therapeutic targets facilitate the development of clinical strategy for stroke, Hou et al. identified Semaphorin3A (Sema3A) as a critical factor mediates vascular permeability and contributes to ischemic brain damage. The article was published on Scientific Reports, recently.

 

The injection of recombinant Sema3A to mouse skin or into cerebral cortex led to an increase of vascular permeability in dose- and time-dependent manners which had similar degree with that caused by a known factor vascular endothelial growth factor receptors (VEGF). The function of Sema3A was confirmed by its effect on increasing endothelial monolayer permeability and disrupting F-actin stress fibre bundles in cultured endothelial cells, which can be suppressed by inhibiting Mical2, a F-actin modulator. Mechanically, Sema3A activates Mical2 by interacting with the neuropilin1/VEGFR1 receptor complex. In addition, deletion of Sema3A in mice significantly reduced vascular permeability and ischemia-induced brain damage. The findings demonstrated a previously unknown role of Sema3A in regulating celebrovescular permeability and provided a promising target for novel therapeutic strategy of ischemia-induced brain damage.

 

Reference:
Sci Rep. 2015 Jan 20;5:7890.

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