Molecular basis of cerebrovascular disease with protein tyrosine phosphorylation in brain capillaries and therapeutic strategies

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This study sought to determine the role of tyrosine phosphorylation of proteins in the pathophysiological alteration of the blood-brain barrier and subsequent brain injuries after stroke. This study demonstrates that the increase in the tyrosine phosphorylation of tight junctional protein occludin is linked to the disruption of tight junctions and the development of cerebral infarction after stroke and that the prostanoid EP1 receptor is involved in the tyrosine phosphorylation of occludin. In addition, this study suggests that protein tyrosine phosphorylation may be linked to the increase in the level of NADPH oxidase subunits, which are known as an important source of a reactive oxygen species, after stroke.