Transgenic expression of HuR increases vasogenic edema and impedes functional recovery in rodent ischemic stroke

Academic Article


  • Background and purpose Ischemic stroke produces significant morbidity and mortality, and acute interventions are limited by short therapeutic windows. Novel approaches to neuroprotection and neurorepair are necessary. HuR is an RNA-binding protein (RBP) which modulates RNA stability and translational efficiency of genes linked to ischemic stroke injury. Methods Using a transgenic (Tg) mouse model, we examined the impact of ectopic HuR expression in astrocytes on acute injury evolution after transient middle cerebral artery occlusion (tMCAO). Results HuR transgene expression was detected in astrocytes in perilesional regions and contralaterally. HuR Tg mice did not improve neurologically 72 h after injury, whereas littermate controls did. In Tg mice, increased cerebral vascular permeability and edema were observed. Infarct volume was not affected by the presence of the transgene. Conclusions Ectopic expression of HuR in astrocytes worsens outcome after transient ischemic stroke in mice in part by increasing vasogenic cerebral edema. These findings suggest that HuR could be a therapeutic target in cerebral ischemia/reperfusion.
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    Author List

  • Ardelt AA; Carpenter RS; Iwuchukwu I; Zhang A; Lin W; Kosciuczuk E; Hinkson C; Rebeiz T; Reitz S; King PH
  • Start Page

  • 126
  • End Page

  • 131
  • Volume

  • 661