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

Full Text via DOI: 10.1016/j.neulet.2017.09.062 PMID: 28982595 Web of Science: 000415912800022

Cited authors

  • Ardelt, Agnieszka A.; Carpenter, Randall S.; Iwuchukwu, Ifeanyi; Zhang, An; Lin, William; Kosciuczuk, Ewa; Hinkson, Cyrus; Rebeiz, Tania; Reitz, Sydney; King, Peter H.


  • 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.

Publication date

  • 2017

Published in


International Standard Serial Number (ISSN)

  • 0304-3940

Start page

  • 126

End page

  • 131


  • 661