Transgenic over-expression of slit2 enhances disruption of blood-brain barrier and increases cell death after traumatic brain injury in mice

Neurosci Lett. 2016 Sep 19:631:85-90. doi: 10.1016/j.neulet.2016.08.013. Epub 2016 Aug 10.

Abstract

Traumatic brain injury (TBI) is the leading cause of mortality and disability among male adolescents and young adults; and mild traumatic brain injury is the most common type of traumatic brain injury. The disruption of blood-brain barrier (BBB) plays an important role in brain trauma. Previously, we have found that slit2, a member of slit protein family, increases permeability of BBB. In the present study, we examined the role of slit2 in the pathogenesis of mild TBI in a mouse model of micro TBI. Rhodamine BandPI (PropidiumIodide) staining were used to detect the permeability of BBB and cell death, respectively. The leakage of Rhodamine B and cell death were significantly increased in Slit2-Tg mice than in C57 control mice after micro TBI. The present results suggest that over expression of slit2 plays a detrimental role in the pathophysiology of mild TBI.

Keywords: Blood brain barrier (BBB); Cell death; Micro traumatic brain injury (TBI); Silt2; Transgenic mice.

MeSH terms

  • Animals
  • Blood-Brain Barrier / metabolism*
  • Brain Injuries, Traumatic / metabolism*
  • Cell Death*
  • Disease Models, Animal
  • Intercellular Signaling Peptides and Proteins / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Nerve Tissue Proteins / metabolism*

Substances

  • Intercellular Signaling Peptides and Proteins
  • Nerve Tissue Proteins
  • Slit homolog 2 protein