Spinal cord injury induces a long-lasting upregulation of interleukin-1β in astrocytes around the central canal

Neuroscience. 2015 Jan 22:284:283-289. doi: 10.1016/j.neuroscience.2014.10.013. Epub 2014 Oct 19.

Abstract

Under inflammatory conditions, interleukin-1β (IL-1β) modulates neural stem cells at neurogenic niches. Here we show that spinal cord injury in rats increases IL-1β expression in astrocytes located around the spinal cord ependyma, a region that also holds a neurogenic potential. IL-1β increases from day 1 after lesion, reaches maximal levels between days 3 and 7, and declines from 14 days to low levels after 28 days. At the time of maximal expression, periependymal upregulation of IL-1β extends beyond 5 mm from the epicenter of the lesion both rostral and caudally. Since IL-1β controls proliferation and cell fate of neural stem/precursor cells, its modulation in periependymal astrocytes might create an appropriate environment for cell replacement after injury.

Keywords: contusion; cytokines; neural stem cell; neuroinflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism*
  • Disease Models, Animal
  • Gray Matter / metabolism
  • Interleukin-1beta / metabolism*
  • Male
  • Neural Stem Cells / metabolism
  • Rats, Wistar
  • Spinal Cord / metabolism*
  • Spinal Cord Injuries / metabolism*
  • Stem Cell Niche / physiology
  • Time Factors
  • Up-Regulation

Substances

  • IL1B protein, rat
  • Interleukin-1beta