Noggin protects against ischemic brain injury in rodents

Jayshree Samanta1, Tord Alden, Kevin Gobeske

  • 1Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ill, USA.

Stroke
|December 19, 2009
PubMed
Abstract

Insights

Overexpressing noggin, an inhibitor of bone morphogenetic protein signaling, significantly reduced brain injury and motor deficits after stroke in mice. This neuroprotective effect involved increased microglia and oligodendrogenesis.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Ischemic Stroke Research

Background:

  • Bone morphogenetic proteins (BMPs) and their receptors are present in adult brains.
  • BMP expression increases after cerebral ischemia (stroke).
  • Noggin, a BMP signaling inhibitor, is also found in the brain, but its role in stroke is unknown.

Purpose of the Study:

  • To investigate the role of noggin in ischemic brain injury.
  • To determine if inhibiting BMP signaling affects stroke outcomes.

Main Methods:

  • Used transgenic mice engineered to overexpress noggin.
  • Induced permanent middle cerebral artery occlusion (MCAO) to model ischemic stroke.
  • Assessed infarct volume and motor function deficits.

Main Results:

  • Mice overexpressing noggin exhibited smaller infarct volumes and reduced motor deficits compared to wild-type controls.
  • Increased numbers of microglia (CD11b+, IBA1+) and oligodendroglial progenitors were observed in noggin-overexpressing mice 14 days post-MCAO.

Conclusions:

  • Genetic evidence shows noggin overexpression confers neuroprotection against ischemic stroke.
  • Noggin reduces brain injury by enhancing microglial activation and promoting oligodendrogenesis.