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Updated: Jun 17, 2026

Quantification of Neurovascular Protection Following Repetitive Hypoxic Preconditioning and Transient Middle Cerebral Artery Occlusion in Mice
Published on: May 4, 2015
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.
Background And Purpose:
Bone morphogenetic proteins and their receptors are expressed in adult brains, and their expression levels increase after cerebral ischemia. The brain also expresses an inhibitor of bone morphogenetic protein signaling, noggin, but the role of noggin in ischemic disease outcome has not been studied.
Methods:
We used transgenic mice overexpressing noggin to assess whether inhibition of bone morphogenetic protein signaling affects ischemic injury responses after permanent middle cerebral artery occlusion.
Results:
Transgenic mice overexpressing noggin mice had significantly smaller infarct volumes and lower motor deficits compared to wild-type mice. CD11b(+) and IBA1(+) microglia along with oligodendroglial progenitors were significantly increased in transgenic mice overexpressing noggin mice at 14 days after permanent middle cerebral artery occlusion.
Conclusions:
These results provide genetic evidence that overexpression of noggin reduces ischemic brain injury after permanent middle cerebral artery occlusion via enhanced activation of microglia and oligodendrogenesis.
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.

