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Tenascin-C induction exacerbates post-stroke brain damage

Bharath Chelluboina1, Anil K Chokkalla1,2, Suresh L Mehta1

  • 1Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|October 25, 2021
PubMed

Insights

Tenascin-C (TNC) knockdown reduced brain damage and inflammation after ischemic stroke in mice. This suggests TNC is a key mediator of secondary brain injury, offering a potential therapeutic target for stroke recovery.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Tenascin-C (TNC) is associated with cerebrovascular diseases, but its role in ischemic stroke pathology remains unclear.
  • Understanding TNC's function is crucial for developing new stroke therapies.

Purpose of the Study:

  • To investigate the effect of TNC knockdown on post-stroke brain damage.
  • To elucidate the mechanism of TNC action in ischemic stroke.

Main Methods:

  • Adult male and female mice underwent transient middle cerebral artery occlusion.
  • TNC siRNA or negative siRNA was administered intravenously post-reperfusion.
  • Motor function, infarct volume, blood-brain barrier (BBB) damage, and inflammation were assessed.

Main Results:

  • TNC siRNA treatment significantly reduced TNC protein expression.
  • Knockdown of TNC curtailed motor dysfunction, infarct volume, BBB damage, and inflammation.
  • These effects were observed in both male and female mice.

Conclusions:

  • TNC induction in the acute phase after stroke mediates post-ischemic inflammation and secondary brain damage.
  • TNC plays a sex-independent role in stroke pathology.
  • Targeting TNC may be a promising therapeutic strategy for ischemic stroke.
Keywords:
Matricellular proteinblood-brain barrierinflammationischemia-reperfusionneuroprotection

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