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Spatial Analysis of Neural Cell Proteomic Profiles Following Ischemic Stroke in Mice Using High-Plex Digital Spatial

Jessica M Noll1, Catherine J Augello2, Esra Kürüm3

  • 1Division of Biomedical Sciences, University of California-Riverside School of Medicine, 900 University Ave, Riverside, CA, 92521, USA.

Molecular Neurobiology
|September 23, 2022
PubMed
Summary

This study reveals distinct spatial proteomic profiles in the brain after ischemic stroke, identifying specific molecular changes in different injury zones. These findings highlight potential therapeutic targets for stroke by understanding spatiotemporal mechanisms.

Keywords:
AutophagyDigital spatial profileInflammationIschemiaProteomicsStroke

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Stroke is a leading cause of death and disability, with neuronal damage resulting from complex glia-neuron interactions.
  • Effective treatments require targeting the detrimental effects arising from these interactions post-stroke.

Purpose of the Study:

  • To investigate the spatial cellular and neuroinflammatory mechanisms early after ischemic stroke.
  • To utilize Nanostring Digital Spatial Profiling (DSP) technology to analyze proteomic changes in distinct brain regions.

Main Methods:

  • Photothrombotic middle cerebral artery occlusion (MCAO) in male C57bl/6 mice.
  • Analysis of ipsilateral hemisphere regions: ischemic core, peri-infarct tissues, and peri-infarct normal tissue (PiNT) compared to the contralateral hemisphere at 3 days post-ischemia.
  • Utilized Nanostring DSP technology and immunohistochemical markers (FJB, GFAP, Iba-1).

Main Results:

  • Distinct spatial proteomic profiles were identified in the ipsilateral hemisphere.
  • The core border showed increased neuronal death, apoptosis, autophagy, and neurodegenerative proteins, with decreased Map2 and NeuN.
  • Peri-infarct regions exhibited increased astrocytic, apoptotic, and neurodegenerative markers, including GFAP and hyperphosphorylated tau.

Conclusions:

  • Apoptosis and inflammation occur in distinct spatial domains following ischemic stroke.
  • Dysregulation of autophagic pathways may contribute to neurodegeneration in peri-infarct tissues.
  • Spatiotemporal identification of post-ischemic mechanisms can lead to precise therapeutic targets for stroke treatment.