Authors
Ching-Yi Lin, Hugh Hiunam Chan, Jason Lin, David Trent, Kenneth B Baker, Yu-Shang Lee
Published in
Brain research bulletin. Pages 112091. Aug 19, 2026. Epub Aug 19, 2026.
Abstract
Ischemic stroke is caused by obstruction of a blood vessel reducing blood supply to a specific brain region and is one of the leading causes of disability worldwide. The pathophysiology of ischemic brain damage involves the formation of glial scars that can further limit functional recovery. Inhibitory chondroitin sulfate proteoglycans (CSPGs) are the major components of glial scars, but there is little information regarding their expression and distribution in either the damaged brain or, secondarily, in the more distant cervical spinal cord region after the chronic ischemic stroke. Here, we used a preclinical photothrombotic model to induce ischemic stroke and immunohistochemistry to characterize the expression of various CSPGs and neuroinflammatory cells that may produce CSPGs in (1) the peri-infarct area, a potentially salvageable area surrounding the ischemic core, and (2) the white (corticospinal tract) and gray matter regions of the cervical spinal cord. Our results demonstrate upregulation of neuroinflammatory cells and CSPG molecules in the damaged brain and cervical spinal cord at two months post-stroke. Reductions in aggrecan+ perineuronal nets (PNNs) and increases in wisteria floribunda agglutinin (WFA)+ PNNs were identified in the lesional cortex. In the spinal cord, aggrecan levels were similar, but there was increased WFA+ intensity. In addition, reactive astrocytes and microglia were increased and colocalized with CSPGs, which are responsible for the generation of CSPGs to persistent chronic neuroinflammation post-ischemia stroke.
PMID:
42617923
Bibliographic data and abstract were imported from PubMed on 20 Aug 2026.
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